MINISTRY OF HEALTH FROM REPUBLIC OF MOLDOVA

PUBLIC INSTITUTE OF STATE UNIVERSITY OF

MEDICINE AND PHARMACY ‘‘NICOLAE TESTEMITANU”
IMPLANT SURGERY CLINIC TEL-AVIV ISRAEL

FAHIM ATAMNI

LATERAL WALL SINUS FLOOR AUGMENTATION

STATE OF THE ART

CHISINAU, 2016

~1~
 Preface

Maxillary sinus augmentation occupies a respected part in clinical research since the first
publications by Philip Boyne in 1980. In the perusing 35 years, researchers, experts, clinicians
and inventors have produced more than 2000 scientific articles dealing with maxillary sinus
augmentation.
This book brings together the most recent scientific publications and the most updated innovative
clinical research with an emphasis on simplifying the surgical procedures of sinus grafting.
This book demonstrates the various approaches used for maxillary sinus augmentation, together
with recently adapted protocols based on the evidence.
The rational basis and specific clinical indications for each graft material are shown.
Both traditional and current techniques for maxillary sinus surgery are comprehensively
discussed with supporting reviews of large statistical power.
In the past 20 years, many excellent books on maxillary sinus augmentation and implant
dentistry have been published. What is evident is that there has not been enough focus on
possible complications that may be associated with this procedure. Complications are a “growing
problem” due to an increase in treating patients with dental implants.
The chapter on early and late complications addresses the various complications related to sinus
floor augmentation with respect to their etiology, prevention and treatment.
The review of current literature is of unique interest.
This book is envisioned to be a tremendous resource, with each chapter systematically focusing
on a specific issue that confronts clinicians in their daily practice.
The book begins with anatomy, physiology and pathology of the maxillary sinus, biology of
bone healing and osseointegration and goes on to cover diagnosis, patient evaluation, ENT-
assessment and surgery. This comprehensive text allows students, clinicians, experts, surgeons
and researchers to enter the world of modern bone grafting and implantology.
My hope is that this textbook will be used to improve the clinician's knowledge about maxillary
sinus augmentation.
Writing a scientific book is an exciting, and unforgettable experience, for several reasons. First
and foremost is to be part of the debate, interexchange and comparison of scientific innovations
that occurs in the scientific community.

Fahim Atamni

Reviewers
Dumitru Scerbatiuc, University Professor, State University, Chisinau, Moldova
Ofer Moses, University Professor, School of Dentistry, Tel-Aviv University

~2~
 Acknowledgement

I sincerely thank my teacher, Prof. Valantin Topalo, who taught me that research comes through
knowledge, dedication, discipline, professional ethics and a love of the scientific way of
thinking. My deepest gratitude goes to the lecturers of the State University of Medicine and
Pharmacy "Nicolae Testemitanu" from Republic of Moldova who welcomed me to their
university.
My thanks also go to the people who have supported this book to be published.
Special thanks go to Ofer Moses, a friend and expert in his field who with his wide horizon,
inspired, coordinated and encouraged my writing of this book.
Last but not least, my thanks to my wife Manal and my children, Nadin and Kinan, for
supporting me and accepting my absence, lack of attention and company.
Finally, my appreciation goes to all people who, thanks to their scientific contribution, have
supported the writing of this book that will contribute to improve the ultimate goal, our patient's
health.

Fahim Atamni

~3~
Author

Fahim Atamni, DMD, PhD

Director, Implant Surgery Clinic
Email: dr.atamni@gmail.com

1980-1984 Studied dentistry at the Johann Wolfgang Goethe University Frankfurt am

Main, Germany
1984: Licensed to practice dentistry in Germany
1984-1987 Doctoral Thesis Dr.med.dent. (Manga cum Laude) at the Johann Wolfgang
Goethe University Frankurt am Main, Germany
1985-1989 Specialty training in oral surgery at the Department of Oral and Maxillo-Facial
Surgery (Prof. Dr. Frenkel, Prof. Dr. Bitter) klinikum Johann Wolfgang
Goethe Univeristy, Frankfurt am Main, Germany
1989: Specialist certificate in oral surgery from the State Medical Board of
Registration of the Federal State Hessen, Germany
1988-1990 Clinical instructor and lecturer for undergraduate and postgraduate dental
students at the Department of Oral and Maxillo-Facial surgery klinikum Johann
Wolfgang Goethe University, Frankfurt am Main, Germany
2000: License for production of implant systems (Medi-Oss) from the Ministry of
Health, Medical Devices Department, Israel
2004-2016: Postdoctoral education in oral surgery - Dr. Habilitat, Department of Oral and
Maxillo-Facial surgery, Orthopedic Stomatology and Oral Implantology
Prof. Dr. Dr. Topalo, USMF "N. Testemitanu", Chisinau, Moldova

Clinical experience:
Author and co-author of over 40 Scientific Publications in the field of Maxillary Sinus Floor
Augmentation and alternative methods
Active member of the European Association for Osseointegration EAO
Several oral communications and poster presentations in the annual scientific meetings of the European
Association for Osseointegration EAO
Honorary Professor of the International Personal Academy
Member of the German Association of Oral Surgery
Member of the DGOI Deutsche Gesellschaft für Zahnӓrztliche Implantologie
Member of the Israeli Association of Oral Implantology
Member and lecturer of the Arab Dentist’s Association in Israel
Member and lecturer of the Palestinian Dentist’s Association
Lecturer of the Palestinian Oral and Maxillofacial Surgery Association
Member of the International Congress of Oral Implantologist ICOI

~4~
 CONTENTS

Preface 2
Acknowledgment 3
Author 4

1. PROPERTIES OF THE POSTERIOR MAXILLA RELATED TO DENTAL

IMPLANTOLOGY
1.1 The anatomic and physiologic features of the posterior maxilla 9
Morphology of the maxillary alveolar arch 11
Factors influencing alveolar morphology 13
Pterygomaxillary region 14
Surgical importance for implant placement 15
Mucosal tissues 16
Innervation and blood supply of the maxilla 17
1.2 Anatomy of the maxillary sinus 20
Anatomical variations and lesions of the maxillary sinus 30
Arterial vascularization of the maxillary sinus 35
Innervation of the maxillary sinus 43
Venous and lymphatic drainage 44
Maxillary sinus septa 45
1.3 Physiology of the maxillary sinus 51
The anatomy and physiology of the maxillary sinus membrane 54
The mystery of the maxillary sinus membrane 55
Mucosal thickening 56
1.4 Morphofunctional changes of the maxilla following tooth loss 69
Soft tissue changes after tooth loss 63
Sinus pneumaization 64
Classification of maxillary atrophy 69
1.5 Bone density 71

2. GENERAL CONCEPTS ON TISSUE INTEGRATION AND IMPLANT

OSSEOINTEGRATION
2.1 Osseointegration of dental implants 75
Surface properties of dental implants 78
The biologic process of implant osseointergration 81
Time sequence of implant osseointegration 84
Osseointegration of implants placed early post extraction 85
2.2 Bone regeneration, modeling and remodeling 87
2.3 Ridge preservation 90
2.4 Mechanisms of bone graft consolidation 95
2.5 General aspects of guided bone regeneration and sinus augmentation 100

~5~
3. PREOPERATIVE ASSESSMENT AND TREATMENT PLANNING FOR IMPLANTS
IN THE POSTERIOR MAXILLA
3.1 Clinical examination of patients with edentulous posterior maxilla 104
Medical history 104
Clinical examination 106
Treatment planning 109
Informed consent 112
3.2 Risk factors related to implantology
patient-related factors 112
Genetics 112
Systemic diseases 113
Osteoporosis, Diabetes mellitus, Xerostomia (Sjogren syndrome),
Ectodermal dysplasia 113
Local risk factors 114
Bone quantity, Bone quality, Keratinized mucosa, Gingival biotype,
Microbiologic factors 114
Factors involving a high risk 118
Periodontitis, Bone biomarkers, Acute sinusitis, Use of bisphosphonates 118
Factors involving a moderate risk 121
Bruxism, Smoking, Mucosal thickening of the sinus membrane, Pathologic
Alterations, Secondary sinus cavities, Unfavorable interarch relations,
The condition of the adjacent remaining teeth, Oral hygiene 121
3.3 Radiographic examination 129
Radiographic techniques 129
Intraoral periapical radiographs, Lateral (profile) radiography,
Panoramic radiographs 129
Computed tomography, Cone beam computed tomography (CBCT),
Microtomography 134
Clinical application of CT images in maxillary sinus surgery 138
3.4 Evaluation of bone density 140
Evaluation of bone density via CT-Images 140
Evaluation of bone density during implant site preparation 141
3.5 Evaluation of implant stability (IS) 142
Evaluation of Primary stability via tapping test 143
Evaluation of primary stability via insertion torque (IT) 143
Evaluation of implant stability using periotest device 144
Evaluation of implant stability using Osstell device (Implant Stability Quotient ISQ) 146
Evaluation of secondary (biologic) stability via reverse torque test (RTT) 150

4. IMPLANT PLACEMENT IN THE ATROPHIED POSTERIOR MAXILLA

THROUGH LATERAL WINDOW SINUS FLOOR AUGMENTATION
4.1 History of maxillary sinus grafting 154
4.2 Indications and contraindications for sinus floor augmentation 156
Indications for sinus augmentation 156
Contraindications for sinus augmentation 159
4.3 Diagnosis and treatment options 160

~6~
 Importance of ENT assessment in stratifying candidates for sinus floor elevation 161
Apprecial of needed bone volume 163
Maxillary sinus floor augmentation by lateral access and simultaneous implant
placement 165
Maxillary sinus floor augmentation by lateral access and delayed implant placement 171
4.4 Surgical approaches and techniques 181
Antrostomy techniques of the lateral wall 182
Elevated antrostomy 182
Complete antrostomy 183
Repositioning antrostomy 186
Double window antrostomy 194
Size and location of the lateral window 196
Presence of an artery 200
Piezoesurgery for sinus augmentation 204
Membrane elevation 208
Implant site preparation and implant installation 210
Grafting the sinus 213
Barrier membrane over the lateral window 215
Surgical technique for two-stage sinus augmentation 217
Surgical technique for local sinus augmentation 221
Reentry sinus augmentation 223
Sinus augmentation combined with horizontal guided bone regeneration (GBR) 227
Sinus augmentation combined with vertical augmentation 233
Sinus augmentation combined with molar extraction 238
Sinus augmentation combined with standard implantation 242
Managing septa 243
Postoperative considerations 245
Second Stage Procedure and Follow-up 246
Guidelines for choosing the proper surgical technique 247
4.5 Marginal bone loss (MBL) in augmented maxillary sinus 248
4.6 Apical bone loss (ABL) in augmented maxillary sinus 251
4.7 Bone grafting materials (BGMs) 256
Autogenous bone (AB) 257
Allograft 258
Xenografts 259
Alloplasts 261
Composite graft material 261
Plasma rich growth factors (PRGF) 262
Guidelines for choosing the proper grafting material 262

5. COMPLICATIONS IN LATERAL WINDOW SINUS FLOOR AUGMENTATION

SURGERY
5.1 Intraoperative complications 264
Schneiderian membrane Perforation (SMP) 264
Anatomical and technical factors, which implicate SMP 266

~7~
 Treatment 270
Prevention of perforation 273
Intraoperative Bleeding 274
Techniques to control bleeding 278
Recommendations 278
Perforations in the buccal flap 278
Injury to the infraorbital nerve (ION) 278
5.2 Postoperative complications 279
Sinus graft infection 279
Dome phenomenon 285
Clinical case presentations 286
Sinusitis following sinus augmentation 289
Treatment 290
Displacement and migration of implants into the maxillary sinus 294
Various mechanisms explain the migration 296
Treatment 297
Clinical case presentations 299
Prevention 300
Postoperative maxillary cyst 300
Accidental grafting of the nasal passage 301
Exfoliation of grafting material 301
Wound dehiscence 302
Peri-implantitis 302
Persistent idiopathic facial pain (PIFP) 303
Cholesterol granuloma 304
Benign paroxysmal positional vertigo 304

CONCLUSIONS 306
TERMINOLOGY AND DEFINITIONS OF USED TERMS 308
LIST OF ABBREVIATINS 315
REFERENCES 318

~8~
 1. PROPERTIES OF THE POSTERIOR MAXILLA RELATED TO DENTAL
IMPLANTOLOGY

INTRODUCTION AND BACKGROUND

Complete or partial maxillary posterior edentulism is very frequently encountered in
dentistry. These conditions occur 35 times more frequently than complete mandibular edentulism
opposing maxillary teeth [1]. Functional and aesthetic rehabilitation following tooth loss in the
posterior maxilla necessitating dental implant placement and implant-supported reconstructions
are widely accepted and well established in reconstructive dentistry [2].
The maxillary posterior edentulous region offers many challenging and unique conditions
in implant dentistry. The maxillary posterior region is many times involved in implant treatment
plans for supporting a removable or fixed prosthesis. Existing accepted treatment modalities make
procedures in the maxillary posterior region similarly predictable to any other intraoral region.
Due to local anatomical conditions, the posterior maxilla’s edentulous alveolar ridges may not be
favorable for placing implants. Implants are prosthetic device aids and therefore need to be placed
in perfect three dimensional anatomical locations. Simulations of natural anatomical contours are
important even if no tooth or root is existent in the alveolar process.
Successfully placing oral implants capable of supporting reconstructions needs a thorough
understanding of the physiologic and anatomic features of the maxilla, the maxillary sinus, the
morphofunctional changes of the maxilla following tooth loss, the anatomical manifestations of
different bone resorption patterns in the posterior maxilla, the character of the overlying soft tissues
and neurovascular structures. Knowledge of the anatomy is also needed to understand the
complications that may inadvertently occur during surgery, such as injury to nerves or blood
vessels, postoperative complications such as infections and the spread of infections caused by
implants in the head and neck region.

THE ANATOMIC AND PHYSIOLOGIC FEATURES OF THE POSTERIOR MAXILLA

The midface’s osseous foundation is formed by the zygomatic bones and paired maxillae
(Fig 1.1a). The two prominent zygomatic bones along with the vomer and palatine bones
contribute structurally to the maxilla, maxillary sinuses, and nasal cavity. The midface’s skeletal
architecture reflects the osseous response to the mastication forces. The maxilla consists of a
central bone body containing the maxillary sinus. The central bone body is pyramidal in shape
with four-sides. Its apex extends to the zygomatic process and the base forms the lower border of
the piriform aperture reaching to the nasal cavity. The four sides are:
1) The greater portion of the orbital floor established by the superior orbital side.
2) The greater portion of the facial skeleton created by the anteriolateral zygomatic side.
3) The surface and wall of the infratemporal fossa contributed by the posterior infratemporal side.
4) The inferior side projecting to the hard palate.
The maxillary alveolar arch is supported or buttressed by three pairs of vertical pillars transferring
masticatory forces to the cranial base. These buttresses are increased dense bone regions capable
of supporting nasal, oral and ocular endosseous implants.

~9~
 a b
Fig 1.1a: Frontal view of the midface formed by the paired Fig 1.1b: Lateral sinus wall and maxillary tuberosity.
maxillae and zygomatic bones.

The alveolar processs of the maxilla related to the anterolateral surface carries the incisors,
the canines, and the premolars (Fig 1.2a). Where as that of the posteriolateral surface carries the
molars and ends as the maxillary tuberosity. Intraorally it is possible to palpate the canine
eminence, the canine fossa, the maxillary tuberosity, and the hamular notch (Fig 1.2b).

a b
Fig 1.2a: View of incisors alveoli, the canine eminence and the Fig 1.2b: Lateral view of the maxillary tuberosity and the
canine fossa. hamular notch.

The vertical plate of the palatine bone articulates with the maxilla’s base. It additionally
has a pyramidal process that interposes between the pterygoid process of the sphenoid bone and
the maxillary tuberosity (Fig 1.3a). The median wall of the maxilla begins at the sharp edge of the
anterior nasal aperture and extends posteriorly, with a concavity that pounds the nasal fossa and
continues distal to the canine. It shapes the maxillary sinus’s medial wall and continues all the way
back to the maxillary tuberosity. The maxilla’s medial wall provides attachment to the vertical
plate of the palatine bone and to the inferior nasal concha. The opening of the maxillary sinus is in
the maxilla’s medial wall, close to the orbit’s floor. The diameter of the opening is decreased by
the uncinated process of the ethmoid bone which provides the superior and middle conchae of the
lateral nasal wall. The maxilla’s orbital plate forms the floor of the orbits and also the maxillary
sinus’s roof (Fig 1.3b).

~ 10 ~
 a b
Fig 1.3a: Caudal view of the palatine bone with the pyramidal Fig 1.3b: Frontal view of the orbital plate which forms the floor
process between the maxillary tuberosity and the pterygoid of the orbit and the roof of the maxillary sinus containing the
process. infraorbital canal.

The infraorbital nerve and vessels are found in the infraorbital canal, and the canal forms
the ridge that can be discerned in the sinus cavity.
The zygomaticomaxillary complex is composed of a portion of the maxilla and entire
zygomatic bone and contributes to the structure of the orbit and maxillary antrum (Fig 1.4b). The
zygoma or malar bone is the most prominent facial bone. It is also part of the composition of the
maxillary sinus’s lateral wall.
We use the term”the zygomatico-maxillary complex” to emphasize the region’s clinical
and surgical anatomy (Fig 1.4a). This term ensures that we understand the key elements for
planning diagnosis and surgical treatment.

a b
Fig 1.4a: View of the zygomatico-maxillary complex. Fig 1.4b: Lateral view of the posterior maxilla and the entire
zygomatic bone.

MORPHOLOGY OF THE MAXILLARY ALVEOLAR ARCH

Masticatory forces transmitted to the alveolus through the teeth and periodontal ligament
affect the osseous morphology of the dentoalveolar process. The maxillary posterior teeth are 5 to
10 degrees buccally inclined and oppose the mandibular posterior teeth, which are lingually
inclined. This transverse curvature of the dental arches, also referred to as the curve of Wilson,
should definitely be considered when placing posterior dental implants. With the resorption of the

~ 11 ~
alveolus, the discrepancy in arch width progressively worsens, making a normal occlusal
relationship difficult to maintain. The inclination of opposing dentition and the effect of
periodontal disease and prior occlusal trauma must be taken in consideration to ensure adequate
bone support when planning implantations. In contrast to the mandible, which possesses an
alveolar arch of cancellous bone supported by a dense basal bone foundation, the entire maxillary
arch is composed of cancellous or spongy bone extending superiorly to a thin plate of compact
bone forming the nasal floor anteriorly and the floor of the maxillary sinus posteriorly. In addition,
the maxillary alveolar arch generally has thin buccal/labial and palatal cortical plates (Fig 1.5a,b).

a b
Fig 1.5a: lateral view of the maxillary alveolar arch showing a Fig 1.5b: palatal view of the maxillary alveolar arch exhibiting
thin buccal plate a thin palatal plate.

Due to progressive bone resorption, the functional alveolar ridge may resorb on anatomic
structures making implant placement difficult. Laterally, buccinators muscle attachment and the
inferior extent of the zygomatic buttress may approximate the crest. Posteriorly, the hamular notch
may become less distinct following tuberosity resorption. Failure to recognize the altered anatomy
may lead to injury of vital structures during surgical dissection with subsequent damages.
Available bone height in the posterior maxilla is generally less predictable than in the anterior
region and pneumatization of the maxillary sinuses decreases bone height availability.
There is significant variation in the growth of the maxillary dentoalveolar ridge in the
vertical dimension and is a major variant in determining lower facial height [3]. The
dolichocephalic (long face) individual generally exhibits a deep palatal vault with a greater
alveolar arch height (Fig 1.6a). Conversely, the brachycephalic (short face) individual presents
with a shallow palatal vault and less alveolar height (Fig 1.6b).

~ 12 ~
 a b
Fig 1.6a: Anterior view of the Fig 1.6b: Anterior view of the
dolichocephalic (long face) individual. brachycephalic (short face) individual

In addition to having a decreased alveolar height, brachycephalic individuals exhibit

greater bite forces than dolichocephalic individuals. In edentulous patients, these compressive
forces might accelerate alveolar bone loss. Brachycephalic individuals initially present with less
alveolar bone height and subsequently present greater alveolar ridge resorption in the edentulous
sites. This is significant in that greater bite forces result in greater compressive forces that are
transmitted to the alveolar ridges in edentulous patients with implant supported prostheses or
complete dentures. The premolar/molar maxillary crests have a parabolic shape in the transverse
plane, with medium or low trabecular bone density and surrounded by a thin cortical bone layer.
In most cases, the width between the buccal and lingual cortical walls is great. Therefore, the
implant morphology could contribute to stabilize the implant.

FACTORS INFLUENCING ALVEOLAR MORPHOLOGY

Bone remodeling is a continuous physiologic process involving osteoclast activation, bone
formation, and bone resorption. The rates of these processes vary which affects the overall height
and density of the maxillary bone. Bone remodeling is influenced by many factors including age,
race, gender, nutritional status, systemic disease, medications, periodontal health, previous
prostheses, and developmental factors.
Systemic diseases, such as diabetes mellitus, can contribute to bone loss by compromising
the effectiveness of host defense mechanisms. This results in an accelerated progression of
periodontal disease. Hyperparathyroidism increases parathyroid hormone serum levels,
stimulating osteoclastic activity and resorption of both cortical and trabecular bone. Long-term
corticosteroid therapy can also decrease trabecular bone formation as a result of catabolic effects.
Steroids also compromise bone formation by lowering the amount of available calcium through
decreasing intestinal absorption and renal resorption of calcium. Other systemic disorders, such as
chronic nutritional deficiencies and osteoporosis, may also adversely affect the alveolar bone
density. Postmenopausal osteoporosis is common after the fifth decade exhibiting defects in
osteoblast function and physiological remodeling. Although all types of bone are affected by
systemic diseases, the cancellous bone with its high metabolic rate and trabecular morphology
increases the susceptibility of the maxillary edentulous to hormonal imbalances and osteoporotic
changes. This vulnerability is caused by increased surface area lined with vascular endosteum in
the trabecular bone as compared with the cortical bone. Although considerable losses in bone

~ 13 ~
density are commonly acknowledged, these changes may not be readily apparent on radiographs.
All the various factors affecting bone density and overall morphology should be carefully
considered during preoperative evaluation. In addition to the ongoing maxillary bone remodeling,
there is also potential for significant bone loss from the basal surface secondary to expansion of
the maxillary sinuses.
After tooth loss, ridge resorption invariably results as a shifting of the remodeling process
toward bone resorption according to Wolff’s law [4]. The reduction of the posterior maxilla seems
to be influenced by the duration of the edentulousness as well as osteoporotic changes [5].

PTERYGOMAXILLARY REGION
The pterygoid process, with its lateral and medial plates, projects downward from the body
and greater wing of the sphenoid bone. The inner surface of the two plates forms the pterygoid
fossa, the origin of the medial pterygoid muscle. The outer surface of the lateral pterygoid plate is
the origin of the inferior head of the lateral pterygoid muscle. Inferiorly, the medial plate forms a
slender hamulus to which the pterygomandibular raphe attaches. Anteriorly, the pterygoid process
abuts with the maxillary tuberosity and the pyramidal process of the palatine bone. Superiorly, this
bony union divides forming the pterygomaxillary fissure, which opens into the pterygopalatine
fossa (Fig. 1.7a,b).

a b
Fig 1.7a,b: Inferior/caudal view of the skull base illustrating the medial and lateral pterygoid plates. The pterygoid process abuts
with the pyramidal of the palatine bone and the maxillary tuberosity.

The pterygopalatine fossa contains the maxillary artery’s terminal portion, which diverges
into the posterior-superior alveolar artery (PSAA) and the infraorbital artery (IOA). Successful
management of hemorrhage from the maxillary artery may require direct transantral exposure and
ligation, or in severe cases, ligation of the external carotid artery. An additional source of
hemorrhage is the pterygoid muscle and the maxillary artery. Although the pterygopalatine fossa
and its contents appear remote on the dentate skull, the distance is markedly reduced in the atrophic
edentulous maxilla. Additionally, the implants placed in the pterygoid region are significantly
longer than those typically used in the maxilla, ranging from 13 to 18 mm in length. The potential
for hemorrhage must be considered when placing implants into pterygoid plates. Implants placed
in the maxillary tuberosity that engage the pterygoid process are generally directed medially,
posteriorly, and superiorly (Fig 1.8). The goal is to engage the pterygoid process while avoiding
the posterior-inferior extent of the sinus. Although it is important to maintain the proper orientation
of the implant within the occlusal table, overangulation in the medial direction risks injury to the
descending palatine neurovascular bundle within the perpendicular plate of the palatine bone

~ 14 ~
medially. When placing implants into the pterygoid process as described by Tulasne [6], the
implants engage the pterygoid process or plates and may enter the pterygoid fossa.

a b
Fig 1.8a,b: Illustration of an implant placed in the tuberosity and is engaged in the pterygoid process.

Hemorrhage associated with this technique is likely muscular (pterygoid muscles) or

venous (pterygoid plexus) in origin; both types are controlled by inserting the implant or applying
pressure.
To avoid possible complications, it is important to understand the anatomical structures
and the course of neurovascular structures in all phases of implant surgery.

SURGICAL IMPORTANCE FOR IMPLANT PLACEMENT

The lower half of the pterygomaxillary suture consists of three different structures: the
pyramidal apophysis of the palatine bone, the maxillary tuberosity, and the pterygoid apophysis of
the sphenoid bone [7]. According to Lee et al., the mean length of the pterygomaxillary suture, or
the height of the pyramidal process of the palatine bone, is 13.1 mm, and 83% of the cases show a
pyramidal apophysis of more than 10 mm height [8]. According to Rodriguez et al., the mean
length of the pterygomaxillary area is 22.5 +- 4.8 mm [9]. Pterygomaxillary implant placements
require meticulous knowledge of each patient’s unique anatomy (Fig 1.9). Some authors
recommend that pterygomaxillary implants be placed in the anteroposterior axis (sagittal view)
with a 45-degree angulation relative to the frankford plane [10]. Other authors recommend placing
the pterygoid implant vertically, with an angulation of about 70 degrees on the anteroposterior axis
[11].

a b

~ 15 ~
 c d
Fig 1.9a-d: Panoramic radiographs of unilaterally edentulous patients with pterygomaxillary implants after 5 years of
function.

The implant angulation recommended by those authors would allow the implant to fit
completely within the pterygoid bone and at the same time to imitate the angulation of the molars
[12]. Several authors have suggested placing the implant in a buccal direction, about 75 to 80
degrees relative to the frankfort plane and to the sagittal view [6,11]. Most of the palatine bone is
made of compact bone tissue. The angulation of the implant axis toward the palatine bone allows
us to use the palatal cortical bone to achieve a good primary stability, which would also improve
bone-implant contact (BIC). The width of the pterygomaxillary suture is influenced by the
pyramidal apophysis of the palatine bone (Fig 1.10). Some authors have recommended a
supracrestal placement of implants in the posterior regions to reduce bone resorption, because this
allows establishing a biologic width. Tulasne and others suggest placing implants no shorter than
13 mm in the pterygoid region, because this length increases primary stability, allows supracrestal
implant placement, and prevents damage to nearby vascular structures [6]. The verticalization of
the pterygoid implant’s long axis would allow it to reach the distal most bone area, minimizing the
horizontal forces over rehabilitation.

a b c
Fig 1.10: Schematic drawing showing the pterygomaxillary column where the pterygomaxillary implant is supposed to be placed
[11].

MUCOSAL TISSUES
The mucosal tissues associated with the maxillary alveolar and palatal bone include
masticatory and lining mucosa. Keratinized masticatory mucosa covers the alveolar ridge and hard
palate, whereas non-keratinized lining mucosa covers the vestibule, cheeks, uvula, soft palate, and
vassal portion of the alveolar process. Lining mucosa is composed of non-keratinized stratified

~ 16 ~
squamous epithelial tissue with a distinct submucosal layer of loose connective tissue containing
blood vessels, fat, and glandular components. It is the presence and composition of the submucosal
layer that determines the mobility of the overlying mucosa. In contrast to lining mucosa,
masticatory mucosa is generally immobile, and with the exception of the hard palate, generally
lacks a distinct submucosal layer. The masticatory mucosa covering the alveolar ridge
(mucoperiosteum) is bound firmly to the underlying periosteum by heavy collagenous bands
extending from the dense lamina propria into the periosteum without an intervening submucosal
layer. The transition from attached gingiva to alveolar lining mucosa on the buccal/labial surface
of the alveolus is defined by the mucogingival junction. With resorption of the alveolar ridge, the
mucogingival junction migrates crestally with a net loss of attached, immobile keratinized mucosa.
Implant placement into a severely resorbed ridge may necessitate a palatal or skin graft
vestibuloplasty or other graft procedures to regain adequate attached tissue buccally.
The maxillary mucoperiosteum often obscures underlying osseous deficiencies owing to
the proliferation of dense fibrous tissue in response to occlusal trauma or chronic inflammation.
This proliferative response is also seen in the posterior or tuberosity region with fibrous
hyperplasia distorting the contour of the underlying osseous ridge. Reduction of hyperplastic tissue
is often needed in regions where implants are being placed. The hard palate is lined with
keratinized masticatory mucosa and is frequently used as a donor site when keratinized tissue is
required. The median raphe separates the two lateral regions of the palate extending posteriorly
from the incisive papilla to the soft palate. The median raphe represents the fusion site of the
palatine processes, and in contrast to the lateral palatal regions, there is no submucosa. The tightly
bound mucoperiosteum is analogous to the attached mucosa of the alveolar ridge. The lateral
regions of the hard palate exhibit a distinct submucosal layer containing mostly adipose tissue
anteriorly and minor salivary glands posteriorly. This loose submucosal layer provides a cleavage
plane that facilitates palatal mucosal graft harvesting. The clinician must be familiar with the
characteristics of the different oral tissues to ensure an adequate margin of attached gingiva at the
implant site.

INNERVATION AND BLOOD SUPPLY OF THE MAXILLA

The maxillary nerve (V2) or second division of the trigeminal nerve innervates the
maxillary dentition and alveolar bone. Multiple superior alveolar nerves innervate the maxillary
dentoalveolar arch. The superior alveolar nerves are described as three divisions: posterior, middle
and anterior. The posterior-superior alveolar nerve consists of three branches that separate from
the maxillary nerve within the pterygoid palatine fossa. The three branches descend the maxilla’s
posterior wall and emerge from the pterygomaxillary fissure. Two of the branches typically enter
the bone of the posterior/lateral maxillary wall above the apices of the posterior-most molar. These
two are considered true dental branches extending anteriorly within the lateral wall of the maxilla
supplying the posterior teeth and periodontium, forming a plexus with the middle superior alveolar
nerve in the first molar-premolar region. A third branch of the posterior superior alveolar nerve
does not enter the bone but instead courses laterally innervating the posterior buccal gingiva. The
middle superior alveolar nerve is the most variable division of the superior alveolar nerves. The
middle superior alveolar nerve arises from the infraorbital nerve in the posterior orbital floor
coursing laterally and descending the lateral wall of the maxillary antrum, terminating in a plexus
over the premolar teeth with the anterior and posterior superior alveolar nerves (Fig 1.11).

~ 17 ~
 Fig 1.11: Innervation of the posterior maxilla [13]

The anterior superior alveolar nerve and artery originate from the infraorbital nerve and
artery within the middle-to-distal portion of the infraorbital canal. The anterior superior alveolar
nerve and artery course laterally along the floor of the orbit, then inferiorly and medially turn
across the anterior wall of the maxillary sinus, terminating in a plexus above the apices of the
anterior teeth. The superior alveolar nerves and arteries also contribute branches to the mucosa of
the maxillary sinus and portions of the nasal cavity. Due to their placement in the outer wall of the
maxillary sinus, the superior alveolar nerves are at risk for transection during antrostomy
procedures. The Caldwell-Luc approach enters the sinus through the canine fossa, frequently
transecting the branches of the anterior superior alveolar nerve and innervating the maxillary
anterior teeth. When operative complications necessitate accessing the sinus, it is often useful to
identify and avoid the larger neurovascular structures within the sinus wall. Innervation and blood
supply to the posterior buccal mucosa is by branches of the posterior superior alveolar nerve and
artery. Branches of the infraorbital nerve and artery supply the labial mucosa adjacent to the
maxillary premolar region. The buccal artery, a branch of maxillary artery, courses with the buccal
nerve. The palatal mucosa is posteriorly supplied by the greater palatine nerve and descending
palatine artery, which divide within the greater palatine canal forming the greater and lesser
palatine nerves and arteries. The lesser palatine neurovascular bundle emerges from the lesser
palatine canal supplying the soft palate, uvula, and palatine tonsils. The greater palatine
neurovascular bundle exits through the greater palatine foramen, which lies at the junction of the
hard palate and alveolus near the distal side of the second molar. The greater palatine nerve courses
anteriorly, innervating most of palatal mucosa except for the extreme anterior region, which is
supplied by the nasopalatine nerve emerging from the incisive foramen (Fig 1.12).

~ 18 ~
 Fig 1.12: The course of the greater palatine artery and nerve on the surface of the hard palate. Note the
nasopalatine nerve emerging from the incisive foramen [13].

The greater palatine artery courses anteriorly along with the greater palatine nerve,
supplying the palate and finally ascending the incisive canal and anastomosing with the septal
branches of the sphenopalatine arteries. Following resorption and subsequent palatal migration of
the anterior maxillary ridge, the incisive foramen may emerge from the crest of the residual ridge,
making its contents vulnerable to injury. The position of the greater palatine neurovascular bundle
should be considered as well when planning a palatal approach to the posterior alveolus or
harvesting a palatal mucosal graft. The nerves are accompanied by the superior alveolar arteries.
Blood supply to the maxillary alveolus is provided by the superior alveolar arteries and the
vessels that supply the mucosa of the nasal cavity, palate, buccal gingiva and maxillary sinus (Fig
1.13).

~ 19 ~
 Fig 1.13: The maxillary artery supplying the posterior maxilla, the course of the posterior superior alveolar
artery and infraorbital artery are well demonstrated [13].

ANATOMY OF THE MAXILLARY SINUS

An understanding of the maxillary sinus’s anatomy is essential for the success of this
fragile type of surgery and allows clinicians to prevent local bone necrosis while optimizing
regional healing via proper vascularization of the graft material [14]. There are four pairs of the
paranasal sinuses: frontal sinus, ethmoid sinus, sphenoid sinus, and the maxillary sinus (Fig 1.14).

a b
Fig 1.14a-b: Illustrate the four pairs of the paranazal sinusis

~ 20 ~
 Of these, only the maxillary sinus is of significant interest to implant dentistry. The
maxillary sinus was first illustrated and described by Leonardo Da Vinci in 1489 and later
documented by the English anatomist Nathaniel Highmore. Highmore was the first to describe the
clinical significance of the maxillary sinus, also known as the "antrum of Highmore," in his treatise
Corporis Humani Disquisito Anatomicain 1651, [15] (Fig 1.15a,b).

a b
Fig 1.15a: Leonardo Da Vinci in 1489 Fig 1.15b: Nathaniel Highmore in 1651

The maxillary sinus or antrum of Highmore lies within the maxillary bone body and is the
largest of the paranasal sinuses and the first to develop. Six bone walls that contain many structures
of concern during sinus graft surgery surround the maxillary sinus. Knowledge of these structures
is crucial for both preoperative assessment and post surgical complications. The maxillary sinus
has approximately 15 ml volume of air space, which occupies the body of the maxilla, ranging
between 4.5 and 35.2 cm2 with a mean size of 24 cm2 in males and a significantly lower average
of 16 cm2 in females [16]. The size of the maxillary sinus correlates significantly with the external
dimensions of the facial skeleton. In a study published in 1930, Dr Harry Nievert observed the
following: "It is truly fascinating to see how sinuses vary, just as faces do" [17]. This means that
the maxillary sinus can vary greatly in size, with sinus pneumatization increasing continuously
with advancing age and after tooth loss [18] (Fig 1.16).

a b
Fig 1.16a,b: Panoramic radiographs showing bilateral pneumatization of maxillary sinuses

The average dimensions of the maxillary sinus are 34mm anteroposteriorly, 25mm
transversely, and 33mm in height. When viewed from above in a transverse section, the sinus

~ 21 ~
appears triangular, with its base formed by the lateral wall of the nasal cavity and its apex
projecting into the zygomatic process of the maxilla. The maxillary sinus is a hypodense pyramidal
airspace occupying most of the maxilla, with clearly defined bony margins. It can exhibit
anatomical variations, such as asymmetry, antral septa, hypoplasia, and exostosis. The limits of
the maxillary floor are usually marked anteriorly by the first premolar and posteriorly by a small
recess posterior to the root of the third molar. The septa divide the sinus into two or more cavities
that can communicate [19].
The anterior wall corresponds to the facial surface of the maxilla and the posterior wall
to the infratemporal surface of the maxilla (Fig 1.17).

a b
Fig 1.17a: Frontal view of the anterior wall of the maxilla, notice Fig 1.17b: Clinical view of the anterior wall, access area to the
the canine eminence and molar eminence maxillary sinus.

c d
Fig 1.17c: Clinical view of prominent malar eminence Fig 1.17d: Clinical view of average malar eminence

The maxillary sinus’s roof is the orbital surface of the maxilla, which is approximately
twice as wide as the floor, formed by the alveolar process of the maxilla. The anterior wall of the
maxillary sinus consists of a thin, compact bone extending from the orbital rim to just above the
apex of the cuspid. With the loss of the canine, the anterior wall of the antrum may approximate
the crest of the residual ridge. Within the anterior wall and approximately 6 to 7 mm below the
orbital rim, with anatomic variants as much as 14mm from the orbital rim, is the infraorbital
foramen (Fig 1.18).

~ 22 ~
 a b
Fig 1.18a: Frontal view of the infraorbital foramen. Fig 1.18b: Lateral view of the infraorbital foramen.

The infraorbital nerve runs along the roof of the sinus and exits through the foramen. The
infraorbital neurovascular bundle lies on the superior wall directly and within the sinus mucosa.
The infraorbital canal is open towards the sinus in 14% of the population and thus in direct contact
with the sinus membrane. Because of the infraorbital canal’s superior location, it rarely presents a
concern for the implant surgeon. The anterior wall of the maxillary sinus may serve as a surgical
access during Caldwell-Luc procedures to treat preexisting or post-sinus graft, pathologic
conditions [20]. The superior wall of the maxillary sinus is bordered with the thin orbital floor.
The orbital floor runs inferiorly in a mediolateral direction and is convex into the sinus cavity. A
bony ridge is usually present in this wall that contains the infraorbital canal with the infraorbital
nerve and arteries.
The posterior wall of the maxillary sinus corresponds to the pterygomaxillary region,
which separates the maxillary sinus from the pterygopalatine fossa and is formed by the maxillary
tuberosity (Fig 1.18).

a b
Fig 1.19a: The pterygomaxillary region with the pterygopalatine Fig 1.19b: The pterygomaxillary region with the pterygoid
fossa and the maxillary tuberosity. process

The posterior wall usually has several vital structures in the region of the pterygomaxillary
fossa, including the internal maxillary artery, sphenopalatine ganglion, pterygoid plexus, and the
greater palatine nerve. The posterior wall should always be identified on the radiograph (Fig 1.20).

~ 23 ~
 a b
Fig 1.20a,b: The posterior wall is clearly visible on the panoramic radiograph (arrows).

It should be noted that pterygoid implants placed through the posterior sinus wall and into
this region might come near vital structures, including the maxillary artery. Therefore, a blind
surgical technique of placing a pterygoid implant through the posterior wall may have increased
surgical risk. Since pterygoid implants are often positioned in the third molar region, they are
preferred primarily when the third molar is needed for prosthetic reconstruction or when sinus
grafts are contraindicated and an available bone posterior to the antrum is present [20].
The medial wall of the sinus communicates with the lateral wall of the nasal cavity and is
the most complex sinus wall. There are three spaces created in the nasal cavity by the inferior,
middle, superior conchae. Each of these cavities is known as a meatus. The ostia of the frontal and
maxillary sinus drain into a groove located in the middle meatus, the infundibulum (Fig 1.22a,b).
On the nasal aspect, the lower section of the medial wall corresponds to the lower meatus and floor
of the nasal fossa. The upper aspect corresponds to the middle meatus. On the antral side, the
medial wall is vertical and smooth. The ostium is positioned high on the sinus’s medial wall
making passive drainage nearly impossible. An additional hindrance to effective drainage is the
configuration of the ostium. The ostium is not a simple orifice into the nasal cavity going through
the bony wall. This duct-like orifice measures 3.5 to 6.0 mm in length and 3.5 by 6.0 mm in cross
section and does not open directly into the nasal cavity but into the floor of a narrow triangular
space, the ethmoidal infundibulum. This infundibulum is demarcated by the lamina papyracea
laterally, by the uncinate process medially, and by the ethmoidal bulla posteriorly. It communicates
with the middle meatus of the nose through its nasal opening, the semilunar hiatus [21]. The
infundibulum is approximately 5 to 10 mm long and drains via ciliary action in superior and medial
directions. The sinus ostium is the main opening through which the maxillary sinus drains its
secretion via the ethmoid infundibulum through the hiatus semilunaris into the middle meatus of
the nasal cavity. The ostium is a 7-11mm long with 2-6mm wide elliptical aperture with a mean
surface area of 16.5mm [22]. The ostium emerges into the nasal cavity beneath the middle concha.
The dimensions of the opening are frequently reduced during infectious or allergic inflammatory
processes, which cause edema of the lining mucosa and partial or complete obstruction of the
ostium. Careful surgical technique must be employed to avoid introducing debris and pathogens
into the sinus, which may cause acute or chronic sinusitis. Introduction of foreign bodies (displaced
implants or graft particles) or other surgical debris may lead to a chronic suppurative infection
with obstruction of the ostium, requiring surgical debridement and reestablishment of drainage
[23] (Fig 1.21).

~ 24 ~
 a b
Fig 1.21a: Displaced implant in the maxillary sinus. Fig 1.21b: Displaced graft particles in the maxillary sinus.

Smaller, accessory or secondary ostia may be presented that are usually located in the
middle meatus posterior to the main ostium. The secondary ostia are of questionable physiologic
significance. However, it is important to know about this occurrence, since during an operation to
augment the maxillary sinus floor, the mucosa must not be detached up to this point. It has a non-
physiologic drainage port high on the medial wall that drains into the middle meatus of the nose.
The ostium is considered non-physiologic because it serves as an overflow drain rather than a
dependent complete drainage system. These additional ostia are usually the result of chronic sinus
inflammation and mucous membrane breakdown. They are present in approximately 30% of skulls
and range from a fraction of a millimeter to 0.5cm and are commonly found within the
membranous fontanelles of the lateral nasal wall. Fontanelles are usually classified as anterior
fontanelles or posterior fontanelles, depending on their relation to the sinus wall. They are
sometimes used to create additional openings into the sinus to treat chronic sinus infections.
Primary and secondary ostia may on occasion combine and form a large ostium within the
infundibulum [16] (Fig 1.22).

a b
Fig 1.22a: Natural ostium of the maxillary sinus (10). Fig 1.22b: Natural ostium is clearly visible in the nose cavity.

The lateral (buccofacial) wall of the maxillary sinus is formed by the posterior maxilla
and the zygomatic process. The lateral wall houses an endosseous anastomosis of the infraorbital
and posterior superior alveolar artery (Fig 1.23).

~ 25 ~
 a b
Fig 1.23a: The lateral wall houses an endosseous anastamosis of Fig 1.23b: Through the lateral window the intramembranous
the infraorbital and posterior superior alveolar artery. PSAA is clearly demonstrated.

The “Tatum lateral wall approach sinus graft procedure” uses this area for entrance into
the maxillary sinus [17] (Fig 1.24).

a b
Fig 1.24a: The lateral wall of the maxillary sinus is exposed. Fig 1.24b: The Tatum lateral wall approach sinus graft b
procedure uses this area for entrance into the maxillary sinus.

The wall’s thickness varies greatly from several millimeters in a dentate patient to less than
1 mm in an edentulous patient. The thickness of the lateral (buccofacial) wall also varies widely
among individuals, from 0.5 to 3.0mm, indicating that careful individual case consideration is
needed [24]. We should also be aware about significant variations between specific regions, such
as the first molar areas, where the wall is thinnest [25] (Fig 1.25a-j).

a b
Fig 1.25a: CT scan demonstrates a thick lateral (buccofacial) Fig 1.25b: Clinical view of separate thick lateral bony wall
wall

~ 26 ~
 c d
Fig 1.25c: Totally removed lateral bony window; note the Fig 1.25d: Clinical view of a thin lateral window; note the bluish
thickness of the bony lateral wall. looking sinus membrane

e f
Fig 1.25e:Thin lateral bony window is well demonstrated. Fig 1.25f: Totally separated think lateral bone plate designed for
replacement after grafting.

g h
Fig 1.25g: CT scan demonstrates a thin lateral bony window Fig 1.25h: A thick lateral wall is demonstrated after complete
antrostomy.

i j
Fig 1.25i: The thickness of the lateral (buccofacial) wall varies Fig 1.25j: Clinical view of average thickness of the lateral wall.
widely among patients, from 0.5 to 3 mm.

~ 27 ~
 Intact mucoperiosteum of the sinus wall is important in sinus augmentation procedures and
extra precautions should be taken in thick lateral walls. Yang et al. [26] found that the thinnest
area is above the maxillary first molar and maxillary second premolar, with a mean thickness of
1.2mm, whereas the wall was thickest in area of maxillary first premolar, between maxillary first
premolar and second premolar, and between maxillary first molar and maxillary second molar.
Neighboring structures such as the zygomatic buttress, the canine eminence, and the maxillary
tuberosity might influence topographic differences in thicknesses in the vertical and horizontal
direction, and hence, these anatomical sites which can be easily detected deserve special attention
during surgery (Fig 1.26a,b).

a b
Fig 1.26a: The lateral wall – notice the zygomatic buttress. Fig 1.26b: Prominent zygomatic buttress – notice the
topographic differences in thickness.

We can estimate the thickness of the buccofacial wall of the maxillary sinus vis CT-scan
to minimize the occurrence of a mucoperiosteal perforation during an osteotomy. The angle
formed by the lateral and the medial walls varies from 22 to 76 degrees with a mean angulation of
36 degree at the second premolar, 58 degree at the first molar and 48 degree at the second molar
[27].
The sinus floor includes the alveolar process of the maxilla and part of the hard palate.
The characteristics of the maxillary sinus floor have a mostly (53%) flat rather than an oblique
contour in the edentulous sites [28]. The floor in the edentulous posterior maxillae is normally
located about 1 cm below the floor of the nasal fossae and in adults with a full dentition,
approximately at the level of the nasal floor. The floor of the maxillary sinus is the strongest of the
bone walls surrounding the cavity, with various recessions and depressions near to the first molar
and premolar teeth. The sinus floor is in close relationship with the apices of the maxillary molars
and premolars (Fig 1.27a,b). Beginning with the first premolar tooth, the dental roots can protrude
into the maxillary sinus following the development of the secondary teeth. These teeth can be
covered by an osseous plate of varying thickness. Bony dehiscences at the apices of the roots can
also be found, such that the roots are covered only by the mucosa of the maxillary sinus.

~ 28 ~
b
 a
Fig 1.27a: The sinus floor – notice the palatal root of the molar Fig 1.27b: The sinus floor with bony dehiscence and the apices
protruding into the hard palate. of the root.

Consequently, surgery of the maxillary sinus may inadvertently result in the injury of the
dental roots. This close relationship of the premolar and molar teeth to the maxillary sinus also
explains complications involving the sinus of dental origin [21]. The teeth are usually separated
by the sinus mucosa by a thin layer of bone. However, occasionally, the teeth may perforate the
floor of the sinus and directly contact the sinus membrane. These perforations may remain for
many months after a tooth extraction and it is therefore, necessary to be extremely careful during
the elevation of the membrane from the exposed apices. The sinus floor is usually convex with its
lowest point around the first and second molars in 8%, its anterior border is located in the second
premolar, 58% in the first premolar, 33% in the canine, while 94% of cases its posterior border
can be found in the third molar [23].
A maxillary sinus classification with three categories (narrow, average, and wide) was
proposed [29]. This new sinus classification could add diagnostic and treatment planning values
to sinus augmentation procedures [29].
The maxillary sinus generally narrows in its anterior border in the premolar region. In the
mediolateral dimension, maxillary sinuses are divided into three categories: narrow, average, and
wide (Fig 1.28a-d).

a b
Fig 1.28a: CT scan demonstrates a wide maxillary sinus with a Fig 1.28b: CT scan demonstrates a wide maxillary sinus with a
thin lateral wall. thick lateral wall.

~ 29 ~
 c d
Fig 1.28c: CT scan demonstrates an average maxillary sinus. Fig 1.28d: CT scan demonstrates a narrow maxillary sinus with
a parallel wall sinus.

Possible implications for the different categories might include determining the easiness of
a sinus elevation procedure, calculation of the amount of bone grafts, and the selection of grafting
material and sinus augmentation approaches. For example, sinuses with average widths are optimal
candidates for a lateral window approach because of their easy access for membrane elevation. For
narrow width sinuses, the wall-off technique might be preferred to avoid difficulties in membrane
elevation from limited space. For wide-diameter sinuses, a crestal approach is indicated so that the
medial wall could be reached more easily. The sinus width at the usual lower boundary of the
lateral window osteotomy (average 2.3 mm from the floor of the sinus) is 9.0 (2.8) mm, with the
33rd and 67th percentile sinus width values being 7.6 and 9.9 mm, respectively. The mean sinus
width at the usual upper boundary of the lateral window osteotomy (15 mm from crest) is 16.0
(4.4) mm, with the 33rd and 67th percentile sinus width values being 14.0 and 17.3 mm,
respectively.
In the dentate individual, the bony walls of the sinus are usually thin, except for the anterior
wall and the alveolar ridge. In the edentulous individual, the alveolar bone has frequently atrophied
and may be only 1 to 2mm thick, making it unsuitable for an implant site without appropriate
grafting.

ANATOMICAL VARIATIONS AND LESIONS OF THE MAXILLARY SINUS

The maxillary sinuses are significant anatomic structures in dental practice. Therefore,
recognizing anatomic variation and lesions of the maxillary sinuses is required knowledge for
dental implant planning. The maxillary sinus can exhibit anatomic variations, such as
pneumatization, hypoplasia, antral septa, exostosis, ethmoid maxillary sinus, secondary ostium,
and Haller cells. In addition, the following maxillary sinus lesions, diseases and pathologies are of
considerable importance: Mucosal thickening ( ≥3mm), polypoid lesions (mucus retention cysts
and/or antrochoanal polyps), discontinuity of the sinus wall, air fluid level, bone thickening,
antrolith, sinus opacification, foreign bodies, and sinusitis [30].

Anatomical variations
The most common anatomic variation of the maxillary sinus is pneumatization which is
characterized by the maxillary sinus extending to the alveolar ridge, maxillary tuber, anterior
region, palate, zygomatic bone, and/or orbital region [31]. Antral septa are defined as a pointed
bone structure and maxillary sinus exostosis is defined as a rounded bone structure, both
originating from any maxillary sinus wall. Antral septa can cause difficulties when lifting the bone

~ 30 ~
plate and of the sinus membrane during sinus surgery. A rare but significant anatomical variation
of the maxillary sinus is called maxillary sinus hypoplasia (MSH). The hypoplastic sinus cavity is
much smaller than a normal cavity and frequently features considerable bony thickening of the
inferior and lateral walls. The etiology is uncertain, but some theorize that it is related to deficient
bone absorption or to the inability to adequately aerate the sinus cavity [32]. A history of childhood
facial trauma is not uncommon for those with MSH. Studies vary on MSH’s prevalence with
different studies reporting 4.8% [33] 2.1% [34], and 0.2% [35]. The maxillary sinus can become
hypoplastic during its embryological development or later due to trauma, iatrogeny, or structural
causes. The narrow infundibular passage associated with the absence of a natural ostium can cause
mucosal thickening of the hypoplastic sinus. Furthermore, MSH also causes lateral extension of
the lateral nasal wall, making surgical procedures difficult.

Maxillary sinus lesions

Antral pseudocysts are the most frequently encountered pathologies of the maxillary sinus
with an incidence of 1.4% to 9.6% in the general population (Fig 1.29). These cysts are classically
described as dome-shaped, sessile soft tissue elevations on the maxillary sinus that occur due to
accumulation of inflammatory exudates enclosed by loose connective tissue (Fig 1.30). Their
formation is generally asymptomatic and their pathogenesis is somewhat controversial [36].

Fig 1.29: Antral pseudocyst in the right maxillary sinus region 14-15.

a b
Fig 1.30a: Panoramic view of an antral pseudocyst. 1.30b: Ct slices demonstrate and antral pseudocyst.

The indications for maxillary sinus augmentation in the presence of antral pseudocyst are
also controversial. For example, Zicardi et al. [37] and Lin et al. [38] state that the existence of an
antral pseudocyst is a contraindication to sinus floor augmentation. In contrast, recent reports of

~ 31 ~
Mardinger et al. [36] and Kara et al. [39] state that antral pseudocysts are not a contraindication
for maxillary sinus floor augmentation but may cause membrane perforation during a sinus
elevation [40]. In the literature, different healing times (3 to 12 months) have been proposed for
sinus augmentation after removal of an antra pseudocyst to allow for the regeneration of new
respiratory ciliated epithelium. Increased membrane thickness generally occurs in the presence of
a pseudocyst and tearing of the sinus membrane is unusual in this situation. The presence of a
pseudocyst in the sinus is thought to be relevant to drainage-related factors, as it diminishes the
size of the sinus and may block it, causing retention of fluids that could result in sinusitis. However,
considering the large size of the antrum, the high position of the ostium, and especially the
increased size of pneumatized sinuses, antral pseudocysts (especially those of small size) are most
likely not going to disturb sinus drainage after sinus floor augmentation [37]. Considering the law
percentage and rate of postoperative sinusitis, maxillary sinus floor augmentation in the presence
of an antral pseudocyst would appear to be safe using either the lateral approach or an osteotome-
assisted technique. I recommend the aspiration of a pseudocyst during sinus floor augmentation to
decrease the cyst’s size and consequently to avoid blockage of the sinus drainage (Fig 1.31).

a b
Fig 1.31a: Aspiration of pseudocyst. Fig 1.31b: The aspirated fluid of the pseudocyst.

The paranasal sinus mucosa normally shows 1mm of thickening [31]. However, when
inflamed, there can be an increase of 10- to 15-fold in the sinus mucosa thickness [31]. Mucosal
thickening is characteristic feature in both acute and chronic sinusitis, and mucosal thickening >3
mm is usually considered pathologic (Fig 1.32) [31,41].

Fig 1.32: Mucosal thickening of about 4mm.

Mucosal thickening, air–fluid level, and sinus opacification are characteristic findings of
an inflammatory sinus disease. The only distinctive feature of acute sinusitis is the air-fluid level,

~ 32 ~
whereas the characteristic feature of chronic sinusitis is the bone thickening of the maxillary sinus
wall [42]. Sinus opacification and the air-fluid level are the most specific signs of bacterial
rhinosinusitis [43]. Discontinuity of the sinus floor is usually accompanied with mucosal
thickening > 3mm [44] (Fig 1.33a-e).

a b
Fig 1.33a: Discontinuity of the sinus floor. Fig 1.33b: Discontinuity of the sinus floor due to extracted molar
– despite the existing discontinuity sinus augmentation
combined with GBR can be accomplished.

c d
Fig 1.33c: Lateral wall sinus augmentation - notice the existing Fig 1.33d: Lateral wall sinus augmentation with implant
discontinuity. placement can be accomplished despite the existing
discontinuity.

e f
Fig 1.33e: Lateral wall complete antrostomy - notice the Fig 1.33f: Lateral wall complete antrostomy with existing
discontinuity. discontinuity of the lateral wall

Odontogenic sinusitis usually occurs following dental infection, maxillary sinus floor
augmentation, tooth extraction, orthognathic surgery, and dental implants [45]. Odontogenic
sinusitis should be managed by a combination of antibiotic therapy, sinus surgery, and removal of
~ 33 ~
the infection source. Several studies using conventional radiographic techniques suggest that
periodontitis is associated with greater prevalence/severity of sinus abnormalities [46]. Sinusitis is
more prevalent in patients with certain conditions such as asthma, allergies, transplants, and AIDS
[47].
The polypoid lesions of the maxillary sinus are identified by the mucus retention cyst, the
antrochoanal polyp and mucoceles [48] (Fig 1.34a,b).

a b
Fig 1.34a: Lesion of the maxillary sinus membrane. Fig 1.34b: Maxillary sinus polypoid.

Polypoid lesions may contraindicate SFE per se, but they are associated with an increased
risk of ostium obstruction and may warrant a prior ENT referral, especially in patients with
coexisting sinonasal symptoms (headache, facial pain, nasal obstruction etc.) or a history of
chronic sinusitis [48].
The mucus retention cyst is characterized by a dome-shaped radiopacity extending from
the sinus wall. It occurs due to an obstruction of mucus-secreting glands of the maxillary sinus, is
usually asymptomatic and can be visible as incidental finding in 2-5% of the sinus radiographs
[26]. A wait and see approach may be appropriate in the absence of any complications, since the
majority of mucus retention cysts show spontaneously resolution or no significant volume change
[49].
Antrorochoenal polyps are benign polypoid lesions that originate from the maxillary sinus
mucosa and extend through its ostium to the choncha. The frequency and incidence of these polyps
was reported in only four studies (18.2%) based on CBCT scans [50]. Both polypoid lesions
represent fluid density in the sinus of CT scan.
Generally, the difference between retention/mucosal cysts and polyps is based on
radiographic characteristics, with polyps exhibiting a roundish, pedunculated morphology usually
originating from the roof or lateral walls of the maxillary sinus. Its etiology remains unclear and
should be treated by surgical removal.
Anteroliths are circumscribed pathologic calcifications formed as a result of mineral salt
deposition around an organic nucleus in the paranasal sinuses [51]. Radiographically, this lesion
is a radiopaque mass with variable sizes and shapes. Treatment by surgical removal is indicated
only for large antroliths associated with clinical symptoms.
Foreign bodies may access the maxillary sinus through an oroantral communication which
remains as an oroantral fistula. Furthermore, this access can also occur by the dental alveolus of a
newly extracted tooth, by means of the root canal or due to a surgical procedure near the maxillary
sinus [52]. Although spontaneous removal of the foreign body from the maxillary sinus has been
previously reported, it can cause complications, such as chronic sinusitis and should be surgically
removed [52].
~ 34 ~
 Ostium stenosis has been observed in 24% of patient [53] and is strongly associated with
chronic maxillary sinusitis [54] and nasal polyps/cysts [55]. Nasal septum deviation, with a
prevalence of 29%, may contribute (along with other abnormal conditions affecting the
osteomeatal complex, e.g., ostium stenosis) to maxillary sinus disease [53] (Fig 1.35a,b). It should
be noted that septum deviation is never the sole diagnosis. A thorough examination of the maxillary
sinus prior to sinus grafting is recommended to resolve any sinus disease or infection and thereby
minimize postoperative complications. The current standard for radiographic imaging to identify
a sinus disease is the CT scan.

a b
a 1.35a: 1) A large pneumatized bulla ethmoidalis
Fig Fig 1.35b: Chronic maxillary sinusitis. Note the endo-
2) Stenosis of the ethmoid infundibulum due to edema antral odontic material migrating towards maxillary
of the mucosa 3) Basal maxillary sinus cyst. natural ostium.

Fibrous scars attached to the schneiderian membrane can be occur after chronic
inflammation of the maxillary sinus which doesn’t necessitate any surgical intervention prior to
surgical sinus augmentation (Fig 1.36a,b).

a b
Fig 1.36a: Fibrous scars attached to the schneiderian membrane Fig 1.36b: Sinus augmentation despite the existing fibrous scars.
due to chronic inflammation.

ARTERIAL VASCULARIZATION OF THE MAXILLARY SINUS

A sound knowledge of the maxillary sinus’s arterial supply is mandatory for surgical
procedures involving this area, such as sinus floor elevation and implantation of grafting materials,
and is also pertinent to the vascularization of sinus grafts [56]. Various studies demonstrate that
there are variations in the maxillary sinus vascular connections with respect to potential risks of

~ 35 ~
surgical hemorrhage [57, 58]. Wound healing following sinus floor elevation depends, in part, on
the affected bone’s blood supply.
The loss of maxillary teeth and progressing age cause marked reductions in bone
vascularization. There is a positive correlation between micro-vascular defect development, bone
atrophy and advanced age. Stenotic processes in the elderly reduce the blood flow to bone marrow,
preventing osteoblast activity and delaying mineralization processes. Atrophy of the maxilla’s
alveolar processes, an event that quite common in the elderly, is associated with micro-circulation
vessel reduction and consequently with a decrease in the blood flow to the area, resulting in
progressive loss of cancellous bone [59]. However the periosteal blood supply still exists even
after centro-medullary vessels have completely disappeared in severe maxillary atrophy [57]. The
head and neck region had an abundant blood supply, with many anastomoses. The blood supply
of the maxilla is derived from the external carotid artery, a branch of the common carotid artery.
The bone of the maxilla is supplied by branches of two major vessels, the infraorbital artery and
the posterior superior alveolar artery. The major branch of the infraorbital artery which supplies
the maxilla is the anterior superior alveolar artery. The posterior superior alveolar and infraorbital
arteries are branches of the maxillary artery, which is one of the two branches of the external
carotid artery. The descending palatine artery travels a short distance within the pterygopalatine
fossa and then enters the greater palatine canal. It travels approximately 10 mm within the canal
in an inferior, anterior, and slightly medial direction and exits the greater palatine foramen in an
anterior direction immediately opposite or even distal to the maxillary third molar or in the region
between the second and third molars. While in the greater palatine canal, it branches off into lesser
palatine arteries and supplies the soft palate and tonsils. After exiting from the greater palatine
foramen, the greater palatine artery and nerve travel across the hard palate to the incisive foramen
and enter the nasal cavity to the anastomose on the septum along with the sphenopalatine artery.
The maxillary artery terminates at the sphenopalatine artery, which passes through the
sphenopalatine foramen to partially supply the lateral wall of the nose and the septum. It reaches
these areas through the posterior lateral nasal arteries and septal branches [14]. The posterior
alveolar artery is a branch of the maxillary artery which subsequently divides into branches
accompanying the posterior superior alveolar nerves.
Arterial vascularization of the maxillary sinus is supplied by the maxillary artery, the larger
terminal branch of the external carotid artery (Fig 1.37). Within the pterygopalatine fossa, the
maxillary artery breaks off to many branches for the maxillary sinus [57, 58]. After entering the
pterygopalatine fossa, the maxillary artery branches to the posterior superior alveolar artery
(PSAA). This artery enters the posterior superior alveolar foramina on the maxillary tuberosity
and divides to dental branches and alveolar branches to supply the pulp tissue of the posterior
maxillary teeth by way of each tooth’s apical foramen, and the alveolar branches supply the
periodontium of the posterior maxillary teeth.

~ 36 ~
 Fig. 1.37: Blood supply to the maxillary sinus relevant to sinus floor elevation. The
external (EA) and internal anastomosis (IA) from the PSAA and IOA are located at
23 and 19mm, respectively from the crest [61].

Dental and alveolar branches also supply the maxillary sinus [57].
The courses of the intraosseous branch of the PSAA on the buccal wall of the sinus are
classified into two categories: the straight (S) type (78.1%) and the U shaped (21.9%) [61]. The
anterior superior alveolar artery (ASAA) rises from the infraorbital artery (IOA) and diverges to
dental and alveolar branches. The dental branches supply the pulp tissue of the anterior maxillary
teeth. The alveolar branches supply the periodontium of the anterior maxillary teeth. The IOA
shares a common trunk with the PSAA in the pterygopalatine fossa. The IOA enters the orbit
through the inferior orbital fissure. The artery runs through the infraorbital canal, provides orbital
branches, and gives off the ASAA. These vessels connect with the formation of the intraosseous
and extraosseous network. Maximum diameters of the PSAA and IOA may reach to 2 and 2.7 mm
[57].
The preservation of such anastomosis is important not only to avoid bleeding complications
but also to support bone graft angiogenesis [62]. In this perspective, during a sinus augmentation
procedure, its concomitant reflection with the Schneiderian membrane should be seriously
considered, if possible and especially when its diameter is consistent. Extraosseous anastomosis
are made up on the alveolar branches of the PSAA, also known as alveolar antral artery (AAA),
the interior branches of the IOA and the alveolar branches of the ASAA [63, 64]. Such anastomosis
although radiographically evident in almost 50% of cases [65, 66], are reported in the width of the
lateral wall in 100% of cases [57, 64] in that they course intraosseously halfway up the lateral sinus
wall. The anastomosis forms a concave arch, with the first molar area being the lowest point of the
bony canal arch. An endosseous anastomosis of PSAA and IOA was found in 100% of cadaveric
specimens [57, 64]. This suggests that an undetected intrabony canal in a CT scan does not exclude
its existence but merely implies that it may not be visible due to its small diameter [66]. The
anastomosis between the PSAA and IOA provides blood supply to the periosteal tissues, to the
sinus membrane, and especially to the anterolateral wall of the sinus [57, 64].
Apostolakis used the term “superior alveolar canal” to describe the bony canal at the lateral wall
of the maxillary sinus that hosts both the PSAA and IOA branches [67] (Fig 1.38a,b). It has been
shown that the canal also hosts numerous nerve fibers, possibly contributing to postoperative
discomfort after sinus graft procedures [68].

~ 37 ~
 a b
Fig 1.38a: The bony canal at the lateral wall. The “superior Fig 1.38b: The posterior superior alveolar artery is attached to
alveolar canal” is clearly visible. the Schneiderian membrane.

A canal diameter of up to 2 mm found in 93.3% of the cases has no real clinical significance
since the resulting bleeding can readily be managed [66]. For canals of greater diameter,
management may be more complicated and the ensuing situation more alarming, especially for an
unprepared and inexperienced dental surgeon [67]. The canal is mainly identified in the 3rd molar,
2nd molar, and 1st premolar positions with a smaller percentage of the canals identified in the
position of the second premolar (44%) and of the 1st molar (40%). The canal is found at various
distances from 0 mm from the maxillary floor to up to 28.5 mm from the maxillary floor. This
great distance variation mandates a case by case evaluation of the position of the canal and in no
way should the surgeon use of a mean value for surgical procedures involving the canal.
A canal of greater than 2 mm diameter is relatively rare. The canal is identified, in at least
one tooth position, in 82% of the sinuses, which by far exceeds the proportion of canals reported
on other radiographic studies. The artery may not run entirely intraosseous and in certain sites does
not completely adhere to the sinus membrane and those places it is not radiographically visible.
However, in places where the artery enters a bone as in the maxillary tuberosity, the canal is more
readily observed. The scientific literature reports that this vessel is located at an average distance
of 19mm [57], 16.4mm [56], 16.9mm [66] from the alveolar crest of the posterior maxilla. This
distance is shortest at the first molar region (14.79 mm) and longest at the first premolar region
(18.92 mm).
For the most atrophic cases the ridge height is less than 3 mm. Such a distance is
significantly lower than seen in lesser atrophic cases. Nevertheless, such data can be misleading
because the height of the residual bony ridge, the maxillary atrophy class and the presence of teeth
are all relevant in determining the location of the vessel. Mardinger et al. [67] and Rosano et al.
[65] found that the AAA is located at a mean distance of 10.9 mm from the crest in classes D, E
and at a distance greater than 15mm in classes A, B and C. Rosano reported that the average
distance of the AAA from the alveolar ridge in atrophic maxilla of Cawood & Howell [70] class
V and VI is 11.25 mm. This confirms that the more resorbed the bone crest, the higher the risk of
violation of such a vessel during sinus augmentation procedure. Since the vessels in older patients
have a reduced diameter this reduces the incidence of bleeding. Although variations exist between
all patients, it has been suggested to limit the superior border of the lateral window up to 18 mm
from the ridge to avoid any potential vascular damage [71]. The entirely intra-sinusal location of
the vessel would justify the contradiction between a 100% prevalence of this artery found by
dissection and an only 47% prevalence detected by CT scans [72].

~ 38 ~
 The course of the AAA was identified in different studies as intra-osseous, intra-sinusal
and sub-periosteal "superficial" courses [73, 63]. The AAA, whose reported diameter is up to 3
mm, supplies the sinus membrane and the antero-lateral wall of the sinus, and therefore can
potentially cause bleeding complications during lateral window antrostomies [65,66]. The
transection of such an artery is not life threatening because its hemorrhage mostly resolves itself
due to a reactive contraction [64]. However, an impairment in vascularization of the Schneiderian
membrane may occur, especially when the AAA diameter is relevant, making its elevation more
difficult and interfering with the placement of the graft material, i.e. the washing out effect. The
preservation of such anastomosis is important not only to avoid bleeding complications but also to
support bone graft angiogenesis [64]. These arteries influence the vitality of the bone, the
vascularization of the grafting material and soft tissue healing.
Vascularization of the grafting material placed in sinus augmentation procedures occurs
through three routes: the extraosseous anastomosis (EA), the intraosseous anastomosis (IA) and
branches of these vessels (PSAA, IOA and IA) in the sinus membrane. The middle portion of the
Schneiderian membrane is supplied by the sphenopalatine artery, the terminal branch of the
maxillary artery. Healing and remodeling of the graft mainly depends on the vascularization
branch from the sinus walls, from which the new blood vessels grow inside the graft. It is important
to preserve the blood flow to other structures involved in the surgical procedure, such as the
Schneiderian membrane and the mucoperiosteal buccal flap. In most cases, there is no vessel
visible or no vessel present with a diameter less than 0.5mm. Sinus arteries with a diameter of
0.5mm to 2.5mm are present in approximately 10% of the cases. Rosano et al. [64] found the
diameter of the anastomosis ≤2mm in a very few cases (3.3%). This is worthy to be taken into
serious consideration.
During the sinus augmentation, several parameters must be considered, particularly the course of
the arteries and their intraosseous or extraosseous locations and anastomoses. In the lower two
thirds of the antero-lateral wall, the arteries may occur in three positions on the sinus wall (Fig
1.39-1.44) [65, 66]: The artery is intraosseous (Fig 1.40a),The artery is attached to the
Schneiderian membrane (Fig 1.40b),The artery has a subperiosteal position (Fig 1.41a,b).

Fig 1.39: Transversal view of a left sinus on a CT scan: variations of the arterial position in the lateral wall of the sinus. (1) The
artery is in the Schneiderian membrane. (2) The artery is intraosseous. (3 and 4) The artery has a subperiosteal position

~ 39 ~
 a b
Fig 1.40a: Intrabony course of the PSAA. Fig 1.40b: Intramembranous course of the PSAA.

a b
Fig 1.41a: The arteries have a subperiosteal position. Fig 1.41b: Capillaries in the Schneiderian membrane are clearly
visible.

a b
Fig 1.42a,b: CT slices demonstrate the course of the PSAA – notice the mucosal thickening of the sinus mucosa.

a b
Fig 1.43a,b: The dissection of the PSAA during lateral wall sinus augmentation is well demonstrated.

~ 40 ~
 a b
Fig 1.44a,b: The dissection of the PSAA during lateral wall sinus augmentation is demonstrated.

c d
Fig 1.44c,d: The separated lateral wall is totally removed leaving theaposterior superior alveolar artery intact.

e f
Fig 1.44e,f: Clinical view of the PSAA – notice the intrabony–intramembranous course of the PSAA.

g h
Fig 1.44g,h: Clinical view of removed lateral bone-notice the created perforation.

~ 41 ~
 i j
Fig 1.44i,j: The Schneiderian membrane with the attached PSAA is elevated, the perforation is covered with collagen membrane
and the sinus is grafted.

k l
Fig 1.44k,l: Clinical view of the course of PSAA. The artery is attached to the Scheinderian membrane.

Because of the location of the intraosseous artery, the potential of bleeding complications
is approximately 20% compared to the normal positioned lateral window osteotomies. A thicker
sinus lateral wall corresponds to a larger vessel diameter. During sinus elevation of a thicker lateral
wall, there is an increased risk of bleeding. Therefore, when there is a thick sinus lateral wall, the
risk of bleeding should be considered even if the CT image shows no intraosseous vessel. It is also
a strong possibility that as the age of the patient increases, the lateral wall on the area of 13 mm
from the sinus floor thickens. In the elderly edentulous population, the number of vessels and
vessel diameter decreases, while tortuosity of the vessel increases [5]. Some authors state that as
the patient ages the diameter of the vessel widens [66,74]. Men have a greater mean lateral wall
thickness 3 mm from the sinus floor and greater vessel diameter than women [74]. This ideally
explains why men exhibiting a greater tendency for bleeding than women during surgical
procedures. According to Kang et al., the vessel position can be classified into three groups:
intraosseous (64.3%), intrasinusial (29.1%), and superficial (6.6%), which correlate well with
previous studies [56,66], that reported that an intraosseous vascular canal at the lateral wall has
been identified in over 50% of the examined CT images [74].
According to Kang, 69% of the arteries are located more than 15 mm from the alveolar
crest, whereas 31% are located less than 15 mm from the alveolar crest [74]. This indicates that
31% of the cases present the potential for intraoperative bleeding. Previous studies have produces
similar results. Elian et al. have reported that 80% of arteries are located more than 15 mm above
the alveolar crest, therefore only 20% of the cases present potential surgical complications [56].
Temmerman et al. have identified a bony canal at the palatal aspect of the canine region in 32.9%
of all analyzed CT images, probably containing an artery, which may empirically supply the

~ 42 ~
maxillary sinus from the palate [75] (Fig 1.45a,b) . However, the authors could not find any
anatomic or radiographic study confirming the existence of such vessels. The mean diameter of
this bony canal is 1.23 mm. This bony canal could be visualized on all cross-sectional images as
well as on axial slices. On the latter, the course of the canal should be followed from its bony entry
point at the most apical position to the bony exit point at the most coronal position. It is possible
to follow this bony canal over a mean distance of 6.71 mm. At present, we have no evidence
indicating that damaging this bony vessel can exert any adverse effect on the maxillary sinus [69].

a b
Fig 1.45a: CBCT showing the bony canal located palatal to the Fig 1.45b: CBCT showing the course of the bony canal
upper canine [69]. located palatal to the upper canine and distally to the first
premolar.

INNERVATION OF THE MAXILLARY SINUS

The nerves supplying the maxillary sinus originate from the maxillary nerve directly, the
second branch of the fifth cranial nerve (trigeminal nerve) with posterior middle and superior
alveolar branches (Fig 1.46). It innervates the sinus floor in the posterior area, together with the
molar and premolar teeth including the anterior palatine and infraorbital nerve. The infraorbital
nerve is purely sensory and traverses the pterygopalatine fossa, where it splits off the posterior
superior alveolar nerve, which pierces the posterolateral sinus wall, courses between the bone and
the sinus membrane and forms a nerve plexus that supplies the sinus membrane [75]. The middle
and anterior superior alveolar nerves lie within the bony sinus wall and form the superior dental
plexus, which is located in the alveolar process. Both the superior dental plexus and the plexus
innervating the sinus membrane are present also in the absence of teeth [76]. The infraorbital nerve
is of concern in sinus elevation surgery because of its anatomical position. This nerve enters the
orbita via the inferior orbital fissure and continues anteriorly. The nerve lies in a groove in the
orbital floor, before exiting the infraorbital foramen. The anterior superior alveolar branch, with

~ 43 ~
branches from the infraorbital nerve at the infraorbital foramen, reaches the anterior sinus wall and
the superior dental plexus, running below the Schneiderian membrane. Some branches starting in
the infraorbital nerve branch out from the trunk before exiting the infraorbital foramen and
innervate the maxillary sinus medial wall. Anatomical variants have been reported including a
dehiscence and malpositioned infraorbital foramen, along with the nerve traversing the lumen of
the maxillary sinus rather than running within the sinus orbital floor through the bone. Other
branches involving the sinus mucosa are branches of the pterygopalatine ganglion and the
sphenopalatine ganglion, with the long and short sphenopalatine nerve.

Fig 1.46: Innervation of the maxillary sinus besides arterial vasculization of the maxillary sinus. The
external (EA) and internal anastomosis (IA) from the PSAA and IOA are clearly visible [13].

VENOUS AND LYMPHATIC DRAINAGE

Venous drainage is ensured by the posterior and inferior alveolar veins. These veins are
usually symmetrically located and receive branches from the same areas of the maxillary zone as
supplied by the arterial network. The veins may also be the route for spreading infection emanating
from the maxillary sinus, which may involve adjacent anatomic areas, as the inferior of the
cranium. These infections may result in meningitis or phlebitis. The veins of the maxillary sinus
empty into the facial vein and the pterygoid plexus [77], while the nasal sinus wall drains into the

~ 44 ~
sphenopalatine vein [78]. The significance of sinus venous drainage is that, apart from joining
typical maxillary pathways to the jugular veins, it may also take an upward course to the cavernous
sinus through the oval foramen and the superior or inferior ophthalmic veins [79]. From the
cavernous sinus the blood flows into the deep middle cerebral vein, which communicates with the
brain's superficial venous system through the white matter [80]. The spread of infection along this
route is a serious complication of maxillary sinus infection.
The lymphatic system of the maxillary sinus empties into collector lymph vessels within
the mucosa of the medial nasal turbinate and reaches the preauricular lymphatic plexus [78]. In
addition, the lymph drains into the deep facial and deep cervical lymph nodes. Less studied
connections are to the auditory tube and the nasopharynx.

MAXILLARY SINUS SEPTA

Inside the maxillary sinus, bony septa are often found. They originate from the sinus floor
and rise to variable heights on the lateral wall (Fig 1.47a,b). These anatomic variations were first
illustrated by Underwood in 1910 in a detailed description of the maxillary sinus anatomy and are
therefore referred to as "Underwood's septa" [79]. The septa may carry out a biomechanical
function to transfer masticatory loads in an optimal manner.
They are made up of bone cortex in a vestibular-palatal or in anteroposterior direction that
divide the maxillary sinus into multiple compartments called posterior recesses.

a b
Fig 1.47a: Bilaterally maxillary sinus septa Fig 1.47b: Maxillary sinus septa in diverse directions

Underwood described the septa as arising between the areas of two adjacent teeth and
usually presenting in three specific regions of the sinus floor, thus dividing the floor into 3 basins:
anterior, between the second premolar and first molar roots; middle, between the first and second
molar roots; and posterior, distal to the third molar roots. These are also called the puzzle
perpendicular maxillary septa. The same author mentioned that the septa were most commonly
observed in the posterior region. He also noted that the size of septa could be accentuated by further
pneumatization of the alveolar process. Occasionally, the septa reach from the base to the upper
sinus wall resulting in two sinuses of a smaller size draining into the nose through separate
openings. The shape of septa has been described as resembling an inverted gothic arch arising from
the inferior and lateral walls of the sinus and coming to a sharp edge along its most apical border
[80] (Fig 1.48a,b, Fig 1.49a,b).

~ 45 ~
 a b
Fig 1.48a: Clinical view of maxillary sinus septa in vestibular Fig 1.48b: Clinical view of maxillary sinus septa in vestibular
anteroposterior direction. palatal direction.

a b
Fig 1.49a,b: Panoramic view of CT scans demonstrating the presence of maxillary sinus septa.

The normal anatomy of the maxillary sinus can assume different shapes. Its upper margin
is in contact anteriorly with the lacrimal bone and posteriorly with the ethmoid bone creating
different shapes of sinus septa. The punctum convergii is located immediately posterior to the
maxillary sinus ostium. From this punctum, a partial-more or less-perpendicular-septum can
develop into the maxillary sinus, somewhat dividing the sinus into anterior and posterior
compartments, called partial perpendicular septations of the maxillary sinus. The third type of a
possible partial septa in the maxillary sinus is a horizontally-located maxillary process from the
palatine bone and the inferior concha which is called a partial horizontal septa (Fig 1.50a,b,c).

a b
Fig 1.50a: A panoramic radiograph showing a left maxillary Fig 1.50b: Panoramic view of a CT scan showing a left
sinus septa. maxillary sinus septa.

~ 46 ~
 c
Fig 1.50c: CT slices demonistrate maxillary sinus septa up to 2 mm.

Maxillary sinus septa can be successfully used for engaging dental implants in the posterior
maxilla according to the author’s experience. Much skill is needed to accomplish this intricate
surgery. The results obtained are very encouraging due to the high density cortical bone composing
the sinus septa. It’s not worth mentioning that the marginal bone loss is limited in those cases due
to the density of the bone surrounding the implants (Fig 1.51a,b).

b
Fig 1.51a,b: Implants placed in the maxillary septa, 15 years post-surgery - notice the septa bone maintenance due to functional
loading.

If surgery of the maxillary sinus reveals the sinus cavity to be very shallow in an antero-
posterior direction, the possibility of an accessory sinus space should be considered. A second type
of accessory sinus results from excessive pneumatization of the posterior part of the maxilla by a

~ 47 ~
large ethmoid air cell (Fig 1.52). In this case, a pathologic process involving the ethmoid bone will
also involve this accessory sinus.
Krennmair et al. [81] further classifies septa into primary septa (which arise from
development of the maxilla) and secondary septa (which arise from irregular pneumatization of
the sinus floor following tooth loss). Both primary and secondary septa seem to undergo resorption
during progressive edentulism. The prevalence of sinus septa is 10 to 48% [82, 83]. This wide
variation may be due to the different analysis of anatomic cadavers, surgical procedures, computed
tomography (CT) or panoramic radiographs [79, 84].
Studies based on panoramic radiographs can only approximate the size and location of the
septa because of two-dimensional image [84], therefore the lower prevalence of the septa were
detected in panoramic radiographs compared to the methods used in other studies.

Fig 1.52: Demonstration of a partial intersinus septum and accessory maxillary sinus [13].

Studies based on CT scans generate 3 dimensional data, which are highly clinically relevant
for the detection and localization of septa. Clinically, a prevalence of up to 57.6% has been
observed [84]. This discrepancy may be explained by the selected patient group or by the
difference between direct clinical inspection and imaging results.
A meta-analysis study of published articles in England from 1910 to 2011 addressed the
prevalence, size, and locations of the septa by retrospective analysis. A total of 7,061 sinuses were
investigated in 19 studies [79-81, 84-87]. The meta-analysis showed that 41% of patients had at
least one septated sinus, while 17% had bilateral septa. Twenty-five percent of sinuses showed a
single septum, while multiple septa were present in 4%. Regarding their antero-posterior position,
24% of the septa were located in the anterior basin, 55% in the middle basin, and 21% in the

~ 48 ~
posterior basin. Most of them were transverse (88%), some horizontal (11%), and few sagittal
(1%). The majority of the septa was incomplete (99%) and had a mean height of 7.5mm (maximum
of 20.6 mm). They are usually thicker at the base on the sinus floor, and then thin out in the middle.
Septa can be found in all parts of the maxillary sinus but they are mainly found medium–
laterally [87]. They are thin and slightly developed vertically. They are generally higher on the
media of the sinus and are rarely found in multiple formations.
Previous studies using radiologic examination methods reported septa in 13% to 35.9% of
sinuses and 16% to 38% of patients. In 1,024 panoramic radiographs a total of 307 septa were
found with a prevalence of 14.9% calculated for both sinuses [85, 86]. The total prevalence of
radiologically detected septa described in the study of Ella et al. [84] appears to be the highest
reported in the literature so far, with 47% of patients and 33.2% of sinuses featuring at least one
septum. The distribution of septa in the anterior region has been reported to be higher than in the
posterior region (20.3% and 2.5%, respectively). This was not observed in other studies which
found 23.1% of septa in the canine and premolar areas and 76.9% of septa posteriorly (molar
areas). These low numbers can be explained in part by the method used to detect and describe the
septa.

Partial perpendicular septa

Beginning at the location of the penctum convergii is an area immediately posterior to
maxillary sinus ostium. In this area, a partial perpendicular septum can develop into a maxillary
sinus, dividing into complete compartments. A septum of this type may cause difficulties in
orientation during surgical elevation of the sinus membrane.

Partial horizontal septa

This septum is horizontally located in the maxillary process arising from the palatine bone
and the inferior concha. This type of septum can be ignored if it is positioned much higher than
the area to be grafted. Otherwise, such a horizontal septa will impede sinus drainage and lead to
sinus graft failure. If these occur, neither process will follow the normal development of the sinus
in its inferomedial direction. While the floor of the sinus is gradually lowered as development
progresses, both processes will maintain their primary horizontal positions. Such horizontal septa
can cause difficulties in diagnosis, as well as impede sinus drainage after planned sinus
augmentation procedures.

Complete separation of the maxillary sinus

A complete vertical septum usually divides the sinus into a big anterior and a smaller
(accessory) posterior sinus. The anterior sinus drains into the middle meatus, while the posterior
sinus opens into the superior or nasal meatus through a bony hiatus delimited by structures similar
to those of the normal hiatus semilunaris (i.e., the maxillary process of the middle concha and the
posterior maxillary process of the palatine bone). Each of those sinuses can show isolated signs of
pathology and thus must be treated separately. The accessory sinus develops in the cartilaginous
nasal capsule concomitantly with the normal sinus. It is the result of an excessive pneumatization
of the posterior part of the maxilla by a large ethmoid air cell. In this case, a pathology involving
the ethmoid bone will also involve the accessory sinus.
Uemura thought that maxillary sinus septa were formed by pressure, such as that generated by
chewing [88]. Forty-two percent of septa and 67% of exostosis are antero-posteriorly positioned

~ 49 ~
according to the transverse palatine suture [89]. The anatomical distribution of the septa, according
to Zyl and Heerden [90] is 26% in the anterior region, 49% in the middle region and 25% in the
posterior region. The implication for clinicians is that 75% of all septa occur in the area anterior
to the third molars, which is the area most often involved in sinus floor elevation procedures.
Septa that could not be classified as either single or multiple are also encountered. These
septa are termed ‘complex’ septa and are counted as single septa. Septa with inclination can be
very challenging if not impossible to navigate during sinus floor elevation and the same would
apply to the complex septa.
Inclined and complex septa, coupled with the high prevalence of septa seen in Zyl and Heerden’s
study [90] and the inaccuracy of panoramic radiographs, are reason enough to consider reformatted
CT scans as the standard of care for all sinus floor elevation cases.

AL-Faraje classification of the maxillary sinus septa into six categories prior to sinus bone
graft surgery [13] (Fig 1.58):

Class I - Single basal perpendicular septum.

Class II - Multible (two or more) basal perpendicular septa.
Class III - Single partial perpendicular septum.
Class IV - Multible (two or more) partial perpendicular septa.
Class V - Partial horizontal septa.
Class VI - Complete perpendicular septa (complete separation of the maxillary sinus).

~ 50 ~
 Fig 1.53a-f: Al-Faraje classification of maxillary sinus septa [13].

Frequently measuring less than a millimeter in width, septa are very subtle structures that
have sufficient resolution in all directions of space. Knowledge of the location and morphology of
the septa is essential in determining the surgical approach. The presence of these septa may cause
complications in maxillary sinus elevation surgery. The use of CT radiographs prior to sinus
elevation permits the clinician to observe and plan the necessary modifications to the sinus
augmentation procedure as a result of the septa. Modifications to the surgical procedure are
variable, depending on the septa’s location.

PHYSIOLOGY OF THE MAXILLARY SINUS

The functional role of the paranasal sinuses is controversial and no exclusive analysis of
the function of the maxillary sinus has been established. Some authors argue that they merely
represent non-functional evolutionary remnants. Due to their inherent disadvantages, such as a
marked susceptibility to chronic diseases, we can reasonably assume that these sinuses, if they did
not serve any physiologic or anatomic function, would probably have been selected out and
obliterated during the evolutionary history of humans [91]. The physiology of the maxillary sinus
is closely related to its microanatomy.
Theories of the maxillary sinus’s physiologic function include [92]: (a) protection of
intracranial structures: the sinus architecture may be suited to act as a shock absorber and stress
distributor to protect the skull base against trauma; (b) humidification and warming of inhaled air:
since it takes 50 breathing cycles to exchange the entire air volume of the sinus, conditioning of
air cannot be a significant function; (c) weight reduction to maintain equipoise of the head:
maxillary sinus pneumatization reduces the skull weight by only 1% of the total weight. Therefore,
weight reduction may not be the main function; (d) thermal insulation of a vital part: if an
insulating mechanism to maintain cranial temperature is assumed, why do Africans have larger
sinuses than Eskimos?; (e) imparting resonance to the voice: the physical properties of the sinuses
make them poor resonators and maxillary sinus augmentation does not modify the voice’s spectral
characteristics [93]; (f) secretion of mucus to moisten the nasal cavity: in contrast to the nose with
its 100,000 submucosal glands, the sinuses have 100 glands at most; (g) increasing the area for
olfaction: the sinus membrane is made up of non-olfactory epithelium; (h) influence on facial
growth and architecture: the architectural theory is far more likely in that the craniofacial shape
has an important bearing on sinus growth and the maxillary sinus plays an important role in the
formation of facial contours (Fig 1.54a-c).

~ 51 ~
 Ventilation of the maxillary sinus
Ventilation of the maxillary sinus is accomplished by gas exchange with the nasal cavity
through the sinus ostium (Fig 1.54a-c). Sinus ventilation may be quantified using xenon-enhanced
CT techniques (inhalation of a xenon-oxygen-air mixture and repeated CT scans every 3 minutes)
[94]. The mean washout time for a 95% exchange of sinus air is 5 to 20 minutes and shows
extremely wide inter-and-intra-individual variations [95]. Both the size of the sinus ostium and the
angle between the ostium and the nose affect the strength of the air stream and the amount of
circulation [96].
Air movement through the sinus ostium undergoes four phases during one respiratory
cycle. During inspiration, the velocity of air rises to a peak quickly and then declines. The same
two movements of air are observed during expiration, although the peak velocity is lower. The
respiratory fluctuations in the nose induce a stream of circulation in the sinus. Differences in air
velocity between the sinus and the nose are 1:50 to 1:100 and can be measured endoscopically by
hot-film anemometry [97]. Maximal values of air velocity have been recorded near the ostium,
and minimal values have been found at the center of the sinus and at the border of the zygomatic
recess. Exhalation stops the air movement in the sinus, while mucociliary action is not thought to
influence sinus ventilation. Wider ostia and a shorter infundibular passage result in higher
velocities and therefore, are capable of higher transport rates [95]. Air velocity in the sinus rises if
the nasal mucosa contracts in response to decongestants.
Under normal conditions, the temperature of the maxillary sinus is constant even when the
external temperature changes [96]. An increased sinus temperature (higher than the body
temperature) is seen in acute sinusitis, while allergic conditions, chronic sinusitis, or impaired
sinus ventilation leave the temperature unchanged [97]. Inspiration causes negative sinus pressure
and expiration causes positive sinus pressure relative to the atmospheric pressure [96].
Gas exchange between the nose and the maxillary sinus is caused by fluctuations in
breathing pressure and regulated by diffusion through the ostium [95]. Gas exchange in the sinus
depends on (1) sinus volume, (2) the functional diameter of the ostium, (3) size and shape of the
nasal cavity, (4) composition of gases, (5) nasal respiratory pressure, (6) nasal airflow, and (7) gas
absorption by the sinus mucosa [94]. An ostial diameter of less than 2.5 mm has been correlated
with lowered oxygen and increased carbon dioxide levels [27]. Reduced oxygen tension facilitates
the growth of facultative anaerobic bacteria and as a result in a marked reduction of mucociliary
activity [91]. Compared with the nasal cavity, significantly higher concentrations of nitric oxide
(NO) are found in the sinus mucosa [98].
The low natural ventilation of the maxillary sinus may in fact be protective, as it not only
prevents drying of the mucosal surfaces, but also helps in maintaining a near-sterile environment
with high (NO) concentrations and minimal pathogen access [94].
The bacterial milieu of the maxillary sinus under physiologic conditions has been widely
investigated. However, the findings have been quite diverse. While healthy sinuses have
traditionally been thought to be sterile, aerobic as well as anaerobic bacteria have been grown from
20% to 100% of asymptomatic sinuses. The most common aerobic isolates are B-hemolytic
streptococci, staphylococci and Haemophilus sp. Counts of anaerobes routinely residing in the
sinus are predominantly Bacteroides and Peptostreptococcus, with Fusobacterium sp. being less
prevalent [99,100]. In contrast to the nasal mucosa which harbors a physiologic bacterial flora, we
still poorly understand whether these organisms represent normal habitants of the maxillary sinus
or are transitory in nature. Some degree of inflammatory cell infiltration in the submucosa of the
sinus membrane is needed for respiratory tissues. A host of specific and nonspecific defense

~ 52 ~
mechanisms prevent maxillary sinus infection. These include mucociliary transport, neutrophils,
macrophages, and the secretion of antimicrobial proteins and peptides by the sinus membrane
[101].

Mucociliary clearance
The fundamentals of mucociliary clearance have been largely elucidated by Walter
Messerklinger based on observations that the human sinus mucosa and its ciliary activity survive
24 to 48 hours beyond the individual’s death [102]. Mucociliary clearance eliminates both inhaled
foreign bodies and hypersecreted respiratory mucus and depends on complex interactions between
motile cilia and mucus secretion [103]. The 2 L of mucus secreted per day consists of 96-97%
water and 3-4% of glycoproteins, prostaglandins, immunoglobulins, lactoferrins, lysozymes,
leukotrienes, and histamine which act as an important immunological barrier [20]. The sinus
mucosa is covered by a double-layered mucus "blanket," which consists of highly viscous outer
mucus and low-viscosity periciliary fluid [104]. The cilia are in constant motion and act in concert
to propel the overlying mucus blanket at a mean rate of 6 mm per minute [105]. Mucociliary
transport runs along genetically determined pathways originating from the sinus floor and spirally
ascending to the natural ostium, even if alternative openings are created [106].

a b c
Fig 1.54a: A healthy sinus with patent Fig 1.54b: A maxillary sinus ostium into Fig 1.54c: Direction of the mucus floor
ostium. the nasal cavity. in the maxillary sinus.

The flow pattern is specific for each individual sinus and seems to adapt to the inner sinus
shape by means of the so-called "bridging phenomenon," in which secretions thicken at the rising
bony edges and the gel phase slides over the serous phase to cross narrow passages [20]. Certain
areas have been noted to transport mucus faster than others. It is however, unknown whether these
"secretion expressways" are artifacts caused by endoscopy [102]. Since the natural ostium is
located in the upper quarter of the medial wall, secretion can only be removed by the active
drainage transport system and does not take advantage of gravitational forces. Every 20-30
minutes, the entire mucus of the maxillary sinus is renewed. Effective mucociliary activity depends
on multiple factors requiring a normal ciliary structure and function [105]. Although the number
of cilia (i.e., the ciliated area or the percentage of mucosal surface occupied by cilia) may be
normal, defective ciliary function may lead to impairment of mucociliary transport [106].
Little is known about changes of the physiologic function of the maxillary sinus due to
sinus membrane elevation and augmentation surgery. Mucosal thickening is routinely seen in 74%
to 89% of patients in the first post-operative week, [107, 108] while only 4% present with persistent
thickening of the sinus membrane following augmentation [109]. Human sinus membrane biopsies
taken 9 months after surgery do not show morphologic or ultrastructural changes other than

~ 53 ~
increased numbers of goblet cells in the epithelium [110]. However, these static images of mucosal
health are poorly suited for evaluating the functional recovery of proper mucociliary activity after
maxillary sinus augmentation.The normally functioning sinus is very nearly sterile. Postoperative
healing after SFE is largely dependent on adequate sinus drainage into the nasal cavity through the
ostium. It is mandatory to maintain a normal mucociliary clearance following an elective surgery.
It should always be stressed that maxillary sinus floor elevation carries the potential risk of
compromising the sinus physiology and may contribute to diminished mucociliary function by
direct trauma on cilia, ciliary loss, and/or other ultastuctural alterations in the epithelium. Damage
to the function of the mucociliary cells or sinus outflow obstruction could lead to mucous retention
and rhinosinusitis [111]. The most common etiologic factor for developing these disturbances is
viral infection, which may be accompanied by secondary bacterial infection. Obstruction of the
maxillary sinus can also be caused by an edema as a result of an allergic reaction, barotrauma,
trauma, polyp or tumor [111]. Carmeli et al. asserted that a compromised maxillary drainage
system is associated with a higher risk of post-operative sinusitis [112]. Therefore, it is crucial to
know preoperatively whether the maxillary sinus drainage system is functional.

THE ANATOMY AND PHYSIOLOGY OF THE MAXILLARY SINUS MEMBRANE

The maxillary sinus is lined with pseudo stratified columnar epithelium, which is
represented by ciliated columnar cells, goblet cells, and basal cells on the basement membrane,
which is also called the Schneiderian membrane (Fig 1.55a,b). The sinus lining is 0.2 to 0.8 mm
thick with a relatively thin basement membrane in healthy individuals and is invisible on CT scans
unless chronically inflamed. Coating the sinus lining is a bilayered secretory blanket. The inner
layer (called the sol) is thin, serous, and rich in proteins, immunoglobulins, and complement. The
surface layer (called the gel) is viscous mucus that floats on the thinner sol layer. The cilia of the
cells lining the sinus reach up through the sol layer and sweep the gel layer along so that any
surface materials are swept toward the sinus ostium at rate of anywhere from 3 to 25 mm per
minute [38].

a b
Fig 1.55a: Elevated sinus mucosa during sinus augmentation. Fig 1.55b: Elevated sinus mucosa during sinus augmentation -
notice the capillaries supplying the sinus mucosa.

The secretory elements of the sinus membrane consist of goblet cells and the openings of
the submucosal glands, which are interspersed between the ciliated cells. At the apical cell ends
there are 100-150 cilia (per columnar unit) [113], showing the characteristic 9+2 microtubular
pattern (a cylinder of nine pairs of microtubules encircling two single microtubules). Together,
these constitute the secretory elements of the sinus membrane. The goblet cells contain numerous
mucin vesicles and have a mean density of 9,600 cells/mm2 compared with 5,600 cells/mm2 in the
~ 54 ~
nose with wide individual variations, but no differences between the sinus walls [114]. By contrast,
the seromucous glands in the underlying stroma are scarce, with a mean density of 0.2 glands/mm2
which are predominantly located near the ostium. The density of ciliated cells is very high, ranging
from 91% to 98% and 47% of them are close to the ostium [106]. It must be assumed that the
greater part of the mucus in the sinus is produced by goblet cells, while in the nose, the greater
part is produced by glands. Beneath the surface epithelium is a loosely cellular but highly vascular
thin tissue with serum-mucosa glands in the lamina, directly underneath and especially next to the
ostium opening. This epithelium continues from the nasal respiratory epithelium. Beneath this
tissue in all areas is a periosteum. The delicate mucosa of the sinus attaches to the periosteum on
its osseous surface. The periosteum is loosely attached to the bone and is usually elevated during
sinus lift procedures. A thin layer of respiratory epithelium which lines the Schneiderian
membrane cannot be differentiated from the periosteum of the bones to which it is firmly affixed.
Under the relatively diminished activity of the seromucous glands, the delicate and loose
epithelium, as well as the reduced number of cilia (100-150 silica per columnar cell), indicate a
lower resistance to infection and easier penetration of microorganisms [114]. This membrane,
being in contact with outside air, also acts as an immunological barrier, although to a lesser extent
than the nasal mucosa.
Under normal conditions, the epithelium is kept humid by the continuous secretion of fluid
from goblet cells and serum mucosa glands. This epithelium transports the produced mucus
towards the sinus ostium and discharges it into the nasal fossa. This process happens thanks to the
100 to 150 cilia present on each columnar cell, vibrating at a frequency of about 1000 beats per
minute, thus moving mucus and debris actively toward the natural ostium.
Secretion can only be removed by the active transport system of drainage, since the natural ostium
is located in the upper quarter of the medial wall. Every 20-30 minutes the entire mucus of the
maxillary sinus is renewed. Factors compromising mucus production and clearance of the mucosa
can increase the risk of sinusitis development and must be avoided. A typical example for such a
risk factor in surgery is the penetration of the particulate graft material during sinus floor elevation
(SFE). Pommer et al. explored the force needed to cause membrane perforation using isolated
samples of human maxillary sinus floors and facial walls. The burst tension of the sinus membrane
ranges from 5.9 ± 2.5 to 8.6 ± 5.1 N/mm2 [115].

THE MYSTERY OF THE MAXILLARY SINUS MEMBRANE

Srouji et al. tested the osteogenic potential of human maxillary sinus Schneiderian
membrane (hMSSM) using both in vitro and in vivo assays. The results showed that hMSSM cells
could be induced to express alkaline phosphatase, bone morphogenic protein-2, osteopontin,
osteonectin, and osteocalcin and to mineralize their extracellular matrix [116,117]. Conversely,
Scala el al. documented the lack of influence of the Schneiderian membrane in bone formation
apical to implants simultaneously installed with sinus floor elevation performed with a lateral
approach. Bone formation at implants started from the native bone of the sinus floor and extended
coronal toward the apex of the implant. However, this coronal proliferation of bone never exceeded
4.5mm, indicating the limitation dictated by the Schneiderian membrane collapsing over the
implant apex [118].
Along with mucociliary activity, the blood flow of the maxillary sinus mucosa is a key
component of the defense mechanisms that serve to protect the maxillary sinus from infection. The
sinus mucosa has a distinctly sparser vascular network than the nasal cavity, which is situated in
the deepest layer of the lamina propria that rests on the periosteum [56]. However, blood flow to

~ 55 ~
the maxillary sinus mucosa has been shown to be three times more abundant than that of exercised
skeletal muscles [119]. Mucosal blood flow is regulated by the autonomic nervous system, and
other factors such as gravity and endocrine activity [120]. Vascular compromise may set in motion
a series of events that predispose the antrum to the onset of sinus disease [91]. Blood flow and
pulse amplitude in the maxillary sinus mucosa are considerably reduced during physiological
activity, falling to 44% of normal [120]. Microcirculatory blood flow is also significantly reduced
in patients with chronic sinusitis [121]. Decongestant nose drops have been found to strongly
reduce mucosal pulse amplitudes and blood flow to the sinus mucosa while only slightly lowering
the gas exchange in the mucosa [122].

MUCOSAL THICKENING
Our knowledge of the mean thickness and the dimension of the Schneiderian membrane is
limited, and there are no guidelines for assessing and classifying mucosal findings in the maxillary
sinus before an SFE. The mean thickness of the Schneiderian membrane has been evaluated in
different studies. Pommer et al. found a mean thickness value of 0.09 +\- 0.05 mm (range 0.02-
0.35 mm) using 20 fresh cadavers [115]. In a study using biopsies from healthy subjects, Aimetti
et al. measured a mean thickness of 0.97 +\- 0.36 mm [123]. Janner et al. confirmed the great
interindividual variability of the Schneiderian membrane’s thickness, with values ranging from
0.16-34.61 mm [124].
Radiographic observations on the Schneiderian membrane dimensions are scarce. Most
studies have applied different measurement scales and classifications, from the maximum mucosal
thickness in millimeters [177] to the simple description of the shape of mucosal thickening [133].
Diffuse mucosal thickening of the sinus membrane is found in up to 42% of subjects [125]. Carmeli
et al. [126] investigated mucosal thickening and the correlation between maxillary sinus inferior
mucosal thickening and sinus outflow obstruction. They graded mucosal thickening as < 5 mm
(1), < 1 mm (2), < 15 mm (3), < 20 mm (4) and > 20 mm (5), and classified by appearance as
normal, rounded, circumferential, irregular, or complete (Fig 1.56). Maxillary sinus outflow was
classified as patent or obstructed (Fig 1.57a,b). They concluded that rounded mucosal appearance
of any grade is associated with a low risk for sinus obstruction and irregular (> 5 mm),
circumferential and complete mucosal appearances are associated with an increased risk for sinus
outflow obstruction and an ENT consultation is recommended.

Fig 1.56: Classification of mucosal thickening appearance. Mucosal thickening is a characteristic feature of both acute and
chronic sinusitis [112].

~ 56 ~
 a b
Fig 1.57a: Classification of infundibural patency: patent [112]. Fig 1.57b: Classification of infundibural patency: obstructed
[112].

An analysis of 9315 panoramic radiographs revealed a maxillary mucosal thickening in

12% of the subjects and a 7% prevalence of mucosantral cysts [127]. Mucosal thickening is mostly
caused by odontogenic infections, (i.e., periapical lesions and periodontal disease in 58-78% of the
cases), it may also be associated with environmental allergy or upper respiratory tract disease and
is not necessarily a sign of sinus infection.
Structural changes of the thickened sinus mucosa include edema, increased numbers of
seromucous glands and goblet cells, interstitial cyst formation, fibroplasia of the lamina propria
and increased inflammatory cell infiltration [114].
Janner et al. concluded that gender seems to be the most important parameter influencing
mucosal thickness in asymptomatic patients, with male subjects having higher mean values [124].
According to these researchers, endodontic, periodontal, and periapical status of the dentition in
the region of interest has no influence on sinus membrane mucosal thickening [128]. Tearing of
the subjacent sinus membrane may occur because of the irregular nature of the overlying bone
located between the root apices and the small dimension of the access cavity.
Early reports had difficulty in visualizing normal mucoperiosteal structures in the paranasal
sinuses through CT [129] or MRI [130], due to a limited spatial resolution and a low detection
limit for mucosal tissue. The mucosa could only be seen at a thickness of 2 mm and above, and
therefore, historically 2 mm was considered a reliable threshold for pathological mucosal swelling
[131].
Mucosal thickening classification goes according to criteria adapted by Soikkonen &
Ainamo [177] (Fig 1.58a-j):
Flat - shallow thickening without well-defined outlines.
Semi-aspherical - thickening with well-defined outlines rising in an angel of < 30o from the floor
or walls of the sinus.
Mucocele-like - complete opacification of the sinus.
Mixed flat and semi-aspherical thickenings.
Other mucosal thickening types or pathological findings.

~ 57 ~
 a b
Fig 1.58a: Mixed flat and semi-aspherical thickening. Fig 1.58b: Mucocele-like mucosal thickening.

c d
Fig 1.58c: Multiple mucocele-like mucosal thickening. Fig 1.58d: Complete opacification due to migrated implant.

e f
Fig 1.58e: Irrigular mucosal thickening with mucocele-like Fig 1.58f: Rounded mucosal thickening.
appearance.

g h
Fig 1.58g: Mucocele-like mucosal thickening. Fig 1.58h: Flat mucosal thickening.

~ 58 ~
 i j
Fig 1.58i: Circumferential mucosal thickening with patent Fig 1.58j: Circumferential mucosal thickening.
osteome.

In recent CBCT studies, mucosal thickening of >2 mm and >3 mm, was reported in 37%
[129] and 62% [132] of similar patient samples respectively. Membrane thickening and a history
of sinusitis were found to be at a greater risk of developing late signs of sinusitis 12-80 months
after augmentation procedures [133]. Moreover, one radiographic (CT) study found membrane
thickening >5 mm to be associated with a progressively increasing risk for ostium obstruction
[126]. Sinuses with >10 mm of membrane thickening were associated with the greatest risk for
ostium obstruction (35.3%), followed by those with 5-10 mm (24%) and 2-5 mm (6.7%) of
thickening [134]. Therefore, sinus floor membrane thickening can be considered as a reliable
predictor of ostium (out-flow) obstruction. Both membrane thickening and ostium obstruction may
indicate only transient (e.g. seasonal) phases of mucosal inflammation and not a pathology
contraindicating SFE.
A clear transient swelling of 5-10 times of the Schneiderian membrane size after a
transalveolar elevation, disappearing within 1 month after the intervention was observed [132].
The reason of this swelling is not well understood. One possibility is that postoperative bleeding
pushes the membrane away from the bony floor of the sinus.
Preoperative knowledge of membrane characteristics, particularly thickness, can be of
great value to the surgeon.
Routine CT scans, including the maxillary sinus ostium, are recommended.

a b
Fig 1.59a: Foreign bodies migrated into the maxillary sinus Fig 1.59b: Foreign bodies are clearly visible causing chronic
probably through an oroantral communication. sinusitis with almost complete opacification.

MORPHOFUNCTIONAL CHANGES OF THE MAXILLA FOLLOWING TOOTH LOSS

The alveolar processes in the jaws are structurally dependant on teeth. After tooth
extraction, wound healing of the extraction socket is associated with modeling and remodeling

~ 59 ~
processes leading to dimensional alterations of the residual ridge [135-139]. Johnson and
colleagues first demonstrated 40 years ago that a reduction of 2.5-7mm in height and up to 30 mm
in width can follow a tooth extraction [140]. Moreover, they observed that most changes occurred
during the first month, while minor additional decreases in the ridge continued over periods
ranging between 10 and 20 weeks [140]. The amount of vertical and horizontal resorption of the
socket walls has been investigated with different methods, ranging from studying and measuring
cast models [139-141], to radiographic analysis [139], clinical assessment with individually
prefabricated acrylic stents during reentry surgeries [142,143], and historical studies in
experimental animal models [136,138]. These studies have concluded that most of the resorption
occurs during the first three months of healing, although dimensional changes can be observed up
to one year after tooth extraction, resulting in approximately 50% reduction of the bucco-lingual
dimension of the alveolar ridge [139]. This is mainly due to the resorption of the buccal bone plate
which may continue long-term, with highly variable progression rates [138,139]. The walls of the
socket are reduced, and the change of the buccal wall is more pronounced than that of its
lingual/palatal counterpart [138,141].
Findings of Pietrokovski et al. have been interpreted to show that the tooth (root) in
function and its supporting tissue (cementum, periodontal ligament and bundle bone) play a crucial
role in the maintenance of the dimensions of the alveolar process and that the absence of tissue per
se will reduce the demand for tissue support at that site [141,144].
Amler studied tissue regeneration in human extraction wounds. He reported that wound
healing in humans consists of a sequence of cellular and tissue changers occurring within the
alveolus after dental extraction. During this healing process, known as ‘corticalization’, a hard
tissue bridge covers the marginal portion of the extraction site [135,145]. It consists of a series of
proliferative and resorptive events through which a cortical bone wall eventually develops, where
the mucosa lining becomes firmly attached. Bone resorption occurs three months after the removal
of a single tooth until it reaches a level of balance at its midpoint, which can be considered an
indicative fulcrum of healing. Bone resorption occurs principally due to collapse of the buccal wall
of the socket toward the lingual [138]. The exact causes of these phenomena are still being
researched.
Araujo and Lindhe stated that, because the buccal bone of the socket in made up of bundle
bone, and bundle bone is part of the periodontium, the removal of a tooth renders this bone useless,
and its reabsorption is a natural consequence [138]. Conversely, other authors have emphasized
that the changes are due to surgical trauma during extraction and the separation of the periosteum
and its disconnection from the underlying bone surface. This can cause vascular damage and an
acute inflammatory response, which in turn, causes the reabsorption of the bone tissue [146, 147].
Multiple adjacent extractions induce greater apico coronal alterations compared with single
extractions [140]. The magnitude of the short-term (3-12 months) reduction in both the alveolar
socket’s vertical and transversal dimensions has been reported by a recent systematic review by
Van der Weijden [148]. He investigated the different factors that might be related to socket healing,
and therefore, may influence the amount of bone loss that occurs. Width of the buccal plate,
elevation of a mucoperiosteal flap, smoking habits, and use of chlorhexidine postoperatively have
been proposed as factors that may affect the amount of bone remodeling of the post-extraction site.

Loss of the maxillary posterior teeth

The loss of maxillary posterior teeth initially results in a decrease in bone width at the
expense of the labial bony plate. The width of the posterior maxilla decreases at a more rapid rate

~ 60 ~
than in any other region of the jaws. The resorption phenomenon is accelerated by the loss of
vascularization to the alveolar bone and the existing fine trabecular bone type. However, because
the initial residual ridge is so wide in the posterior maxilla, even with a 60% decrease in the width
of the ridge, adequate diameter implants can usually be placed. However, the ridge progressively
shifts toward the palate until ridge is reabsorbed into a medially positioned narrower bone volume.
The posterior maxilla continues to progressively remodel towards the midline as the bone
resorption process continues [149]. These dimensional changes may lead to vertical and transversal
bone deficiencies, significantly limiting the insertion of implants of desired length and diameter
(Fig 1.60a,b).

a b
Fig 1.60a,b: Clinical view of vertical and transversal bone deficiencies after tooth extraction not allowing the insertion of standard
implants.

In particular, the edentulous posterior maxilla was shown to have the least amount of
residual bone height compared with other edentulous regions of the maxilla [150]. Bone height
significantly decreases from premolar to molar edentulous sites. However, edentulous molar sites
show a significantly greater ridge width than premolar sites. The residual ridge height may be seen
as the combined result of bone crest resorption in a coronal-apical direction, and the expansion of
the maxillary sinus. The contribution of these two remodeling processes in determining the final
dimensions of the ridge is still unclear.
Understanding the remodeling process of the posterior maxilla following tooth loss can
provide insight on the need for reconstructive procedures aimed at bone augmentation and for
sinus elevation.
Trombelli et al. observed a mean amount of vertical resorption at edentulous sites, which
was limited to first premolar sites (0.7mm) and is more pronounced at molar sites (2.1-2.4mm)
[151]. The limited reduction in ridge height at first premolar sites may be partly attributed to the
presence of the adjacent canine (Fig 1.61a,b).

~ 61 ~
 a b
Fig 1.61a,b: The limited residual ridge height is the result of the resorption of the alveolar ridge and the expansion of the maxillary
sinus.

In this respect, Trombelli demonstrated that the presence/absence of adjacent teeth to the
edentulous lacuna may significantly affect the extent of bone resorption [151].
Alveolar bone resorption caused by tooth loss is characterized by height loss, which is
accompanied not only by central bone repair but also by marginal or “cortical” bone resorption. It
is therefore important to know whether or not resorption is due to extraction or senescence.
There are two factors that contribute to bone loss. One is related to basal bone loss due to
the reinforcement of the osteoclastic activity of the sinus membrane, and the other is related to
alveolar bone loss due to crestal bone disappearance [152]. Even a slight increase in positive intra-
antral pressure can cause enlargement in the volume of the maxillary sinus [153].
Araujo et al. [137] and Botticelli et al. [154] concluded that after 3 months of healing, the
amount of bone height reduction is similar at implant sites and edentulous sites, despite the
placement of a dental implant. Such bone resorption could be attributed to the following situations:
(a) the bundle bone that lost its function following tooth removal is resorbed and replaced with
woven bone, (b) tissue adjustment occurs to meet genetically determined demands regarding ridge
geometry in the absence of teeth, (c) surgical trauma inflicted along with flap elevation, and (d)
root extraction and implant placement [137,138].
In the apical and middle portions of the socket site, minor dimensional alterations occur
and in the coronal portion of the ridge, the reduction of hard tissue volume is substantial. Four to
eight weeks appear to be an optimal period for deferring implant placement to allow adequate soft
tissue healing without loss of bone volume.
Covani et al. [155] confirmed that the buccal wall tends to reabsorb after extraction
according to a specific pattern. Thus, the reabsorption at midpoint represents the doubling of bone
loss at the distal and mesial points (Fig 1.62a-d).

~ 62 ~
 a b

c d
Fig 1.62: a-d: Panoramic radiographs demonstrating different resorption degrees following tooth loss.

SOFT TISSUE CHANGES AFTER TOOTH LOSS

Tooth removal will generally result in some alveolar bone loss, as well as structural and
compositional changes in the overlying soft tissue [139]. Both horizontal and vertical dimensional
changes are expected in both hard and soft tissue [148]. In the subsequent weeks following tooth
extraction, cell proliferation will result in increased soft tissue volume, and soft tissue will cover
and seal the socket entrance (Fig 1.63a,b).

a b
Fig 1.63a: Soft tissue seal one month after extraction. Fig 1.63b: Complete soft tissue seal three months after
extraction.

The changes in the mucosal contours are dependent on the corresponding changes in the
external profile of the alveolar bone surrounding the extraction site.
Iasella et al. measured soft tissue thickness changes after extraction [156]. There was a 0.4
to 0.5 mm gain in soft tissue thickness on the buccal and lingual sites at 6 months. In addition, this
~ 63 ~
study also demonstrated a trend in which the lingual soft tissues were nearly twice as thick as the
buccal ones.
Soft tissue on the buccal and lingual surface of the alveolar ridge has a tendency to increase
in thickness after extraction. The significance of this finding is as yet unknown. The same study
also documented that a soft tissue cover of 2.1 mm in thickness developed over the original socket
six months post-extraction. This post-extraction soft tissue may mask the real extent of hard tissue
resorption and impact on the overall outcome of any reconstructive procedures.

SINUS PNEUMATIZATION
Pneumatization is a physiologic process that occurs in all paranasal sinuses during the
growth period, causing that to increase in volume [157]. Primary pneumatization of the maxillary
sinus occurs during fetal development at about three months. At birth, the sinuses are filled with
fluid and the maxillary sinus is still an oblong groove on the mesial side of the maxilla. After birth,
the sinus continues to pneumatize into the developing alveolar ridge as the permanent teeth erupt.
Pneumatization of the sinuses develops slowly from birth until seven years and then becomes more
intensive but irregular. By the age of 12-14 years, the paranasal sinuses have nearly completed
taking their final shapes and dimensions, but may continue to increase slightly in size to age 25.
In old age, however, the maxillary sinus can penetrate more deeply into the edentulous alveolar
process.
At 12 to 13 years, the sinus floor is at the same level with the nasal floor and at age 20,
when the eruption of the third molars is complete, the pneumatization of the sinus ends and the
sinus reaches 5mm inferior to the nasal floor [158] (Fig 1.64a-c).
In the posterior maxilla, post extraction remodeling of the residual ridge may also be
accompanied by an increase in the size of the maxillary sinus by pneumatization, which is known
as the fourth expansion phenomenon of the maxillary sinus and has been explained as a type of
tisuse atrophy.

a
Fig 1.64a: Panoramic radiograph showing the sinus floor at the same level with the nasal floor.

~ 64 ~
 b
Fig 1.64b: Panoramic radiograph showing the sinus floor about 5 mm inferior to the nasal floor.

c
Fig 1.64c: Panoramic radiograph showing the expansion of the maxillary sinus combined with alveolar ridge resorption.

Although the adult maxillary sinus maintains its overall size while teeth are present, a rather
rapid expansion phenomenon of the maxillary sinus occurs with the loss of posterior teeth. In fact,
even with the loss of a single molar, the sinus expands between the adjacent tooth roots (Fig
1.65a,b).

~ 65 ~
 b
Fig 1.65a,b: The sinus tends to expand between the adjacent teeth roots in cases of single molar loss.

In the edentulous maxilla, the sinus expands in both inferior and lateral dimension and may
even invade the canine eminence region and proceed to the lateral perform rim of the nose (Fig
1.66a,b).

a b
Fig 1.66a,b: Although teeth are present, the expansion of the maxillary sinus is readily demonstrated between the adjacent teeth
roots.

The results of such an expansion are a lack of available bone in the posterior maxilla and a
greatly decreased height (even reaching values of less than 1mm) from both the sinus expansion
and crestal resorption. Histologic examination has shown that the pneumatization process occurs
by osteoclastic resorption of the cortical wall of the sinus and the layering of the osteoid inferior
to it [159].
The reasons for sinus pneumatization are poorly understood. There are two related factors
that are thought to contribute to the gradual expansion of the maxillary sinus cavity:
(1) osteoclastic activity of the sinus membrane,
(2) increased intrasinus pressure during expiration.
The thin ciliated mucosal lining of the sinus is separated from the underlying periosteum
by an imperceptible lamina propria.
This intimate association between the mucosa and periosteum without the intervening loose
connective tissue is believed to enhance the sensitivity of the periosteum to subtle increases in
intrasinus pressure. The positive intrasinus pressure during expiration may provide the impetus for
gradual sinus expansion through induction of osteoclast activity in the periosteal layer of the sinus
membrane.

~ 66 ~
 This positive pressure is the result of a size discrepancy between the choanal apertures
joining the posterior nasal cavities with the nasopharynx and the smaller anterior nares (nostrils)
creating a slight back pressure within the nasal cavities and communicating paranasal sinuses
during expiration.
In young adults with full dentition, the inferior extent of the sinus is normally in the second
premolar or first molar region. As teeth are lost, the maxillary sinus may expand into the vacated
alveolus (Fig 1.67a,b). The extent to which the sinus invades the alveolus cannot be predicted, and
careful evaluation of radiographs is necessary to avoid violating the sinus membrane during
implant placement.

a b
Fig 1.67a,b: After tooth loss, the maxillary sinus expand into the vacated alveolus, particularly the first molars.

Among the factors that influence sinus invasion is heredity, craniofacial configuration, the
pneumatization drive of the mucous membrane of the nose, density of the bone, growth hormones,
sinus air pressure and sinus surgery [157, 160]. A few experimental studies have described a
resumption of maxillary sinus pneumatization in adults after posterior tooth extraction [158, 149].
The cause for this phenomenon has been explained as a type of disuse atrophy [161, 162]. This
may be due in great part to the absence or reduction of normal masticatory loads transferred to the
bone after tooth loss causing a shift in the remodeling process toward bone resorption [158].
The best explanation for pneumatization of the maxillary sinus is a biomechanical one. It
is a result of disuse atrophy with endosteal (sinus floor) resorption caused by lack of occlusal
function due to missing teeth. This explanation has been validated in both animal and clinical
studies by Boyne. In short, pneumatization is a phenomenon of the mechanostat, a result of disuse
osteopenia, atrophy, and resorption with the effect of enlarging the sinus cavity. This results in
increased sinus volume at the expense of the edentulous alveolar ridge.
The rate and degree of the pneumatization process after tooth loss may be influenced by
the position of tooth roots into the sinus cavity [149]. Roots that protrude into the sinus have a thin
cortical bone lining [159]. During extraction, this thin bone may break and dislocate, thus allowing
the sinus to expand towards the empty socket (Fig 1.68a,b).

~ 67 ~
 a b
Fig 1.68a,b: CT scans showing a thin cortical bone plate above the tooth apex – notice the periapical lesion.

Greater pneumatization has been found after molar extraction in comparison to premolar
extraction [162]. The length of time during which teeth are missing is correlated to the extent of
alveolar resorption and to the pneumatization of the alveolar process in the maxillary sinus (Fig
1.69a-h).

a b

c d

~ 68 ~
 e f

g h
Fig 1.69a-h: Panoramic radiographs Showing different degrees of pneumatization and alveolar bone resorption.

CLASSIFICATION OF MAXILLARY ATROPHY

Bone volume classification was proposed by Lekholm and Zarb in 1985 for residual jaw
morphology related to the insertion of Branemark implants [162]. They described five stages of
jaw resorption, ranging from minimal to extreme (A, B, C, D, and E). The classification of
Lekholm and Zarb does not describe the actual resorption process in chronological order and is
more descriptive of the residual bone.
Another bone resorption classification, which includes the expansion of the maxillary
sinuses, was proposed by Cawood and Hawell in 1988 [68].
Misch [149] established four basic divisions of available bone for implant dentistry in the
edentulous jaws, which follow the natural resorption phenomena of each region (Fig 1.70).
According to this classification, division A is an alveolar ridge with adequate bone for implant
stability and has the following dimensions: > 5 mm in width, > 7 mm in mesiodistal length, > 12
mm in height, and angulation of < 30 degrees to the occlusal load. A minimum residual width of
5 mm is required to support a 4 mm diameter implant. The dimensions of a division B edentulous
ridge are 2.5 to 5 mm in width, 7 mm in mesiodistal length, over 12 mm in height, and angulation
to occlusal load of < 20 degrees. This decreased width in all jaw locations primarily occurs from
the facial to medial. Division C-w ridge consist of 0 to 2.5 mm in width and 10 to 12 mm in height.
A C-h ridge is inadequate in height (<10 mm) and has a crown height space to bone ratio of >1:1.
In division D, severe atrophy with significant loss is present (a crown height to remaining bone
ratio > 5:1).

~ 69 ~
 A B C C.W C.H D
Fig 1.70: Misch classification of available bone (divisions A,B,C,D) [149].

This classification was based on treatment options available at the time it was formulated
and depended very much on the amount of bone height available between the floor of the sinus
and the crest of the residual ridge as it related to ideal implant locations. Each protocol included a
surgical approach, the type of bone graft material to use, and a timetable for healing to take place
prior to prosthetic reconstruction. These original four divisions of bone were further expanded to
two subcategories to include the available bone width related to surgical approach and implant
design.
Moreover Misch presented four subantral classifications related to treatment options, based
on the amount of bone below the maxillary sinus [158].
Subantral option 1 (SA1): conventional implant placement
SA1 is chosen when there is sufficient available bone height of at least 12mm permitting
the placement of a 4-mm-diameter implant according to conventional surgical protocols.
Subantral option 2 (SA2): sinus lift and simultaneous implant placement
SA2 is selected when 10 to 12 mm of vertical bone is present. To obtain the needed 12mm or more
of vertical bone, the antral floor is elevated through the implant osteotomy.
Subantral option 3 (SA3): sinus graft with simultaneous or delayed implant placement
SA3, is indicated when at least 3mm of vertical bone and sufficient width is present between the
antral floor and the crest of the alveolar ridge. The implant may be inserted at the same time as
the sinus augmentation under ideal conditions or delayed for a period of four to six months.
Subantral option 4 (SA4): sinus graft healing and extended delay of implant insertion
In SA4, the subantral region is first augmented. This option is indicated, when less than 5mm
residual bone height remains. The SA4 corresponds to a larger antrum and minimal host bone.
Implant placement takes place after 6 to 10 months post augmentation. The amount of healing is
related to the antral size [20].
In 1995, Misch modified his classification to include the lateral dimension of the sinus
cavity and used this dimension to modify the healing period protocol, since smaller-width sinuses
(0 to 10 mm) form bone faster than larger-width (> 15 mm) sinuses [158].
In 2003, Chiapasco [164] modified existing sinus classifications with the aim of correlating
morphology with current surgical reconstructive protocols. He observed that implant placement in
the residual bone of the posterior maxilla generally becomes less predictable when the absolute
height of the residual alveolar ridge is less than 8mm, regardless of the cause (sinus pneumatization
or vertical alveolar resorption or a combination of both). Therefore, he evaluates and classifies the
atrophic posterior maxilla not only by absolute residual bone height, but also by available width,
intrasinus morphology, and the intermaxillary relationship, since the sinus grafting procedures
represent only one part of the reconstructive effort to restore orthoalveolar form. His classification
is based on three variables: width and height of the residual ridge, and inter-ridge relation.
Evaluation of the maxilla’s horizontal and vertical relationship (and not only of residual
bone volumes) is important to prevent construction of nonaxial prosthetic solutions (i.e., long

~ 70 ~
vertical crown height or unfavorable “crossbite” occlusion). These three variables are used to
define the treatment needs.
Another three subantral posterior alveolar ridges have been distinguished by Nimigean [165]:
SAC 1 with a residual bone height of 10 mm (usually found in edentulism of no more than 5 years
standing).
SAC 2 with a residual bone height of 5-10mm (after 5 to 10 years of edentulism, on average).
SAC 3 with a residual bone height of less than 5 mm (usually after edentulism of more than 10
years).
In 2008, Chiapasco et al. classified defects of the lateral-posterior maxilla according to the width
and the height of the residual alveolar ridge and according to the interarch vertical and horizontal
relationship in the following classes [166]:
Class A: (a) residual alveolar ridge height of between 4 and 8 mm; (b) residual alveolar width ≥ 5
mm (absence of significant horizontal resorption with maintenance if acceptable horizontal
intermaxillary relationship); and (c) absence of vertical resorption of the alveolar ridge with
maintenance of acceptable vertical intermaxillary relationship.
Class B: (a) residual alveolar ridge height between 4 and 8 mm; (b) residual alveolar ridge width
< 5mm (presence of horizontal resorption and unfavorable horizontal intermaxillary relationship);
and (c) absence of vertical resorption of the alveolar ridge with maintenance of acceptable vertical
interarch distance.
Class C: (a) residual alveolar ridge height <4mm; (b) residual alveolar ridge width ≥ 5mm (absence
of significant horizontal resorption with maintenance of acceptable horizontal intermaxillary
relation); and (c) absence of vertical resorption of the alveolar ridge with maintenance of
acceptable vertical interarch distance.
Class D: (a) residual alveolar ridge height <4mm; (b) residual alveolar ridge width <5mm
(presence of significant horizontal resorption unfavorable horizontal intermaxillary relation); and
(c) absence of vertical resorption of the alveolar ridge with maintenance of acceptable vertical
interarch distance.
Class E: the same characteristics of class A but with increased crown height space.
Class F: the same characteristics of class B but with increased vertical crown height space.
Class G: the same characteristics of class C but with increased vertical crown height space.
Class H: the same characteristics of class D but with increased vertical crown height space.
Class I: severe tridimensional atrophy of the edentulous maxilla with increased vertical crown
implant space, horizontal resorption, and sagittal intermaxillary discrepancy with maxillary
retrusion due to a centripetal bone resorption pattern.
A residual height of 4 mm was arbitrarily chosen by the authors as a “cutoff” measurement between
different classes because this height, if associated with adequate bone width and adequate bone
quality, is sufficient to allow primary stability of implants placed at the same time of sinus grafting
procedure. A residual width of 5 mm was arbitrarily chosen as a “cutoff” measurement between
different classes because this width or higher values are sufficient to embed implants of adequate
diameter, whereas lower values generally need reconstruction/regeneration of the deficient
horizontal dimension.

BONE DENSITY
Bone quality is a collective term referring to the mechanical properties, architecture, degree
of mineralization of the bone, chemistry and structure of the bone mineral crystals, as well as its
remodeling properties.

~ 71 ~
 Several classification systems have been proposed for assessing bone quality, but these
classifications have provided only subjective methods for preoperative evaluation. In 1985,
Lekholm and Zarb [163] classified bone density radiographically into four types based on the
amount of cortical versus trabecular bone (Fig 1.71). Quality 1 is composed of homogeneous
compact bone. Quality 2 has a thick layer of compact bone surrounding a core of dense trabecular
bone. Quality 3 has a thin layer of cortical bone surrounding dense trabecular bone of favorable
strength. Quality 4 has a thin layer of cortical bone surrounding a core of low-density trabecular
bone.

Fig 1.71: Lekholm and Zarb classification of bone density [162].

In 1988, Misch proposed four bone density groups independent of the jaw regions, based
on macroscopic cortical and trabecular bone characteristics [149] (Fig 1.72). The jaw regions with
similar densities were often consistent. Dense or porous cortical bone is found on the outer surfaces
of bone and includes the crest of an edentulous ridge. Coarse and fine trabecular bone types are
found within the outer shell of the cortical bone and occasionally on the crestal surface of an
edentulous residual ridge. These four macroscopic structures of bone may be arranged from the
least dense to the densest. These four bone categories described by Misch (D1, D2, D3 and D4)
are located in the edentulous areas of the jaw [149]. D1 bone is primarily dense cortical bone. D2
bone has dense-to-porous cortical bone on the crest and within the bone has coarse trabecular bone.
D3 bone types have a thinner porous cortical crest and fine trabecular bone and composes almost
all of the total volume of bone next to the implant. Bone density D3 is very common in the maxilla.
More than half of the patients have D3 bone in the posterior maxilla (more often in the premolar
region). The softest bone, D4, is most often found in the posterior maxilla (approximately 40%),
especially in the molar regions or after a sinus graft augmentation. Type 4 bone, characterized by
a thin cortex and loose trabeculae, does not achieve primary stability with a high rate of success
[167]. Bone with incomplete mineralization and large intertrabecular spaces may be addressed as
D5 bone. This type is most often immature bone in a developing sinus graft. The molar region of
the maxilla has a trabecular bone volume of 17% in women and 23% in men, with wide variations
in each group. Type 4 bone predominates in the molar of the edentulous (68% in women and 62%
in men) [168].

~ 72 ~
 Fig 1.72: Misch classification of bone density [148].

A more accurate determination of bone density is made with CT before surgery or tactilely
during implant surgery.
Using Misch’s parameters, the bone density classification may be evaluated on CT images
by correlation to a range of Hounsefield units (HU):
D1: > 1250 Hounsefield units
D2: 850 to 1250 Hounsefield units
D3: 350 to 850 Hounsefield units
D4: 150 to 350 Hounsefield units
D5: < 150 Hounsefield units
The bone density may be different near the crest compared to the apical region where the
implant placement is planned [169]. The most critical region of bone density is the crestal 7 to 10
mm of bone, as this is where most stresses are applies to an osseointegrated bone-implant contact
(BIC). Since there is a great difference in the tactile sensation during osteotomy preparation in
different bone densities, Misch proposed the different densities of his classification to be compared
with materials of varying densities [170]. Site preparation and implant placement in D1 bone is
similar to the drill resistance on an osteotomy in oak or maple wood. D2 bone is similar to the
tactile sensation of drilling into white pine or spruce. D3 bone is similar to drilling into a
compressed balsa wood. D4 bone is similar to drilling into a compressed Styrofoam or a light balsa
wood. The surgeon should know how to modify the treatment plan according to this tactile sense
method.
In 1999, Trisi and Rao using the Misch system, tried to establish a new classification among
four classes: D1, D2, D3, and D4 [171]. They suggested combining D2 and D3 into one group,
thus classifying bone density into three groups: D1, D2/D3, and D4.
A method for an objective quantitative classification of bone density that can be applied
preoperatively was recently proposed by Norton and Gamble [172]. They divided the mouth into
four main regions of interest:
Q1 anterior mandible above 850 HU.
Q2/Q3 posterior mandible/anterior maxilla, between 850 to 500 HU.
Q4 posterior maxilla under 500 HU.
Q4 tuberosity under 0 HU called the "failure zone".
Rebaudi et al. proposed a novel bone classification system, dividing bone density and/or
quality into three classes of clinical interest: H=hard; N=normal; and S=soft (HNS) using a simple,
innovative mathematical formula that converts HU into measurements of bone volume [173]. With
such a preoperative appreciation of bone quality/density, the oral surgeon will be able to choose
the best implant site preparation technique, implant positions, and components, as well as establish
a treatment plan that is appropriate for local anatomic conditions. For example, an osteoconductive

~ 73 ~
implant surface, which enhances bone-implant contact during the healing period, may be required
only when the bone is soft as in the posterior maxilla as well as when the use of implants enhancing
stability is indicated, e.g., longer and wider implants equipped with larger and nontraumatic
threads [174].
Shapurian et al. reported that the mean bone density in the posterior maxilla is 321 HU and
presented data supporting the postulate that a density of 180 HU or less is clearly representative
of low-density bone [175]. The distinction of type 4 bone using the Hounsfield scale as a reliable
and objective method is important, since numerous reports have considered bone density in the
recipient site to be an important factor for long-term success of osseointegrated implants [173].
This indicates that some areas of the mouth are safer than others for implant surgery. They reported
a strong correlation between bone density and subjective bone quality scores, as well as between
the bone density score and different regions of the mouth, demonstrating that an objective bone
density scale based on the Hounsfield scale can be established.
Accurate analysis of the bone content and architecture can facilitate clinical decision-
making regarding patient selection, implant type and surface, and the surgical technique used.
Knowledge of Hounsfield values as an objective method of evaluating bone density for a
proposed implant site could alert the surgeon to modify the treatment plan so that primary stability
in bone of less density is ensured and a longer healing period is planned.
Bone density seems to represent the major determinant of primary stability in maxillary
sinus augmentation with simultaneous implant placement. Preoperative bone density assessment
may help to avoid stability-related complications in one-stage implant treatments of the atrophic
posterior maxilla [176] (Fig 1.73a,b). Men generally exhibit greater bone density than women, and
blacks and Asians have greater density than whites.

a b
Fig 1.73a,b: Clinical view of posterior maxillary bone Fig 1.73a,b: Clinical view of posterior maxillary bone
composed of a thin layer of cortical bone surrounding low composed of adequate layer of cortical bone surrounding low
density trabecular bone – notice the resorption pattern after density trabecular bone – notice the moderate corticalization
tooth loss. after tooth loss.

~ 74 ~
 2. GENERAL CONCEPTS ON TISSUE INTEGRATION AND IMPLANT
OSSEOINTEGRATION

Today, the use of osseointegrated dental implants is considered a predictable and successful
treatment method for functional restoration of the fully or partially edentulous patient. Dental
implant therapy is currently among the most popular methods for replacing missing dentition. In
comparison to conventional prosthesis, implant-supported prostheses are associated with better
comfort, stability, and esthetics, positively effecting patients’ oral health-related quality of life.
The success of contemporary dental implants is largely attributed the process of osseointegration.
Since the pioneering, work of Branemark [178] and others [179], the use of dental implants has
become a standard and accepted treatment modality for edentulous patients. Dental implants are
being placed in a variety of biochemically and biomechanically compromised bone tissue, such as
the atrophic posterior maxilla.
Different physio/chemical features of the implant surface influence the biomolecular and
cellular interactions with the implant [180-182]. A comprehensive understanding of the molecular
and cellular processes relevant to peri-implant healing is critical for finding therapeutically
relevant targets to positively influence implant osseointegration.

OSSEOINTEGRATION OF DENTAL IMPLANTS

The dentogingival complex consists of highly differentiated and specialized tissues, while
the oral implant-tissue interface is the result of a foreign body reaction to biocompatible materials.
From this perspective, the two entities cannot be directly compared. Osseointegration is defined
as “a direct structural and functional connection between vital bone and the surface of a load-
carrying implant at the level of light microscopy” [178, 183], which provides a prosthesis
supporting foundation and can transport occlusal load directly to the bone (Fig 2.1).
Histologically, osseointegration has been further defined as direct anchorage of an implant by the
formation of bone directly on the surface of an implant without an intervening layer of fibrous
tissues [184, 185]. This concept was developed by Per-Ingvar Branemark, a professor at the
institute for Applied Biotechnology at the University of Goteborg in Sweden and the inventor of
the well-known Branemark implant system. Branemark discovered during animal studies of
microcirculation in bone repair during the 1950s, a strong interfacial connection between bone and
titanium. Clinically, this suggests ankylosis of implant to bone interface as described by Schroder
and associates [185].

a b
Fig 2.1a,b: Osseointegrated implant in both jaws since 18 years – notice the bone maintenance around the implant nicks.

~ 75 ~
 This ankylotic interface is developed during the healing period immediately post placement
and is dynamically maintained throughout the osseointegration period for the long term (Fig 2.2,
Fig 2.3).

Fig 2.2: Intraoral radiograph exhibiting the papilla-like bone Fig 2.3: CT slices showing well osseointegrated implants 17
maintenance of implants inserted 17 years prior. years prior - note the corticalization due to probal functional
loading.

The long-term success and predictability of dental implants are related to the
osseointegration process [186] (Fig 2.4, Fig 2.5).
Several key factors influence successful implant osseointegration [179, 187] and include
the following:

 The characteristics of the dental implant surface, which can dramatically affect
osseointegrating success.
 Implant design, shape, macro and micro surface topography.
 Initial primary stability is a crucial prerequisite for achieving osseointegration [188].
 Bone density in the host site. Trabecular bone density can affect primary and secondary
stability by guided bone regeneration and remodeling at the tissue implant interface [189].
Maxillary bone density is a given factor. Therefore, implant surface, design, and shape
should be expected to adapt to the specific quantities and qualities of the host bone to
promote osseointegraion.
 The implant-crown ratio which can create a destructive lever arm that may lead to crestal
bone loss in the long term perspective.
 Ridge height and width - When the host bone or graft is inadequate in height, the portion
of the implant body inside the bone has a limited capacity for challenging occlusal loads.
A ridge that is too narrow (i.e. < 5mm) to accommodate standard 3.75mm diameter
implants, will force the clinician to use less desirable reduced diameter implants to obtain
the necessary interfacial implant-to-bone-connect.

~ 76 ~
 Fig 2.4: CT slices demonstrate the interfacial implant-to-bone connection. Note the massive corticalization.

Ideally, the marginal and apical parts of the implants should be fully engaged in cortical bone
or in cancellous bone that presents a high proportion of bony trabeculae to support the implants. It
is crucial to achieve initial stability with a micromotion of less than 150μm of the implant and
osseointegration. Once stability is lost, the implant can only be removed.

a b

c d

~ 77 ~
 e f
Fig 2.5a-f: Panoramic radiographs demonestrating the well osseointegrated implants in different locations. The implant radiographs
are long term follow-up of 10 to 18 years.

SURFACE PROPERTIES OF DENTAL IMPLANTS

The dental implant surface represents one of the key factors affecting successful
osseointegration and may affect the amount of bone formed at the bone implant interface [190].
The influence of the implant design on primary stability is due to the surface characteristics, the
implant body morphology, and the implant thread geometry. The earliest studies indicate that
implant surfaces dramatically influence the retention of the implants due to a greater bone-to-
implant contact (BIC), and provide greater biomechanical interlocking at the implant with the host
bone, despite the recognized effect of surgical technique and loading conditions [191].
The most important surface properties are topography, chemistry, surface charge and
wettability.
Processes such as protein adsorption, cell-surface interaction, and cell/tissue development
at the interface between the implant and host bone are affected by implant surface properties [192]
and are all relevant for the function of the device.
Modifications to the implant surface are commonly made through the use of additive or
abstractive techniques. Today, there is no consensus concerning the most appropriate implant
surface topography, other than to say that rough surfaces are superior to turn surfaces using
additive or abstractive processes.
Additive methods such as titanium plasma spraying, hydroxyapatite (HA) coating, coating
with plasma, or magnetron sputter coating, coatings of calcium phosphate and/or apatites, as well
as various attempts to coat an implant surface with biologic molecules, have also been described.
Subtractive methods of surface modification include abrasion through blasting with titanium
oxides or other soluble or resorbable biomaterials, grit or sandblasting with aluminous oxides, and
blasting and acid-attacking or etching (with a hydrogen sulfate or hydrogen chloride). Other
surface treatments include anodizing, cold working (dimpling), sintering, and bead compaction.
The surface energy, composition, topography, and roughness of an implant are thought to affect
bone formation and apposition [193-196] (Fig 2.6a,b).

~ 78 ~
 a b
Fig 2.6a: Grid-blasted and high-temperature etched dental Fig 2.6b: Micro and macro bits for osteoblast retention.
implant surface.

Some important advantages have been attributed to increased surface roughness. These
include: a) increased surface area of the implant adjacent to the bone; b) improved cell attachment
to the implant surface; c) increased bone present at the implant surface; d) increased biomechanical
interaction of the implant with the bone.
A more potent bone response to moderately roughness surfaces (Sa 1.1-2 um) has been well
investigated [197]. Surface roughness of more than 2 µm is associated with a higher risk of peri-
implantitis [198]. Rough-surface implants support the attachment of the developing blood clot
after placement. The provisional extracellular matrix of the blood clot allows osteogenic cells to
migrate to the implant surface, where they can lay down new bone to supplement the bone that
originates from the implant bed. This can explain the higher degree of bone-implant contact during
early osseointegration.
Intimate peri-implant bone is a prerequisite for strain adaptation, which occurs in trabecular
bone as well as in cortical bone in the form of remodeling and modeling. This mechanism is based
on mechanical strain signal sensing leading to cellular mechanotransduction. Conversion of
mechanical forces into cellular response involves activation of intercellular signals induced by
stretched cytoskeletal molecules and piezoelectric potentials.
Buser et al. compared experimental implant surfaces bearing different surface topographies
that increase surface roughness and resulted in increased bone-to implant contact [200]. The
histologic examination revealed direct bone-implant contact for all implants. However, the
morphometric analyses demonstrated significant differences in the percentage of bone-implant
contact, when measured in cancellous bone. Electropolished as well as the sandblasted and acid
pickled (medium grit; HF/HNO3) implant surfaces had the lowest percentage of bone contact with
mean values ranging between 20 and 25%. Sandblasted implants with a large grit and titanium
plasma-sprayed implants demonstrated 30-40% mean bone contact. The highest extent of bone-
implant interface was observed in sandblasted and acid attacked surfaces (large grit; HCl/H2SO4)
with mean values of 50-60%, and hydroxylapatite (HA)-coated implants with 60-70%.
Wennerberg and coworkers also systematically revealed that increasing surface roughness
improved both bone-to-implant contact and physical interaction with bone (removal torque)
[197,201-204]. According to Kasemo and Lausmaa, roughening implant surfaces with micopits
measuring less than about 100 µm but well above the nanometer scale (i.e., 1/1000 µm) may
influence the biologic response at the bone-implant interface, since the micropits are within the
size range of cells and large biomolecules [205]. In contrast, micropits measuring 100 µm and
larger may serve the strictly mechanical function of aiding in stress transfer. The current literature
related to the surface topography effect on osseointegration at the molecular level supports both

~ 79 ~
histomorphometric and biochemical data of improved osseointegration [204, 206]. When the
surface topography of an implant is altered, the chemistry is also altered. Cell behavior is depended
on both topography and chemistry.
Acid etching removes most of the carbon contaminants introduced onto the implant surface
by machining, together with the outer layer of titanium. Thus, acid-etched and plasma-sprayed
surfaces are generally cleaner and more reproducible than turned and sandblasted surfaces.
Sul concluded in a study investigating bone tissue reactions to various surface oxide
properties that, either separately or together, surface chemistry and topography play important
roles in the bone response to the implant surface [207]. There is clear evidence that rough-surfaced
implants decrease the integration time and may decrease overall treatment time appreciable [193]
which means that implants with rough surfaces are more likely to be successful when used for
immediate loading [208, 209]. Rough surfaced implants demonstrate enhanced bone apposition
and higher removal torque values indicating a direct relationship between the biological and
mechanical qualities of the interface [193, 210-212]. Ferguson and coworkers confirmed the
benefits of a sandblasted, acid-etched titanium implant surface, and as such this surface treatment
should be considered the gold standard [213].
Chemical and biochemical surface modifications are assumed to be especially
advantageous for accelerated healing. Fluoride surface modification seems to enhance osteoblastic
differentiation and interfacial bone formation [214]. The use of modified titanium surfaces with
extracellular matrix components enhances bone remodeling in the early stages of healing. A newer
approach is surface modification with bioactive molecules. Drug-eluting coatings are the most
probable future developments. Local delivery of bisphosphonates has resulted in increased
mechanical fixation of implants [215], while the potential of growth factors such as bone
morphogenetic protein 2 has been shown in many studies [216]. It has been suggested that
bioactive implants may offer certain advantages [197, 201]. Coatings of calcium phosphate,
bisphosphonate, and collagen containing chondroitin sulfate could potentially enhance peri-
implant bone healing, but no significant difference was shown compared to the performance of
the reference standard of a sandblasted acid-etched titanium implant. The local delivery of
bisphosphonates to enhance local peri-implant bone formation is promising avenue requiring
further study. Indeed, a higher percentage of bone contact was found around bisphosphonate-
coated implants by Fiorellini et al. [216] and Peter et al. [215]. Calcium-phosphate (CaP), mainly
hydroxyapatite, is the main inorganic element of native bone. Coating with CaP is one of the
strategies used to improve the surface characteristics of titanium. The bioactivity of hydroxyapatite
is due to a chemical cohesive bonding of the apatitic coat with the surrounding osseous tissue
through ion exchange [217]. This osteogenic exchange enables bidirectional bone formation on
both the osseous recipient site and CaP coating [218]. The resorbable CaP coating has a low
coating thickness of 20-30 µm, a micro-crystalline structure with a large active surface, and
microporosity with a high capillarity effect on blood. According to Schiegnits et al. [219] CaP
coated surfaces on supracrestal-inserted implants may have osteoconductive characteristics at the
implant shoulder and support the concept that bioactive CaP-coated implants may have the
capacity to guide supracrestal bone growth.
Titanium is basically considered to be bioinert and not likely to form direct bonds with
bone. Therefore, a bioactive material, coated onto the surfaces of Ti implant, could increase
optimal surface reactivity. Several studies have indicated that an enhanced calcium composition
on the outer oxide layer can improve cell adhesion on titanium surfaces by increasing protein
adsorption [220]. Several in vivo studies at the molecular level indicate that surface topography

~ 80 ~
influences adjacent cellular functions, including the process of bone matrix biosynthesis and
mineralization [220].
Most recent investigations focus on mRNA expression profiles of cells adjacent to the
implants or adherent cells on implant surfaces. The findings include increased expression of
mRNA involved in the regulation of cell proliferation, angiogenesis, osteoinduction, and
osteogenesis [221].
Charge is defined as the energy at the surface of a dental implant and it is positive, negative,
or neutral. Charge density affects the hydrophilic or hydrophobic characteristics of the surface
[222]. A hydrophilic or easily wettable implant surface is proposed to be superior during the initial
phase of wound healing and osseointegration process. Increasing attention has been paid to the
potential of hydrophilic implant surfaces to further stimulate osseointegration [223, 224]. To date,
two different technologies are used and are commercially available to prepare hydrophilic dental
implants: i) rinsing the titanium surface after etching process under nitrogen protection, followed
by storage in isotonic saline [225], and ii) chair-side treatment of dental implants with aqueous
sodium hydroxide [224]. In vitro, hydrophilic surfaces support the adhesion of monocytes, platelet
activation, and blood clot formation, which are the initial events in osseointegration [226, 227].
Hydrophilic surfaces are favorable for the osteogenic differentiation of mesenchymal stem cells,
and have demonstrated anti-inflammatory properties [180, 228]. All of the dental implant studies
show a benefit in hydrophilicity for early osseointegration.
The wettability of an implant surface is directly influenced by its surface energy.
Wettability is important in the accessibility of an implant surface for aqueous biologic liquids.
Increased wettability enhances the interaction between the implant surface and the biologic
environment.
Research has shown that in low-density bone, primary stability may be influenced by
different implant designs [229, 230]. The choosing of implant design features that optimize surface
area available for bone contact can increase mechanical anchorage and primary stability in low-
density bone and reduce initial micromotion during the remodeling of the trabecular network at
the interface [231, 232].
Beside the diameter and length of the dental implants, the thread configuration has been
modified over time [233]. Threads have been incorporated in the implant design to increase
primary stability via mechanical friction with the host bone. A modified thread configuration such
as length and diameter can be particularly important in the posterior. Studies have shown that
initial primary stability and consequently early endosseous integration in poor density bone is
improved with a reduced thread pitch and depth which results in increased BIC [234]. Therefore,
the presence of large BIC areas undergoing resorption and areas with no initial BIC for prompt
new bone deposition might promote better osseointegration [234], and the subsequent healing
interval might be shortened.
Tapered implant designs increase the compression of bone and primary stability when
placed into a conventional parallel osteotomy [235]. O’Sullivan et al. [235] demonstrated that a 1o
taper had more initial stability than parallel implants and a 2o taper could not be inserted completely
in the same osteotomies.

THE BIOLOGICAL PROCESS OF IMPLANT OSSEOINTEGRATION

Current theories of bone biology are an extension of those formed by Marshall Urist in
1952 [236]. Bone formation is a complex series of molecular changes that lead to a newly formed
structural and functional entity. The stages of endosseous wound healing can be subdivided into

~ 81 ~
hematoma, clot resolution, and osteogenic cell migration, which lead to new bone formation at the
wound site [237]. The healing process around an implant is similar to what occurs in endosseous
wound healing. This three stage process is the biologic process of implant osseointegration.
When a rough-surface implant is placed into the cancellous marrow space, blood is initially
present between the implant and bone, and a clot subsequently forms. Only a small amount of bone
is in contact with the implant surface and the rest is exposed to extracellular fluid and cells. During
the initial implant-host interaction, numerous cytokines are released that have a variety of
functions, from regulating adhesion molecule production and altering cellular proliferation to
enhancing collagen synthesis and regulating bone metabolism. These events also correspond to the
beginning of the general inflammatory response to the surgical procedure. By the end of the first
week, inflammatory cells respond to foreign antigens introduced by the surgical procedure. While
the inflammatory phase is still active, vascular ingrowth from the surrounding vital tissues begins,
developing into a more mature vascular network during the first three weeks following implant
placement [238]. In addition, cellular differentiation, proliferation, and activation begin.
Ossification also begins during the first week, and the initial response observed is the migration of
osteoblasts from the endosteal surface of the trabecular bone and the inner surface of the
surrounding cortex to the implant surface. This migration is likely a response to the release of bone
morphogentic protein (BMP) during implant placement and the initial resorption of bone in contact
with the metal surface. The osteophytic phase lasts about one month. Once they reach the implant,
the bone cells spread along the entire implant surface (osteoconduction), laying down an osteoid
layer. Initially, this is an immature connective tissue matrix and the bone deposited is a thin layer
of woven bone called a foot plate (basis stapedis). The fibrocartilaginous callus is eventually
remodeled into bone callus (woven and, later, lamellar) in a process similar to endochondral
ossification. This process occurs during the next three months as more bone is added to the total
surface area of the implant. Four months after implant placement, the maximum surface area is
covered by bone. By this point, a relatively steady state has been reached and no further bone is
deposited on the implant surface [239].
The final, or osteoadaptive, phase begins approximately four months after implant
placement. A balanced remodeling sequence continues even after the implants are exposed and
loaded. Once loaded, the implants generally do not gain or lose bone contact, but the bone thickens
in response to the load transmitted through the implant to the surrounding bone, and some
reorientation of the vascular pattern can be seen.
Because grafted bone integrates with implants to a higher degree than does natural host
bone [239], bone grafting is recommended around implants placed in sites where bone volume or
density is deficient or where there is a history of implant failure. Traditionally, an osseointegration
period of four months prior to loading is recommended for implants placed in grafted bone, and 4
to 6 months prior to loading for implants placed in normal bone, depending on its density.
Bone formation induction at the implant sites is due to a major alteration in the cellular
environment [240]. Davies described peri-implant bone healing as having three distinct phases: a)
osteoconduction, b) de novo bone formation, c) bone remodeling [241]. Albrektsson and
Johansson described the terms osteoinduction and osteoconduction as interrelated but not identical
phenomena that occur during bone wound healing [184].
Osteoinduction involves mesenchymal cells differentiating into bone-forming cells [237].
Primitive, undifferentiated, pluripotent mesenchymal cells are stimulated to develop into the bone-
forming osteoblasts and osteocytes cell lineages [184]. Osteoconduction has been defined as
appositional bone growth permitting bone formation on a surface or down into pores, channels, or

~ 82 ~
pipes [184]. Davies described de novo bone formation around dental implants as the formation of
a mineralized interfacial matrix, equivalent to that found in natural bone tissue, on the implant
surface [237]. The phenomenon of osteoconduction relies on the migration of differentiating
osteogenic cells to the implant surface [241] along with undifferentiated mesenchymal cells that
migrate to the surface of the implant, attach, and proliferate.
According to Boyan and coworkers, environmental factors such as oxygen tension help
determine whether mesenchymal cells will differentiate into fibroblasts, chondrocytes, or
osteoblasts [240]. Adherence can occur when the cell itself directly binds to the surface or when it
binds to arginineglycine-aspartic acid (RGD) –containing proteins that adhere to the surface [242].
During this time, the mesenchymal cells synthesize their own extracellular matrix, including
growth factors and cyktokines, and modify the surface of the implant. Mesenchymal cells then
undergo osteoblastic differentiation. Cells of mesenchymal origin are extremely sensitive to
surface properties such as surface energy, roughness, and topography [243]. The new osteoblasts
produce osteoid, including matrix vesicles and growth factors. Matrix calcification occurs, leading
to woven bone formation which is subsequently remodeled with osteoclast recruitment [194].
Osborn and Newesley proposed that two different phenomena exist by which bone can
become exposed to an implant surface, contact osteogenesis and distance osteogenesis [244].
Contact osteogenesis involves de novo bone formation directly on the implant surface (Fig 2.7a,b,
Fig 2.8). Distance osteogenesis is the formation of new bone on the surfaces of the existing peri-
implant bone. The placement of implants in the alveolar process elicits a sequence of healing
events, including necrosis and subsequent resorption of traumatized bone around the implant body
concomitant with new bone formation [245].

a b c
Fig 2.7a: Contact osteogenesis Fig 2.7b: Contact osteogenesis in Fig 2.8: Secondery osteons next to a microstructured
in spongy bone. cortical bone. surface.

Based on research at the molecular level, implant substrate-osteoblast interactions may be

characterized as specific, protein-mediated, dynamic, signal-generating events. Implant surface
modification may modulate the cell behavior [246]. Following implantation, after hemostasis and
clot formation, fibrinolysis occurs with the formation of a loose connective tissue stroma that
supports angiogenesis [240]. The surface of the implant is conditioned by serum proteins, mineral
ions, sugars, and lipids, as well as cytokines produced by immune cells. The behavior of absorbed
proteins may be related not only to the interaction between the charge of the material and the

~ 83 ~
protein, but also to the protein’s potential for change once adsorbed onto the surface [236]. The
static blood volume surrounding the implant varies considerably as a function of the implant design
and site [234]. Vascular ingrowth or angiogenesis is the most likely mediated by extracellular
matrix components and growth factors [247].
Davies suggested that the implant surface provides anchorage for the fibrin clot to
withstand detachment forces during cell migration and thus maintain a migratory pathway for the
differentiating osteogenic cells to reach the implant surface [237].
Achieving optimum peri-implant healing requires an exact choreography of biological and
molecular events, of cell migration, proliferation, extracellular matrix (ECM) deposition,
angiogenesis, and remodeling. Among the many factors contributing to non-healing is impaired
production of cytokines by local inflammatory cells and fibroblasts and reduced angiogenesis.
Implant adherent macrophages and multinuclear cells are detected prior to bone formation at the
surfaces of different materials inserted in the bone. Osseointegration is a dynamic process, where
there is a delicate interplay between bone resorption in contact regions and bone formation in
contact-free regions [245]. Recent histological data in humans show a potential role for osteoclasts
in modulating osseointegration where no new bone formation was observed in areas with any
visible prior resorbtive processes [248, 249]. The development of the bone-implant interface
requires the colonization of the implant surface with MSCs / osteoprogenitor cells and their
subsequent proliferation and differentiation. The crestal area receives the majority of occlusal
forces that affect the surrounding tissue of an implant. Rough or microthreaded implant neck
designs may inhibit detrimental micro-motion at the bone-implant interface and thus allow stress
transfer to the surrounding tissue [199].
Static load was reported to induce structural adaptation of the peri-implant bone with
absence of bone loss [250]. Dynamic load, by contrast, is seen to have a detrimental effect on peri-
implant bone behavior [250]. Peri-implant bone loss was reported to be significantly higher in the
mandible due to less vascularization and slower bone adaptation compared with trabecular bone.
Interleukin-1B is a sensitive marker for the detection of peri-implant bone alteration [251]. Lam
(1960) stated that the maximum loss of tissue contours occurs during the first month of healing
[252].

TIME SEQUENCE OF IMPLANT OSSTEOINTEGRATION

Immediately after implantation, serum proteins adhere to the implant [193]. During the first
three days, mesenchymal cells attach and proliferate. By six days, an osteoid is produced. By two
weeks, matrix calcification is complete and by three weeks, remodeling is well under way. One of
the most critical factors in successful implant osseointegration is bone stability at the time of
placement. Relative motion between the implant body and the surrounding bone during the early
healing phase is considered to be a high risk factor for early implant loss due to osseointegration
failure.
Following the placement of an endosseous implant, primary mechanical stability is
gradually replaced by biologic stability. The transition from primary mechanical stability, provided
by the implant design, to biological stability provided by osseointegration takes place during early
wound healing [245]. Therefore, presumably, there is a period of time during healing in which
osteoclastic activity decreases the initial mechanical stability of the implant but the formation of
new bone has not yet occurred to a level required to maintain implant stability. During this critical
period, a loaded implant could be at greatest risk of relative motion and would theoretically be
most susceptible to osseointegration failure. Only with bone remodeling will there be a gradual

~ 84 ~
replacement of peri-implant bone, with the possibility of de novo bone formation at the implant
surface [247]. A series of cellular events contributes to this change. Osteogenesis in vivo must find
a balance between achieving adequate coverage of an implant material with osteogenic cells and
the ability of those cells to differentiate into competent osteoblasts in a timely manner [194].
Berglundh et al. described a novel model used to investigate different temporal phases of
wound healing that result in osseointegration. In Labrador dog mandibles, within two hours, the
wound chamber was occupied by a coagulum of erythrocytes, neutrophils, and macrophages in a
fibrinic network [245]. At four days, along the cut surface, osteoclasts were observed and
mesenchymal cells, vascular structures, and densely packed connective tissue cells were found
within the wound chamber. At seven days, woven bone was first seen along the implant surface
and along vascular connecting. Trabecular were lined with osteoblasts and with a provisional
matrix which had collagen fibrils and vasculature. At two weeks, newly formed bone appeared to
be extending from parent bone. At four weeks, marked formation of woven bone combined with
lamellar bone was seen. Finally, at 8 and 12 weeks, there were marked signs of remodeling within
the wound chamber in this animal model. Osteoclastic activity was seen as early as five days
following implant placement, and new bone formation was noted at one week postplacement.
Replacement of the original bone that was responsible for the initial implant stability at
placement was well underway at the two-week mark. The critical time frame for implant healing
in humans is 2 to 3 weeks postplacement. The effect of immediate loading is not clearly understood
as it relates to the timeline of osseointegration. However, it is clear that the processes of osseous
remodeling and osseointegration occur simultaneously with functional loading. Interactions of
these biologic and mechanical forces are critical to the successful integration of the implant. Initial
stability and continued stability during the healing phase is necessary for osseointegration to occur
and splinting of the implants improves the likelihood of success [208, 209].

OSSEOINTEGRATION OF IMPLANTS PLACED EARLY POST EXTRACTION

An understanding of extraction wound healing and subsequent bone resorption,
regeneration, and remodeling of the healing socket is necessary to provide a basis for reviewing
the outcomes of implants placed early after tooth extraction (Fig 2.9a-d). The events that occur in
a healing extraction socket have been extensively studied [135,253-257] and five stages of healing
have been described [135]. In the first stage, an initial clot forms as a coagulum of red and white
blood cells derived from the circulation. In the second stage, granulation tissue replaces the clot
over a 4- to 5-day period. Cords of endothelial cells are associated with budding capillaries. In the
third stage, connective tissue gradually replaces granulation tissue over 14 to 16 days. The
connective tissue is characterized by the presence of spindle-shaped fibroblasts, collagen fibers,
and a metachromatic ground substance. In the fourth stage, calcification of osteoid is apparent,
commencing at the base and periphery of the socket. Early osteoid is seen at the base and periphery
of the socket by 7 to 10 days. Bone trabeculae almost completely fill the socket by six weeks. In
the fifth stage, complete epithelial closure of the socket is achieved after 24 to 35 days. Substantial
bone fill occurs between 5 and 10 weeks [135,255,256]. By 16 weeks, bone fill is complete, with
little evidence of osteogenic activity [257].

~ 85 ~
 a b
Fig 2.9a: Clinical view of extracted premolar and molar three Fig 2.9b: Full thickness flap elevation during sinus floor
weeks hense. augmentation

c d
Fig 2.9c: Clinical view of implants placed early post extraction Fig 2.9d: Guided bone regeneration (GBR) was indicated due to
with guided bone regeneration (GBR). horizontal bone deficiency

Three factors influence ridge alterations after immediate implant placement, the location
where implants are placed, the thickness of the buccal bone crest and the size of the horizontal gap
between the center of the implant and the buccal wall [258]. The marginal defects around
immediate implants placed in molar extraction sites are completely filled after six months of
healing through de novo bone formation [259]. Bone resorption is observed from the external
aspects of the buccal and oral socket walls [259]. Dimensional changes of the external socket walls
are mostly pronounced at the buccal aspects [258]. Any dip in implant stability has fundamental
clinical importance for immediately loaded implants. If the stability decreases below a critical level
during the healing process, a functionally loaded implant cannot withstand masticatory forces,
becomes mobile, and fails. There is a considerable lack of agreement regarding the parameters of
the dip in postinsertion stability. Studies that demonstrated this dip in stability have usually
observed it between the second and eighth week following implant placement [260]. The
maximum stability drop was detected during the third or fourth week postplacement and ranged
from 2 to 12 ISQs below the baseline ISQ [260,261]. The use of an early loading protocol in the
posterior maxilla is doubtful, as this region has always been considered particularly challenging
for long-term successful implants survival because of its deficiency in bone quantity and/or
quality. Roccuzo and Wilson suggest that successful functional loading on SLA implants is
possible after the sixth postoperative week in the posterior maxilla with an implants surface area
that exceeds 125 mm2 [262].

~ 86 ~
 BONE REGENERATION, MODELING AND REMODELING
Bone healing and the restoration of form and function involve well-orchestrated biological
events with systemic factors of bone metabolism and local mediators that regulate recruitment,
differentiation, and function of cells participating in bone turnover [263] (Fig 2.10a,b).
Regeneration of bone follows three different pathways of ossification: endochondral,
transchondroid, and intramembranous ossification. Typically, endochondral ossification can be
found in long bone fracture healing [264]. Endochondral ossification is seen during the embryonic
development of long bones [265, 266]. Transchondroid ossification produces chondroid bone and
was identified as intermediate tissue between cartilage and bone [265, 267]. Intramembranous
ossification is characterized as direct bone formation by differentiated osteoblasts with no pre-
existent cartilage [268].

a b
Fig 2.10a: Differentiation and activation of osteoclasts by Fig 2.10b: Differentiation and activation of osteoclasts by
osteoblast/osteoclast coupling during physiological remodeling inflammatory cytokines during pathological resorption [269].
[269].

Published data have elucidated a close interaction between angiogenesis and osteogenesis
in fracture healing [270-274] to achieve biologically functional tissue. The ossification is
accompanied by angiogenesis of new capillaries from pre-existing ones which maintains oxygen
homeostasis to deliver nutrients and provide biological mediators [271, 275]. Endothelial cells
involved in angiogenesis, participate in the construction of microvasculature and contribute to the
tissue response by expressing osteoblast adhesion molecules [276].
In contrast to endochondral ossification during fracture healing, histological studies have
shown that intramembranous ossification is observed in alveolar bone healing [277, 278]. Healing
of an extraction socket, and external changes drive to the loss of the alveolar ridge width and height
[139]. A blood clot fills the socket immediately after tooth extraction as a consequence of blood
vessels rupturing from the periodontal ligament and the apical foramen. Then, cells start a series
of events, which lead to the formation of a fibrin network, which will contribute along with the
platelets to create a stable clot within the first 24 h. Successive events include the formation of
granulation tissue, which will completely replace the clot a week later, and the formation of osteoid
tissue at the base of the socket (Fig 2.11a-h). In fact, a hard tissue bridge covers the marginal
portion of the extraction site and this phenomenon is well known as “corticalization” [145]. It
consists of a series of proliferative and resorptive events, which will drive to the formation of a
cortical bone wall.

~ 87 ~
 Fig 2.11a-h: Illustration of the different stages of alveolar healing. (A) The presence of blood cells and an inflammatory infiltrate
after extraction. (B) Neovascularization is rapidly established, bringing new cellular and molecular elements. (C) The signaling
commits local cells to the osteogenic route. (D) High magnification of cellular differentiation associated with matrix synthesis
which leads to the formation of immature tissue. (E) This differentiation process occurs at the center of the socket and over the
alveolar walls. (F) The process is amplified, leading to the formation of a trabecular framework. (G) The trabecular framework
joins and starts to fill the socket. (H) Alveolar filling is carried out with bone that should be remodeled to withstand the local
stress and strain [18].

It is well known today that bone is continually being deposited by osteoblasts and absorbed
by osteoclasts at active sites in the body. It is important to note that bone modeling and bone
remodeling are two different processes in osseous repair, although, many scientist and practitioners
define both processes as remodeling.
Bone modeling typically refers to the sculpting and shaping of bones after they have growth
in length. This process involves the independent, uncoupled actions of osteoclasts and osteoblasts.
Bone is resorbed in some areas and added in others. Bone modeling can also be controlled by
mechanical factors, for example, during orthodontic tooth movement, in which the application of
force causes the bone to resorb on the tooth surface, new bone to form on the opposite surface, and
the tooth to move with the surrounding bone rather than through the alveolus. Bone modeling can
change both the size and shape of the bones. Bone remodeling, on the other hand, refers to the
sequential, coupled actions by these two types of cells. It is a cyclical process that usually maintains
the status quo and does not change the size or shape of bones.
Bone remodeling removes a portion of old bone and replaces it with new bone. Unlike
bone modeling which slows substantially after growth stops, bone remodeling occurs throughout
life (although its rate also slows somewhat after growth). Bone remodeling also occurs throughout

~ 88 ~
the skeleton in focal, discrete packets that are distinct in location and chronology. This suggests
that the activation of the cellular sequence responsible for bone remodeling is locally controlled,
possibly by an autoregulatory mechanism such as autocrine or paracrine factors generated in the
bone microenvironment. Bone modeling also occurs during wound healing (e.g. implant
stabilization) and in response to bone loading. Unlike bone remodeling, it does not have to be
preceded by resorption. Activation of cells that resorb and those that form bone can occur within
the same bone on different surfaces. In addition, bone modeling may also be controlled by growth
factors, as with bone healing, grafting, and osseointegration. Whether the bone is being modeled
or remodeled, it is deposited in proportion to the compressional load it must carry. Therefore,, the
bones of athletes are considerably heavier than those of nonathletes. Likewise, a person with one
leg in a cast who continues to walk using only the opposite leg will experience a thinning of the
unused leg bone. Continuous physical stress stimulates osteoblastic activity and bone calcification
[279]. Bone stress also determines the shape of bones in some circumstances.
Bone remodeling is a continuous physiological process involving activation of osteoclastic
cells, bone resorption, and bone formation. These processes occur at varying rates affecting the
overall height and density of the maxillary bone. Bone remodeling is influenced by many factors
including age, gender, race, medications, systemic disease, nutritional status, periodontal health,
previous prosthesis, and developmental factors.
The severity of bone remodeling may represent an important problem for clinicians for
various reasons. First of all, the absence of adequate bone levels makes implant placement
impossible. Secondly, aesthetic problems in the fabrication of implant-supported restoration could
be caused by serious bone reabsorption.
It is already well known that bone remodeling takes place around the so-called crest
module, which is defined as the portion of a two-piece metal dental implant designed to hold the
prosthetic component in place and to create a transition zone to the load-bearing implant body
[280]. The crest module includes the implant-abutment connection, which is a critical component
of the implant. Design of the implant-abutment connection influences not only the mechanical
behavior of implants but also the biologic responses in hard and soft tissues [281]. First, the
biologic response is related to inflammatory processes around the microgaps found in implant-
abutment connections, and second, stability of the implant-abutment interface is related to load
distribution [282]. However, even if stable connections seem to decrease these factors from a
mechanical engineering standpoint, discrepancies and microgaps between components are
inevitable when different components are fitted together [283]. For these reasons, ongoing
attempts are being made to improve implant design to preserve marginal bone levels and to
increase long-term success. Changes in size, diameter, macrogeometry, surface topography, and
implant-abutment connections are some of the most addressed issues.
Studies involving external hexagons (EH), internal hexagons (IH), internal octagons, and
morse taper connections have been reported in the literature. Stress distribution, micromovements,
structural integrity, and crestal bone reactions around implants have been observed and compared.
The differing behavior of different type of bone grafts or the presence of native bone does not
influence the remodeling of coronal areas of native bone when a biological dimension of the
implant attachment apparatus has been established (Fig 2.12).

~ 89 ~
 Fig 2.12: Panoramic radiograph demonstrating Papilla-like remodeling. The intrasinusal apical bone maintenance with defined
borders is well demonstrated

RIDGE PRESERVATION
It is very important to define terms regarding the various procedures, which have been
described in the literature under the general term of "ridge preservation" or “socket preservation”.
A distinction needs to be made as described below:
Ridge preservation - preserving the ridge volume within the envelope existing at the time
of extraction.
Ridge augmentation - increasing the ridge volume beyond the skeletal envelope existing at
the time of extraction.
Ridge preservation is defined as a procedure undertaken at the time of tooth extraction,
which is designed to minimize external reabsorption of the ridge and to maximize bone formation
within the socket.
The alveolar processes on the jaws are tooth dependent structures that will undergo
significant structural changes whenever the teeth are lost. The dynamics and magnitude of these
changes have been widely investigated in different studies [135, 136,138,254,284-286]. These
investigations have identified key processes of tissue modeling and remodeling after tooth
extraction that eventually lead to a reduction on the overall ridge dimensions with significant
changes in both the buccal and lingual bone crests. The systematic review of clinical studies by
Lang [287] demonstrates that the alveolar ridge undergoes the following dimensional changes
within six months after tooth extraction: Mean horizontal reduction of 3.8mm in ridge width and
1.24 in ridge height. The clinical consequences of these physiological hard and soft tissue changes
may affect the outcome of the therapies aimed to restore the lost dentition, either by limiting the
bone availability for ideal implant placement or by compromising the aesthetic result of the
prosthetic restorations. To counteract these early tissue changes after tooth extraction, different
socket preservation therapies have been proposed, ranging from a careful flapless tooth extraction
aimed at an undisturbed socket healing [288, 289], to the immediate placement of dental implants
[290], to filling the resulting alveolar socket with different grafting materials, with and without
barrier membranes [288, 289].
The possible beneficial effect of a flapless surgery during tooth extraction for limiting the
resorptive process of the alveolar crest has been investigated (Fig 2.13a-d). Although some studies
have shown slightly less pronounced bone remodeling of the alveolar ridge after flapless tooth
extraction [288, 289], other studies have failed to encounter significant differences between flap
and flapless tooth extraction [290].

~ 90 ~
 a b
Fig 2.13a: Clinical view of extracted tooth 16. Fig 2.13b: Implant site preparation for immediate implantation.

c d
Fig 2.13c: Flapless immediate implant placement aiming for Fig 2.13d: Wound closure.
socket preservation without grafting material.

Based on the systematic review by Vignoletti et al. [291] the reasons for ridge preservation
include [292]:
 Maintaining the existing soft and hard tissue envelope.
 Maintaining a stable ridge volume for optimizing functional and esthetic outcomes.
 Simplifying treatment procedures subsequent to the ridge preservation.
Reasons for ridge augmentation:
 Generating adequate soft tissue volume for implant placement thus simplifying
implantation procedures at earlier time points.
 Generating adequate hard tissue volume for implant placement thus simplifying
implantation procedures at later time points.
No high level evidence was found in the literature regarding contraindications specific for ridge
preservation. Hence contraindication for ridge preservation was considered to encompass:
 Infections at the site planned for ridge preservation, which cannot be taken care of during
the ridge preservation surgery.
 Patients irradiated in the area planned for ridge preservation.
 Patients taking bisphosphonates.
 General contraindication against oral surgical interventions.
Various techniques have been described in the literature for so called ridge preservation. These
techniques may be categorized into two different groups:
Techniques used for maintaining the ridge profile (ridge preservation),
Techniques used for enlarging the ridge profile (ridge augmentation).

~ 91 ~
To enlarge the ridge profile, flaps are generally raised and augmentation procedures for ridge
contouring use biomaterials with or without barrier membranes. It appears that primary closure of
the wound is beneficial regarding the volume gained using this approach (Fig 2.14a-d).

a b

c d
Fig 2.14a-d: Flapless tooth extraction with immediate implant placement aiming for socket preservation with grafting material.

Indications for ridge preservation:

 Implant placement is planned at a time point later than tooth extraction i.e.,
a) When immediate or early implantation is not recommendable.
b) When patients are not available for the immediate or early implant placement.
c) When primary stability of an implant cannot be obtained.
d) In adolescents.
 Contouring of the ridge for conventional prosthetic treatment.
 Provided the cost/benefit ratio is positive.
 Reducing the need for elevation of the sinus floor.
Clinical recommendations in general:
 Raising of a flap and placement of biomaterials and barrier membrane.
 Primary wound closure.
 Materials with a low resorption and replacement rate.
 Raising of flaps and placement of devices for contouring the ridge profile.
The application of regenerative bio-materials, such as bone autografts, allografts, guided tissue
regeneration procedures, xenografts and most recently, growth factors, has also been evaluated
with varying degrees of success to maintain the anatomical dimensions of the alveolar ridge after
tooth extraction [293, 294, 298] (Fig 2.15a-d). A recent systematic review [291] evaluated the
efficacy of these therapies in non-molar alveolar regions suggesting that these techniques may not

~ 92 ~
prevent the physiological resorptive bone processes after tooth extraction, although they may aid
in reducing the resulting bone dimensional changes.

a b

c d
Fig 2.15a-d: clinical view of trephine core elevation with grafting material for ridge preservation according to the GBR principles.

It is uncertain whether the socket preservation therapies using different biomaterials, such
as demineralized freeze-dried bone, autologous bone, human morphogenetic proteins, and
xenogeneic graft material improve the outcomes of the different rehabilitation approaches after
tooth loss [293, 294].
Guided bone regeneration (GBR) is advocated for the promotion of new bone formation
and for the preservation of the volume and contour of the alveolar ridge following tooth extraction.
Several studies provide histological evidence of new bone formation in extraction sockets
following the application of barrier membranes in combination with bone grafts of allogenic [295,
296] and xenogenic origin [294,297]. The application of GBR can significantly reduce the loss of
alveolar bone volume in extraction sites. It should be noted however, that the available evidence
supports the use of membranes alone or in conjunction with bone grafting materials for socket
preservation purposes. However, the application of bone grafting materials by themselves may
actually interfere with normal osseous healing processes [298].
Several case reports and human clinical studies show the potential of GBR treatment to
augment atrophic alveolar ridges before implant placement [299, 300] and to attain long-term
stability of the results achieved [301]. Clinical studies have documented that non-resorbable and
resorbable barrier membranes alone or in combination with allografts or xenografts can be
successfully applied in combination with two-or one-stage implants placed in fresh extraction
sockets and promote new bone formation and bone to implant contact [302-306]. Clinical studies
have also demonstrated significantly more bone formation in sites, where immediate implant
placement was combined with uncomplicated application of membranes, compared with sites,
~ 93 ~
which necessitates early membrane removal [307]. To avoid bone tissue damage, the first
procedure should be carried out during tooth extraction. Tooth extraction should be performed
without the raising flap, causing the least possible surgical trauma (which includes separation of
the periosteum and the rupture of its connective tissue attachment at the bone surface).This trauma
induces an acute inflammatory response, which in turn mediates resorption of the surface layer of
the alveolar bone in the exposed area [308].
There is still controversy regarding the ideal biomaterial for ridge preservation.
Deproteinized bovine bone seems to be an appropriate material for alveolar reconstruction [294,
309]. Hydroxyapatite and calcium sulphate were successfully used in these procedures [310].
Autogenous bone still represents the gold standard and provides better results in comparison with
allograft bone [311].
The scientific literature is divided over whether or not soft tissue coverage at the time of
extraction is necessary for optimum healing socket. Barone et al. [312] pointed out that the alveolar
ridge preservation technique performed with collagenated porcine bone and a resorbable
membrane was able to limit the contour changes reported after tooth extraction. However,
scientific articles discuss various methods to detect alveolar changes and different reference points
have been used. According to Barone et al., complete preservation of the alveolar crest, especially
on the buccal side, is still not achievable. Moreover, additional bone augmentation procedures
were required for 46.4% of implants in non-preserved sites compared to 7.1% of implants placed
in preserved sites [311]. Many clinicians prefer to completely preserve the original ridge contours.
Therefore, instead of socket preservation therapy, other alternative therapies should be explored,
like early implant placement with simultaneous contour augmentation with GBR. The early
placement technique is characterized by the following: careful extraction of the tooth without flap
elevation, debridement of the socket, followed by a 4-6 week soft tissue healing period, implant
placement in a correct three-dimensional position, simultaneous contour augmentation on the
facial aspect with GBR using a bio-absorbable collagen membrane combined with autogenous
bone and a low substitution bone filler, and tension-free primary wound closure [312].
Socket preservation techniques may aid in reducing the bone dimensional changes
following tooth extraction. However, they do not prevent bone resorption. Therefore, the loss in
width of up to 3.48 mm and in height of up to 2.64 mm may be still expected [313]. In some
studies, socket grafting apparently showed a successful outcome while in other reports the benefit
of this therapy was more questionable. While the biomaterial placed in a contained bone defect
may promote hard tissue formation and defect resolution, the graft may in fact delay healing. It
must be realized that the degree of reduction at the grafted sites was much smaller than that of the
non-grafted sites. The ability to place implants depends on the bone quantity, but the predictability
of the ultimate aesthetic outcomes is determined by the soft tissue outcome (Fig 2.17a-d).

~ 94 ~
 a b

c d
Fig 2.17a-d: Double implants in buccopalatal location in the posterior maxilla may reduce the bone dimensional changes following
tooth extraction.

MECHANISMS OF BONE GRAFT CONSOLIDATION

Graft consolidation describes graft material that is surrounded and invested by newly
modeled bone and incorporated into the vital host vascular bed followed by functional remodeling.
Graft consolidation is a complex process and involves the interaction of bone substitutes with cells,
extracellular matrix and signaling molecules provided by the host [311]. Thus, the
microenvironment of the maxillary bone can influence the behavior of bone substitutes and the
microenvironment of the bone substitutes can influence the osteogenic response of the maxillary
bone. Graft consolidation in the augmented sinus is a complex process where new bone originating
from the maxillary host bone is guided by the osteoconductive properties of biomaterials up to the
Schneiderian membrane. The gradient of graft consolidation characteristically represents the
interaction of new bone with the biological properties of biomaterials within each region of the
augmented sinus.
To consider these changes in the augmented maxillary sinus, three regions of interest are
selected: (i) a ‘bridging distance’, where new bone is mainly laid onto the host bone, (ii) a region
of osteoconduction, where new bone exclusively grows on the biomaterial, (iii) a region of
osteoconduction that represents the maximal distance of the new bone (Fig 2.18a,b).

~ 95 ~
 a b
Fig 2.18a: intraoral radiograph demonstrating three different Fig 2.18b: intraoral radiograph showing clearly the original
regions in augmented maxillary sinuses: (i) a ‘bridging sinus floor and the apical border of the augmented area. Note
distance’(blue), where new bone is mainly laid onto the host the three different regions described in 2.18a.
bone, (ii) a region of osteoconduction(red), where new bone
exclusively grows on the biomaterial, (iii) and a region of
osteoconduction (green) that represents the maximal distance of
the new bone.

The properties of bone substitutes in the augmented sinus can be initially described as
histological changes with increasing distance from the host bone and later as histological changes
over time within a particular region.
The biological properties of bone substitutes do not only relate to the amount of bone
formation, but to its quality, e.g. mineral distribution, formation and maturation of the non-mineral
matrix, and the birth and death of bone cells [312].
Consolidation of the graft material with the host bone is a prerequisite for osseointegration.
The interconnection between the bone and the implant distributes functional forces within
physiologic parameters. Functional strain limits transferred by dental implants to bone are based
on adequate osseointegration, which in turn requires the presence of vital bone tissue established
by graft consolidation. Consolidation involves the formation of a graft-woven bone complex that
remodels into lamellar bone and further adapts based on functional load. Graft consolidation
requires a blood supply and osteogenic cells, which deposit new bone onto a solid surface [313].
Continuous delivery of osteogenic cells is necessary because mature osteoblasts either end up as
osteocytes and lining cells or undergo apoptosis [314]. Angiogenesis, osteoblast function, and graft
consolidation, therefore, share a functional linkage.
The dense vascular network of the maxilla diminishes after tooth loss and advancing age.
Because 70% to 100% of the blood vessels in the maxilla originate from the periosteum [315], we
must ensure atraumatic elevation of the mucosa. Disruption of the sinus mucosa also impairs local
blood flow, which can compromise graft consolidation and implant survival [316] (Fig 2.19a,b).

~ 96 ~
 a b
Fig 2.19a,b: Disruption of the sinus mucosa may impair local blood flow, which can compromise graft consolidation.

Depending on the processing of graft material, blood vessels sprout into the haversian
canals of block grafts or in the spaces between particulated bony material during the early stages
of bone graft incorporation (Fig 2.20a,b).

a b
Fig 2.20a,b: Clinical view of a grafted sinus. Notice the network of channels and concavities of the particulate materials where
blood vessels supposed to sprout.

Angiogenic signal molecules released at the injury site from activated platelets [317],
migrating macrophages [318], and osteogenic cells organize the blood vessels. Hypoxic conditions
in the early graft site provide a further stimulus for the expression of angiogenic molecules by
macrophages and osteogenic cells [319]. The blood clot serves as a reservoir of angiogenic factors,
such as the vascular endothelial growth factor and the basic fibroblast growth factor [320].
Blood vessels are also needed to provide a continuous source of osteogenic cells. The origin
of osteogenic cells at bone regeneration sites is not entirely clear, although vascular pericytes and
blood-derived cells are potent candidates [321]. Migration, proliferation, and differentiation of
osteogenic cells are orchestrated by autocrine paracrine factors released from macrophages,
activated platelets, neutrophils, osteogenic cells and endothelial cells, as well as from components
in the extracellular matrix [322, 324]. Bone morphogenetic proteins can adsorb to extracellular
matrix proteins, such as collagens I and IV and heparin, thereby increasing local threshold levels
to initiate osteogenic differentiation.
The main source of osteogenic cells during graft consolidation is the periosteum, which
has mesenchymal progenitor cells in the cambium layer and provides a rich source of blood
vessels. The sinus mucosa also contains osteogenic cells, but whether they contribute to graft
consolidation is unclear [325].

~ 97 ~
 Osteoclastogenesis is required for graft-woven bone complex remodeling. A continuous
supply of osteoclasts at the graft site also requires blood vessel formation. Osteoclastogenesis
requires a microenvironment provided by mesenchymal cells triggered into the osteogenic lineage
[325]. Recent findings suggest that osteoclasts are also involved in the coordination of bone
formation [326]. Although the signals that control osteoclast formation, activation, and survival
are known in great detail, the main signal coordinating bone resorption during graft consolidation
remains unknown.
Consolidation depends on the properties of the graft material and the osteogenic potential
of the host site. The graft material should allow ingrowth of blood vessels and formation of bone
on its surface for integration into the host site. Autografts provide a source of both osteogenic cells
and growth and differentiation factors to support bone regeneration. Osteogenic cells within the
autograft contribute to its early consolidation provided that nutrients and growth factors diffuse
through the blood clot [327]. For this reason, autograft processing must be considered. Neither
autograft grinding nor morselizing disturbs the viability of osteogenic cells [328, 329], which will
survive in a hypoxic environment for at least 3 days.
Bone substitutes as well as autografts have also been supplemented with growth factors,
extracellular matrix, and osteogenic cells [330]. However, whether these therapies are substantially
more efficacious is currently unclear. The proliferative capacity and health of the host site are
crucial in early revascularization, maturation, and consolidation of the graft. In general, bone
regeneration is more predictable when a defect is surrounded by host bone. Because of its
immunological acceptability and various mechanisms for bone regeneration, autogenous bone is
the so-called gold standard of graft material [331, 332].
A two-phase theory of osteogenesis during healing has been described. Composite bone
grafts consisting of 50% autogenous bone and 50% DBBM promote predictable bone formation
without exposing the patient to invasive bone harvesting procedures [333]. Allogenic grafts and
xenografts function strictly as scaffold for osteoinduction. Atamni [334] concluded that using
xenogeneic material alone to elevate the maxillary sinus floor makes the procedure simpler, faster
and cheaper without the need of autogenous bone. The success rates of dental implants placed in
areas with xenographic bone to those with autogenic bone are comparable. In another article of
Atamni [335] sinus elevation with β-tricalcium phosphate for programmed bone formation in
advanced maxillary atrophy was performed. The author concluded a comparable success rates of
dental implants placed in areas with β-tricalcium phosphate to those with autogenic bone. Using
at least 50% autogenous bone and placing the graft directly adjacent to the large volume of host
bone, afforded by a wide surgical approach, improves the predictability of the second phase of
bone formation within this scaffold as the graft is gradually replaced. Bone morphogenetic protein
acts as the coupling agent between bone resorption and new bone apposition as it does in normal
bone remodeling. Stem cells found in the graft, the local tissues, and the circulatory system respond
in the form of osteoblast differentiation and new bone formation. Essentially, a greater surface
area (i.e., a larger recipient site) will have a greater number of potentially available stem cells and
endosteal osteoblasts. Loss of autograft bone mass occurs when resorption exceeds formation
during the consolidation phase. Such a situation increases the risk of implant loss because the
compromised bone graft fatigues to failure.
To overcome excessive, at times even complete, resorption of the autograft and to reduce
the volume of bone that must be harvested, bone substitutes that are added to the graft are chosen
for their capacity to resorb slowly. The use of a bone substitute such as bovine bone mineral, either

~ 98 ~
alone or in combination with an autograft, preserves the vertical height of the augmented sinus
over time.
For this indication, slowly resorbing bone substitutes serve as space-maintainers during
consolidation. Host bone, which invests the bone substitutes, retains its capacity to respond to
mechanical force via adaptive remodeling and modeling. The process of graft incorporation, which
varies in duration depending on the graft material used, consists of cellular proliferation, migration,
gene expression, differentiation, adhesion, and apoptosis (Fig 2.21a,b). For autografts, this phase
generally lasts four months, for allograft 7-8 months, and for alloplasts one year or longer. In light
of the relatively long healing process (6 to 8 months), this guided bone regeneration concept is
essential.

a
b
Fig 2.21a,b: CT scan showing graft incorporation in the maxillary sinus three years after sinus floor augmentation – notice the
dense solid grafting materials.

The use of bone substitute material (BSM) is always associated with an inflammatory
reaction, which activates osteoclastic cells and macrophages [336, 337]. These cells induce
resorption and biodegeneration of the BSM particles over time. During biodegeneration, ions such
as sodium, phosphate, and calcium are dissolved from the BSM particles. At the same time, due
to the release of different cytokines with osteogenic effects, new osteoblasts initiate mineralization
of the collagen matrix. The dissolved substances might be directly involved in the mineralization
process. The features of an ideal scaffold delivery system have been recently elucidated [338]. On
the one hand, mechanical support for cells has to be guaranteed until an adequate three-
dimensional, mineralized bone matrix has been produced. On the other hand, the scaffold must
also chemically and biochemically support the cell, allowing, via a sufficient vascular contribution,
and adequate amount of nutrients, oxygen, molecular signals, and growth factors. Vascular support
is a key factor for obtaining new bone formation [339]. For this reason, the three-dimensional
geometry of the scaffold must be studied to support adequate angiogenesis, creating a strong
interconnected new vascular support [340].
Calcium-phosphate ceramic materials with defined and interconnected porosity (with pore
size ranging from 300 to 400 µm) possess a network of channels and cavities capable of supporting
both vascular invasion and angiogenesis [338]. The geometry of the scaffold seems to be able to
influence and even “drive” cellular activity [338, 341] (Fig 2.22a-c).

~ 99 ~
 a b
Fig 2.22a: Biopsy performed at a sinus graft. Fig 2.22b: Penetration of newly formed bone is evident between
the granules.

Fig 2.22c: Histologic section showing direct osseous apposition

on granules, with osteoid material on the borders, indicating
c intensive osseous activity [19].

Several authors, using calcium-phosphate ceramic materials, have shown how the first
bone apposition preferentially occurs in the concavities of the scaffolds [341-343]. The osteoblasts,
in fact, together with growth factors and specific cytokines (that is, molecular signals that govern
cellular activity) tend to preferentially concentrate in the cavities [344].

GENERAL ASPECTS OF GUIDED BONE REGENERATION AND SINUS

AUGMENTATION
Guided bone regeneration (GBR) is the most frequently used technique for bone
regeneration in conjunction with or prior to implant placement. The principle idea of GBR is the
use of a membrane to exclude epithelial cells with a high turnover and to allow the migration of
the desired cells (particularly osteoblasts) in the established wound space [345]. GBR was
introduced as a therapeutic modality whose aim was to achieve bone regeneration via the use of
barrier membranes, provided that bone regeneration is significantly enhanced when the invasion
of soft tissue into osseous defects is mechanically impeded [346] (Fig 2.23a-d).

~ 100 ~
 a b

c d
Fig 2.23a-d: Clinical view of guided bone regeneration with the resorbable membrane after tooth extraction.

The concept of creating a secluded anatomic site with the aim to promote healing was first
introduced 50 years ago, when cellulose acetate filters were experimentally used for the
regeneration of nerves and tendons [347, 348]. Murray reported new bone formation beneath
plastic cages adapted over decorticated femoral defects in dog [349]. Subsequent animal studies
reported enhanced osseous healing of rib, radial bone and femoral bone defects via the application
of cellulose acetate and Millipore filters [350, 351]. In the craniofacial region, successful results
were shown following mechanical barrier placement over jawbone defects in rabbits [352] and
over cranial defects in rats [353]. In these early studies, most of the authors attributed the barriers’
success to the preservation and protection of the blood clot rather than to the colonization of the
created secluded space by an osteogenic cell population.
In the mid 1980s, the guided tissue regeneration (GTR) principle was introduced, according
to which, regeneration of a certain type of tissue is achieved when cells with the capacity to
regenerate the particular type of lost tissue are allowed to populate the defective area during
healing [299]. GBR was a natural outgrowth of the GTR principle. Therefore, the GBR biological
rationale advocated the mechanical exclusion of undesirable soft tissue from growing into the
osseous defect, thereby allowing only osteogenic cell populations derived from the parent bone to
repopulate the osseous wound space [346, 354].
The GBR therapeutic protocol involves surgically placing a cell occlusive membrane
facing the bone surface to physically seal off the skeletal site in need of regeneration [346].
Furthermore, the membrane creates and maintains a secluded space, thus providing an
environment for the osteoprogenitor cells that is permissive for recruitment and proliferation of
osteoprogenitor cells, differentiation along the osteoblastic line age and expression of osteogenic
activity [355, 356]. Various non-resorbable and resorbable membrane materials have been used in
experimental and clinical studies of GBR treatment. The desirable characteristics of barrier

~ 101 ~
membranes utilized for GBR therapy include biocompatibility, integration by the host tissues, cell
occlusion properties, clinical manageability and space making ability [356]. The standard GBR
barriers were of expanded polytetrafluoroethylene membranes (e-PTFE) due to its early and
successful application [357]. Despite the high predictability of bone regeneration using e-PTFE
barriers, the main disadvantages of this material are that the membrane must be removed in a
second surgical intervention and that membrane exposure can cause bacterial contamination [358].
Subsequently, the inflammatory reaction of the surrounding soft tissues may require early removal
of the membrane. To avoid these problems, the use of biodegradable materials was investigated.
In the past 10-15 years, resorbable membranes made of collagen have become the
membrane of choice in many clinical situations. Several biodegradable materials have been tested
with varying success in periodontal and/or bone regeneration including collagen type I,
polyurethane, polyglaction 910, polyglycolic acid, polylactic acid, polyorthoester and different
copolymers of polylactic and polyglactic acid [357].
The efficacy of applying either non-resorbable or resorbable barrier membranes for treating
critical size defects has been further documented in various experimental animal studies [145,358-
363]. A series of animal studies demonstrated that neo-osteogenesis, i.e. de novo bone formation
beyond the genetically determined skeletal envelop, can be predictably achieved via application
of the GBR principle. Studies have shown significant neogenetic bone formation beyond the
anatomic skeletal borders in the secluded space, created via" dome" or "capsule" shaped membrane
barriers fixed on the calvarial bone [345, 364].
The healing period following GBR application is a critical factor affecting the amount of
experimental neogenetic bone formation. It is well established that to ensure occlusiveness against
cellular invasion, the structural integrity of the barrier material and the sufficient adaptability of
its borders to the parent bone, constitute prerequisites for predictable new bone formation via GTR
[365]. GBR can predictably lead to regenerating critical size maxillofacial defects and to de novo
bone formation via a synchronized progression of events recapitulating intramembranous
ossification. In addition, GBR constitutes a successful therapeutic approach for the treatment of
peri-implant bone defects and for preserving the dimensions and the configuration of the alveolar
socket following tooth extraction.
Lateral and vertical bone augmentation of atrophic alveolar ridges before or in conjunction
with implant placement can be achieved via GBR application, albeit with varying degrees of
success. Although there is histological evidence supporting the ability of the GBR principle in
promoting vertical bone augmentation in combination with implant placement, the available
clinical research on the technique’s predictability is presently limited. The ultimate goal would be
to optimize the case selection process and to introduce guidelines in terms of developing the GBR
therapeutic protocol. Furthermore, preclinical and clinical trials investigating the physiology and
pathophysiology of the healing process following GBR application at the molecular level are
warranted, with a view to develop and implement novel therapeutic strategies, e.g. tissue
engineering, drug delivery and/or gene therapy aimed at promoting bone formation and
regeneration potential following GBR treatment. Implants placed simultaneously with GBR
procedures using resorbable or non-resorbable membranes show a high survival rate ranging from
91.9% to 92.6% [250].
The clinical success of sinus augmentation depends on understanding the fundamental
principles of bone regeneration. The newly formed bone in the maxillary sinus floor is a
prerequisite for the osseointegration of dental implants. Like the consolidation of grafting
materials, the osseointegration of dental implants also requires bone regeneration. Thus, the bony

~ 102 ~
consolidation of grafting materials is fundamental for the clinical success of implant treatment.
The grafting materials are not only important for providing primary mechanical implant stability,
they are also needed to guide the new bone into the grafted area, i.e., the implant site, so that
implants are placed in the grafted sites with vital bone. The grafting material undergoes
regeneration and ultimately supports the osseointegration of dental implants. Even if implants are
placed in a region where graft consolidation has not yet occurred, full osseointegration can be
reached once the graft is consolidated. The clinical success of this treatment depends on various
parameters including the grafting material and the bone regenerative potential of the patient. While
clinicians are responsible for selecting the appropriate grafting material, the regenerative potential
of a patient is predetermined. It is therefore clinically important to understand the impact of
grafting materials on the process of graft consolidation. Based on this knowledge, grafting
materials can be selected on an individual basis along with consideration of patient parameters.

~ 103 ~
3. PREOPERATIVE ASSESSMENT AND TREATMENT PLANNING FOR IMPLANTS
IN THE POSTERIOR MAXILLA

Medical history
The goal of preoperative evaluation is to reduce patient risk and surgical morbidity.
Preoperative patient assessment can modify patient care and improve outcome and is important in
developing a safe and appropriate surgical and anesthetic plan [366-368].
Factors in determining the magnitude of the preoperative evaluation include the extent of
the planned surgery, the type of anesthesia employed, and the general health of the patient. During
the preoperative assessment, the clinician interviews the patient to obtain information. This is
followed by a physical examination with special emphasis on the cardiovascular and respiratory
systems to help determine risk. Laboratory tests, imaging, and consultations are ordered as deemed
necessary based on information obtained during the history and physical examination.
Finally, diagnoses are formulated and the treatment options are discussed with the patient
followed by obtaining an informed consent. The importance of an accurate, detailed history cannot
be overemphasized because it provides the framework on which the clinician builds an accurate
diagnosis and treatment plan.
Preoperative questionnaires and computer-driven programs are commonly used to gather
information and save time. Patients should be asked about their chief complaint (CC). The chief
complaint assists the clinician in establishing priorities during the history-taking process. Past
medical history (PMH) alerts the clinician to any coexisting illnesses that may have an impact on
any planned surgeries. Information regarding illness severity should be obtained. Past surgical
history can also help identify factors that may affect the patient’s ability to undergo a safe surgical
procedure.
The practitioner must be familiar with the basic principles of medical perioperative
management in implant patients, how to proceed in evaluating patients, how to manage the
patient’s medications perioperatively, and how certain conditions may affect the surgery and the
healing phase.
Before implant treatment and bone augmentation can be performed, it is mandatory to
thoroughly review the patient's medical history. All relevant aspects of the medical history must
be assessed to determine the patient's suitability for SFE. Special attention should be devoted to
patient-related factors that may affect bone healing prior to determining the suitability of a patient
for SFE. A systematic approach includes: general health status, concomitant medication, allergies,
tobacco and alcohol, and compliance is recommended. Candidates for implant treatment or SFE
should not present with any condition that would affect bone healing, either locally or systemically.
Patients who have undergone head-and-neck radio therapy when the field included the maxilla
should be excluded from implant treatment. Poor glycemic control in diabetic patients (i.e.
uncontrolled diabetes) is associated with increased susceptibility to postoperative infections. These
patients should be treated with great caution. SFE procedures are not, however, contraindicated in
patients with well-controlled diabetes [369]. For transplant patients undergoing long-term
immunosuppressive therapy several experimental studies have shown that immunosuppressive
agents like cyclosporine disturb normal bone healing around dental implants. However, no clinical
data regarding implant placement or SFE procedures are available for immunosuppressed patients.
It is therefore recommended that alternatives to implant treatment and bone augmentation be
preferred until clinical data are available to support these procedures [370].

~ 104 ~
 Whether osteoporosis is a risk factor for implant failure is open to debate. While it is
believed that osteoporosis does not per se contraindicate implant placement or SFE, the risk may
be increased by long-term treatment with oral bisphosphonates [370]. Studies dealing with implant
placement or bone augmentation procedures in patients with neuropsychiatric disorders are
virtually non-existent. Disorders of this type are not contraindications per se, but may affect
compliance. It is extremely important to make sure that these patients will be able to comply with
postoperative instructions and maintain an adequate level of oral hygiene. A complete list of
medications should be obtained well ahead of the surgical procedure, allowing the surgeon to
evaluate whether any of the drugs pose an absolute contraindication to the planned treatment.
Absolute contraindications include IV bisphosphonates, chemotherapy, or indeed any drugs
known to suppress bone healing or immune response. Other types of medication, such as
antithrombotic drugs, indicate that extra caution should be exercised during surgery.
Antithrombotic treatment should generally not be discontinued, as the risk of severe bleeding is
usually much lower than the risk of thromboembolic events [371]. Discontinuation or a dose
reduction from therapeutic to prophylactic levels may be indicated if a complex procedure
involving an increased risk of bleeding is expected (e.g. extensive bone augmentation or extraoral
bone harvesting).
Any adjustments of concomitant medication should only be made in consultation with the
patient's physician. In addition, surgeons need to make sure that regular medications will not
interact with drugs prescribed in relation to surgery. A number of known interactions with
antibiotics and analgesics dictate that the treatment of patients on antithrombotic vitamin-K
antagonists should be considered very carefully. While allergies per se are rarely an issue for SFE,
some patients may be allergic to any of the perioperative medications prescribed, notably including
antibiotics and analgesics. Smoking is a risk factor for implants placed both in native bone and in
the augmented posterior maxilla [372-374]. Although tobacco use should not be considered an
absolute contraindication for SFE procedures, it is mandatory to inform these patients about the
increased risk of implant loss and peri-implant bone infection. They should be motivated to quit
or at least reduce their smoking. Alcohol is known to affect bone grafting. However, the main issue
with alcoholism in implant patients is presumably compounding factors such as a malnutrition,
poor oral hygiene and compliance [375]. Therefore, patients with any kind of abuse issue should
be evaluated with utmost care. In many situations, alternatives to implant therapy including SFE
procedures should be considered. Patients unable to comply with postoperative instructions or
presenting with inadequate oral hygiene should not be considered for SFE procedures.

Fig 3.1: Clinical view of a patient with inadequate oral hygiene.

~ 105 ~
 Clinical examination
A complete physical examination of oral hard and soft tissues is indispensable for each
patient, and an overall dental treatment plan has to be formulated in conjunction with the treating
restorative clinicians. Diagnostic casts are articulated with the use of a face bow on a semi-
adjustable articulator with interocclusal record and record bases (Fig 3.2a-d).

a b
Fig 3.2a: Semi-adjustable articulator. Fig 3.2b: Facebow.

c d
Fig 3.2c: Diagnostic wax. Fig 3.2d: Cast models in semi adjustable articulator.

Teeth are fabricated in diagnostic wax in conjunction with the cast to identify the desired
locations of the dental implants as needed except for those missing single teeth. In addition to the
general examination requirements for implant treatment, specific aspects of the maxillary sinus
must be examined separately. Bone width can be measured preoperatively by a ridge-mapping
procedure with calipers. Two measurements are made at each implant site: one at the level of the
ridge crest and the other at the point approximately 7mm cranially.
Ridge morphology and interarch relation are specifically assessed from a restorative
viewpoint. Following this detailed examination, the final treatment plan is developed based on the
best scientific evidence available. Preoperative evaluation is designed to confirm the
appropriateness of the implant treatment, select the proper implant site, and identify all problems
that require correction before the implant is placed.

~ 106 ~
 Among the factors to be considered are:
-The anatomy and condition of the potential site and its relation to other structures.
- The position, quantity, and quality of the bone.
- The relation of the ridge to the adjacent and opposing teeth.
- The quality and dimension of the soft tissues.
- The occlusal relationships.
The ridge is assessed mesiodistally and buccolingually to ascertain whether it can
accommodate an implant. If there has been considerable resorption, ridge augmentation with grafts
and flaps three dimensionally or applying a membrane around the implant may be necessary to
overcome the bone loss.
The prognosis and role of adjacent and opposing teeth influence long-term restorative
success and therefore should be considered. In some cases, when molars are lost, the opposing
teeth extrude and corrections are required to accommodate the implant. Other pathoses have to be
corrected before an implant is placed. The occlusal scheme is planned to avoid overloading of
individual implants and to direct loading forces axially. This is particularly important for
pterygomaxillary implants because of the magnitude of muscle force in the posterior jaw. During
intra-oral examination, the quantity of keratinized mucosa (KM) and the profile of the alveolar
crest are evaluated (Fig 3.3a,b).

a b
Fig 3.3a: Clinical view of keratinized mucosa. Fig 3.3b: Clinical view of the alveolar crest profile.

Establishing an adequate amount of peri-implant mucosa which is firmly attached to the

underlying periosteum and bone has been proposed as an important factor for the long term success
of dental implants [376]. To provide a functional and predictable implant-supported restoration,
the position and number of implants is determined according to a prosthodontical plan. This plan
takes into account the specific clinical challenges of the posterior maxilla such as resorption which
often proceed in all three dimensions, limiting bone volume not only in the vertical but also in the
horizontal dimension. In mild to moderate resorption, the interarch relationship is considered as
acceptable and SFE is chosen as the only adjunctive procedure. In severe cases of resorption, a
combined approach with three-dimensional site development should be considered, since sinus
grafting by itself may not create ideal tissue contours. Both vertical augmentation of the sinus floor
and horizontal bone augmentation may be needed to optimize the restorative outcome (Fig 3.4a-
d).

~ 107 ~
 a b
Fig 3.4a:Clinical view of lateral window preparation. Fig 3.4b: Augmented sinus combined with GBR.

c d
Fig 3.4c,d: Clinical view of patient requiring both vertical augmentation of the sinus floor and horizontal bone augmentation to
optimize the restorative outcome.

A diagnostic interarch relation is mandatory for assessing the most suitable treatment
option for patients with severe horizontal and/or vertical resorption of the alveolar crest. According
to the aforementioned facts, bone width can be measured intraoperatively using forceps during
sinus floor augmentation (Fig 3.5a,b).

a b
Fig 3.5a: forceps for measuring bone width. Fig 3.5b:forceps for measuring bone width during SFA.

Chiapasco categorized the atrophic posterior maxilla which requires sinus floor elevation
into four groups [166]. Each situation requires a different surgical approach to achieve ideal bone
volume and three-dimensional interarch relations. Table 1 shows the classification of the atrophic
posterior maxilla and the related treatment options of SFE (Fig 3.6a,b).

~ 108 ~
 Table 1 Classification of the atrophic posterior maxilla and related treatment options.
Classification Clinical characteristics Surgical approach
Group 1 Residual bone height ≤ 4mm SFE procedure with bone
adequate width of alveolar ridge substitute and/or autogenous
ideal interarch relations bone from intraoral donor site

Group 2 Residual bone height ≤ 4mm SFE procedure and horizontal

inadequate width of alveolar ridge ridge augmentation with bone
acceptable vertical interarch relations substitute and/or intraoral
autogenous bone and barrier membrane

Group 3 Residual bone height ≤ 4mm SFE procedure and vertical

adequate width of alveolar ridge ridge augmentation with bone
acceptable horizontal interarch relations substitute and/or intraoral
unfavorable vertical interarch relations autogenous bone and barrier membrane
due to advanced crestal reosorption

Group 4 Residual bone height 4 to 8 mm Transcrestal SFE with and

adequate width of alveolar ridge without bone graft
acceptable interarch relations

a b
Fig 3.6a: Frontal view showing the discrepancy between the Fig 3.6b: Lateral view showing the discrepancy between the
upper and lower jaw due to severe bone resorption of the upper and lower jaw due to severe bone resorption of the
maxilla. maxilla.

Treatment Planning
Careful and appropriate selection of patients based on well-defined clinical indications is
critical to the long-term success of implant treatment alone or combined with augmentation
procedures in the posterior maxilla. For proper evaluation, clinicians need to have in-depth
knowledge of the anatomy of the maxillary sinus with its adjacent structures and of the bone
modeling pattern that takes place after tooth extraction. There is a need for clinicians to understand
in detail the indications and contraindications, the various treatment options available, and the
implications of different treatment plans. Only with this information can they select appropriate
treatment modalities including grafting and non-grafting procedures.

~ 109 ~
 For treatment planning it is a prerequisite to assess the existing bone in the posterior
maxilla. There are two different terms of bone. The term “available bone” refers exclusively to the
quantitative assessment of bone without any regard to the location of the teeth within a specific
prosthesis. These data alone should not be used in determining optimal implant positions. Surgeons
must know the locations of the restorations and the positions of the implants prior to treatment
planning. The term “usable bone”, on the other hand, refers to bone volume that allows three-
dimensional positioning of implants according to the planned locations of the teeth within the
implant restorations. It is important to make sure, both clinically and through the use of imaging
CT scans, that there is at least 1.5 mm of bone surrounding dental implants. This thickness ensures
that the labial bone height is maintained after formation of the peri-implant biologic width (Fig
3.7).

Fig 3.7: CT slices demonstrating 1.5 mm of bone surrounding dental implants.

Bone thickness less than 3 mm is frequently encountered in patients with traumatic tooth
loss. In these cases, CT examinations with a radiographic scanning appliance should be performed
to evaluate the amount of usable bone and whether it precludes correct three-dimensional
positioning of the implant. If there is not enough usable bone, bone augmentation is required. It is
also critically important to make an accurate assessment of the soft tissues prior to treatment. In
cases of soft tissue deficits (thin tissues, scarring, marked tissue concavities on the edentulous
areas), tissue management must be achieved prior to initiating bone augmentation procedures. At
the time of surgery (bone augmentation and/or implant), suitable tissue will thus be available for
containing and protecting the regenerative material.
In addition to the general examination requirements for implant treatment, specific aspects
of the posterior maxillary sector need to be examined seperately. A detailed radiographic
examination, usually by CT, is indispensable. Following this detailed examination, the final
treatment plan can be developed. Patients with edentulous posterior maxilla can be treated with
implants placed by one of the five following specified surgical procedures:
1. Standard implant placement
2. Sinus grafting procedure by lateral access with simultaneous implant placement
3. Sinus grafting procedure by lateral access with delayed implant placement
4. Transcrestal sinus elevation with or without graft material
5. Alternative treatment concept using preexisting bone following one of five specified

~ 110 ~
treatment modalities: a. Short implants with or without transcrestal sinus floor elevation (TSFE),
b. Tilted implants, c. Palatal positioned implants, d. Pterygomaxillary implants, e. Implants with
cantilevered prostheses.
A candidate for sinus floor elevation (SFE) presenting with any condition that would affect
bone healing, either locally or systemically, should be rejected. Patients with edentulous posterior
maxilla, a posterior residual height of at least 1mm to sinus floor and no diagnosed bone disease
and not taking medications known to affect bone metabolism are candidates for one of the
aforementioned treatment modalities. In particular, patients should be evaluated for seasonal
allergies, allergic rhinitis, or sinus congestion, all of which may indicate potential sinus pathosis.
A patient with sinusitis, sinus disease or invasive lesions should be referred to an ear, nose, and
throat (ENT) specialist for treatment before any surgery procedure. Because patients with a history
of chronic sinusitis are more predisposed to recurrent pain and infection when their sinus cavities
are manipulated, it is important to correctly diagnose the condition of the maxillary sinus and to
eradicate all evidence of sinus disease or infection prior to sinus grafting.
A careful multi-tasking preoperative management, including an ENT evaluation is needed
to assess the condition of the nasal mucosa, turbinates, septum, meatal grooves and osteomeatal
complexes with fiber optic endoscopy. A radiological evaluation extended to the ostiomeatal
complex should be performed in candidates with potentially irreversible and presumably reversible
ENT contraindications to SFE. The clinical and radiological assessments are also used to detect
conditions which could jeopardize the physiological maxillary ventilation and drainage function,
impairing the antral homeostasis such as sino-nasal anatomical alterations (i.e. septal deviations,
concha bullosa, paradoxical bending of the middle turbinate , etc.), maxillary ostium stenosis, post-
surgical endonasal scars, synechiae of the middle meatal region, nasal polyposis or masses
obstructing the medio-meatal region, antro-ethmoidal foreign bodies, oro-antral fistula and sino-
nasal neoplasms.
It is recommended to make every possible effort to reduce transmucosal loading of the
implants. Whenever possible, fixed provisional restorations supported by the remaining teeth are
recommended, even if their prognosis is poor and ultimately would be extracted. Hopeless teeth
should be extracted after osseointegration of the initial implants, which then support the
provisional restoration that protects the newly placed implants. In situations where it is not possible
to avoid trans-mucosal loading, the implant should be submerged and uncovered later.
Conventional dentures are relined 1 to 3 weeks after surgery. The first provisional prosthesis
should be delivered when the implant is uncovered. After the soft tissue had matured and its
contours stabilized, the provisional prosthesis is adjusted to reflect the contours of the stabilized
tissue (Fig 3.8a,b). Prostheses are removed routinely for assessment of soft tissue healing and
implant integration.

~ 111 ~
 a b
Fig 3.8a: Final restorations before connection. Fig 3.8b: Final restorations in situ.

Informed consent
SFE for implant treatment is a complex surgical procedure. Clinicians need to explain to
the patients its advantages and disadvantages for them to give their informed consent. The
following points should be considered in these discussions:
 Alternative restorative options with their strengths and weaknesses, including fixed dental
prostheses with a distal cantilever and removable dental prostheses.
 Alternative implant options, including shortening of the dental arch, distal cantilever
implants supported fixed dental prosthesis, and angled implants to increase the distal arch
of the implant-supported prosthesis.
 Selection of biomaterials and source (intraoral, extraoral) and volume of needed
autogenous bone.
 Short-term and long-term surgical risks and long-term prognosis (survival and success
rates, complication rates when SFE is performed).
 Cost of treatment, as implant procedures involving SFE are invariably more expensive than
standard implant treatment.
 Duration of treatment, as staged SFE in particular will involve protracted treatment periods.
 Esthetic demands, patient cooperation, and consent to treatment.

RISK FACTORS RELATED TO IMPLANTOLOGY

Patient-related factors

Genetics
An associations between peri-implant bone loss and specific interleukin 1 (IL-1) gene
polymorphisms has been recently discovered. IL-1 has been found to elevate bone resorption thus
stimulating the differentiation of osteoclasts and mature osteoclast activity [377, 378]. A
retrospective cohort study involving 90 patients who had received at least one implant and
supportive periodontal therapy showed that heavy smokers carrying specific polymorphisms of
this gene had an elevated risk for peri-implant bone loss [379]. A controlled, clinical study,
involving patients totaling 251 implants, revealed that the IL-1B-511 2/2 genotype has a significant
association with early bone loss indication around dental implants [380]. In addition, the frequency
of this gene was higher in patients with marginal bone loss in one or more areas of greater than 0.5
mm [381].

~ 112 ~
 Systemic diseases
Osteoporosis
Osteoporosis negatively affects bone mass and causes bone architecture deterioration over time.
The World Health Organization defines osteoporosis based on bone mineral density (BMD)
measurements at the hip, lumbar vertebrae, wrist, or heal (Table 2). Osteoporosis is characterized
by a decrease in mineral density (mass/volume units) of a normally mineralized bone [384]. A
diagnosis of osteoporosis indicates bone fragility and, as a result, increasing risk of fracture.
Holahan and colleagues found that osteoporosis and osteopenia, conditions that could
affect jawbone quality, do not contraindicate dental implant therapy [382]. Slatger and colleagues
are in agreement that dental implant placement in osteoporotic patients is not contraindicated
[383]. However, the connection of systemic measures of bone mineral density and the osteoporotic
status on local jawbone quality remains poorly understood. Table 2 shows the osteoporosis
diagnosis classification.

TABLE 2 World Health Organization osteoporosis diagnosis classification

Normal A value for BMD that is not more than 1 SD below the
young adult mean value
Osteopenia A value for BMD that lies between 1 and 2.5 SDs below
the young adult mean value
Osteoporosis A value for BMD that is more than 2.5 SDs below the
young adult mean value
Severe/established osteoporosis A value for BMD more than 2.5 SDs below the young
adult mean value in the presence of one or more fragility
fractures
BMD = bone mineral density.

Due to estrogen deficiency, postmenopausal women (51 to 75 years old) who have type 1
primary osteoporosis also demonstrate impaired bone metabolism (where resorption exceeds
deposition) [385]. Estrogen deficiency negatively impacts bone healing and bone quality.
However, this situation is not considered an absolute contraindication for dental implant placement
since the maxillofacial bone is minimally affected by this metabolic disorder [386]. Osteoporosis’s
minimal impact on the maxillofacial bone could be explained by the craniomaxillofacial region’s
embryogenic bone derivation. There is growing evidence that endodermal originating bones
(which include most of the cranial bones) differ in certain aspects from ectodermal originating
bones, which include the majority of the postcranial skeleton [387]. However, the reasons for these
differentiations are not yet fully elucidated [388]. In fact, osteoporotic patients do not appear to be
at greater risk for implant failure [389]. Optimal site preparation (e.g., 3.3 mm diameter implants
in sites that are 2.3 mm in diameter, 3.75 mm diameter implants in sites that are 2.70 to 2.85 mm
in diameter, and 4 and 5 mm diameter implants in sites that are 3 mm in diameter) and extended
healing periods (8.5 and 4.5 months in maxillae and mandibles, respectively) can result in less than
1 mm bone loss [390].
Little evidence exists correlating osteoporosis and higher risks of bone resorption around
implants [391]. Unlike the CT numbers of multislice CTs (MSCT), voxel values of CBCT may
not accurately represent bone mineral density (BMD), needed for successful implant treatments
[392]. Hue et al. reported that the voxel values of CBCT are inappropriate for evaluating BMD
[393]. Conversely, Saitoh et al. retrospectively compared CBCT and MSCT images and reported
that the voxel values of CBCT could be used to estimate BMD [394].

~ 113 ~
 Diabetes Mellitus
A wide range of systemic complications are associated with diabetes mellitus, including
susceptibility to infections, microvascular disease, and altered wound healing [395]. All these
factors affect the osseointegration process and consequently influence bone remodeling.
Unfortunately, there are relatively few human studies that directly compare diabetic and
nondiabetic patients for implant survival and success. Furthermore, the issue of glycemic control
is only sporadically addressed in these studies. With what is available, the current thinking based
on the best evidence available indicates that implants placed in patients with well-controlled
diabetes (HbA1c < 6%) have similar long-term outcomes as for nondiabetic patients. However, it
is unclear whether implants placed in patients with poorly controlled diabetes (HbA1c > 6%) have
worse or similar long-term outcomes when compared with implants placed in nondiabetic patients.
A retrospective study found more bone loss around machined implants in diabetic patients
in the first year following occlusal loading [396]. However, dual acid-etched implants in controlled
diabetes patients showed a high amount of bone-implant contact (BIC) (80%) with minimal peri-
implant bone loss [397]. Further research is necessary to clarify this situation.

Xerostomia (Sjogren Syndrome)

Xerostomia or dry mouth, secondary to Sjogren syndrome, is a chronic inflammatory
autoimmune disease that destroys the salivary glands’ secretory components. Reduced saliva
flow impairs food and microorganism clearance [398]. These patients have a considerable risk of
implant failure at the time of abutment connection. Surprisingly, bone loss has been reported in
these patients not to exceed 0.7 mm after 1 year and an additional 0.6 mm after 4 years of
treatment [399].

Ectodermal Dysplasia
Ectodermal dysplasia is comprised of a group of inherited disorders with several oral
manifestations from hypodontia to anodontia. The alveolar processes in patients with this disease
do not develop properly [400]. No relevant studies have measured peri-implant bone loss on these
patients [401-403]. However, a critical review on this topic has shown that implants placed in
young patients have a higher failure risk (88.5% to 97%) [404].

LOCAL RISK FACTORS

Bone Quantity
The implant placement site must be able to provide primary stability and sufficient blood
supply. However, not all the residual alveolar bones provide these conditions. There is currently
little evidence for a minimal buccolingual bone thickness to guarantee optimal esthetic outcomes
[405]. However, when the buccal bone thickness is at least 2 mm beyond the implant surface, bone
loss was shown to decrease significantly, and some increased bone thickness has been
demonstrated [406]. The dimensions of the posterior maxilla’s residual ridge are critical in implant
treatment planning.

Bone Quality
Bone quality is a vague and complex term. Defining bone quality is multifaceted and is
composed of several parameters such as skeletal size, bone mineral density, bone matrix
~ 114 ~
properties, architecture and the three dimensional orientation of the trabeculae [407]. The efficacy
of different clinical methods used to assess bone quality prior to and during implant placement has
yet to be proven, since these methods have not been evaluated as diagnostic or prognostic tests
[408]. There are no long-term clinical studies showing the influence of bone quality-related
parameters on implant treatment outcomes. As a result, dental implant planning and treatment
concerning bone quality have been based to a large extent on personal experience or scientifically
unverified observations.
The term “bone quality” is not clearly defined in the scientific literature. Bone quality
includes many parameters such as physiological and structural aspects and the degree of bone
tissue mineralization [409] and in addition, bone metabolism, maturation, cell turnover,
intracellular matrix and vascularity have also been shown to affect bone quality [410]. The roles
of the individual parameters on bone quality have not been fully elucidated [409].
It has been assumed in implant dentistry that bone quality refers to bone mineral density
[409]. Bone mineral density is usually poor in the maxillary posterior segments. The posterior
maxilla as compared to the other major jaw segments (anterior maxilla, anterior mandible,
posterior mandible) has the lowest bone density in terms of Hounsfield units [411, 412]. One study
found this difference to be statistically significant [413].
When there is a minimal cortical layer, primary stability is difficult to obtain. When
cancellous bone is non-existent, bone regeneration using only bone substitutes is very difficult.
Therefore, in these cases, the use of autogenous bones alone or combined with a bone substitute is
indispensable [414].
According to a recent review, there have not been studies that addressed the influence of
bone quality in peri-implant bone loss [415]. However, one study demonstrated that implants
placed into mandibular molar sites have a lower cumulative survival rate and the peri-implant bone
remodeling than those that are placed in maxillary and mandibular anterior segments. These
outcomes are possibly due to bone quantity and quality [416].
Without having clear-cut definitions of poor, moderate, and good bone quality, different
classifications are used. For this reason, bone quality evaluation methods are not routinely used,
and there are no guidelines as to a “gold standard”. For this reason, not all implants placed in poor-
quality bone fail and not all implants placed in good-quality bone survive. Clearly, bone quality is
only one factor in implant failure/survival and should be viewed in the context of other factors
affecting the patient’s short and long term clinical outcomes.

Keratinized Mucosa (Quality and Quantity)

The keratinized gingiva (KG) consists of the free and the attached gingiva, extending from the
gingival margins to the mucogingival junction [417] (Fig 3.9a). This tissue is covered with keratin
or parakeratin, and having a stippled appearance [418]. The width of the KG around teeth varies
between 1 and 9 mm according to the jaw, frenum pull, tooth location and position, and the
individual’s age [419]. In recent years there is a renewed interest in the keratinized mucosa (KM)
around dental implants. There are studies that examined the structure and function of the mucosa
that surrounds implants [420]. It was found that the transmucosal attachment is comprised of two
parts which are the barrier epithelium and connective tissue attachment. The barrier epithelium
resembles the junctional epithelium, and is about 2mm long. The barrier epithelium has a
continuous width of 1-1.5mm of a connective tissue zone that is attached to the implant. It contains
collagen fibers, which enters into the periosteum of the bone crest, and runs in parallel with the
implant surface [421] (Fig 3.9b).

~ 115 ~
 a b
Fig 3.9a: Clinical view of keratinized gingiva. Fig 3.9b: Histological view of keratinized gingiva.

Zigdon and Machtei suggest that KM thickness around implants determine the soft tissue’s
future dynamics around dental implants to either mucosal recession, or the formation of peri-
implant pockets in mucosal areas of a thin or a thick biotype (respectively) [422]. The
characteristics of the soft tissue covering the edentulous alveolar crest can influence marginal bone
stability around dental implants. Some authors consider as being insufficient a keratinized tissue
thickness of >2mm for the maintenance of the peri implant bone marginal level after transmucosal
abutment connection [423]. Evidence from clinical prospective studies [424] have shown that soft
tissue recession occurs during the first half a year of healing independently of the quality of peri-
implant mucosa.
Since there is no periodontal ligament around the implants, peri-implant mucosal tissue is
unable to produce a keratinized mucosa as opposed to the soft tissue around a tooth that is
influenced by the connective tissue of the periodontal ligament during healing [425]. The
keratinized mucosa quantity depends on (i) the period of edentulousness, (ii) the amount of the
alveolar crestal bone resorption and (iii) the position of the border between the masticatory and
the lining mucosa [426,427].
Regardless of the quality of the soft tissue surrounding the implant, the marginal bony level
can be maintained for a long period of time [428,429]. Reducing the width of the peri-implant soft
tissue has been shown to lead to crestal bone resorption during reformation of the mucosal seal.
This process is a biological one, involving bone resorption, which takes place to restore a new
“biological width”. Sites with a buccal bony crestal thickness between 1.8 and 2mm show a
significantly lower marginal bone loss compared with sites with thinner bony plates. Implants
should be surrounded by both buccal and lingual masticatory mucosa. A marginal bony crest
resorption must occur to allow the biological width to reach the physiological dimensions required.
From a clinical point of view, Bengazi et al. showed that a larger horizontal and vertical buccal
bony crest resorption at the implant site without keratinized mucosa is to be expected when
compared with implant sites with maintained keratinized mucosa sites [430]. However, evidence
of the necessitation of keratinized tissues around implants for health and tissue stability is very
limited [431]. Patients who have implants for more than 10 years demonstrate that the width and
keratinized mucosa do not have a significant influence on plaque control or on health conditions
as determined by bleeding on probing [432]. Conversely, reduced keratinized mucosa and plaque
have been correlated with higher bone loss [433]. The bony crest appears to undergo resorption
after implant installation, [434] and when there is a thick bony wall, there seems to be more
resorption as compared with thin bony walls at the buccal site to allow the establishment of a
biological width of proper dimensions.

~ 116 ~
Opinions differ regarding “adequate” or “sufficient” dimension of gingiva. Several studies stress
the importance of keratinized mucosa around dental implants to maintain peri-implant health and
patient comfort [433,435,436], while other studies found comparable implant survival rates and
peri-implant parameters irrespective of keratinized mucosa width [424,428,432]. The absence of
root cementum, periodontal ligaments, and connective tissue attachment around dental implants,
as well as the margin’s submucosal location of the majority of cement-retained restorations, may
increase the susceptibility of peri-implant tissues to developing a robust inflammatory response
against dental plaque accumulation and microbial invasion [437]. A cuff-like mucosal barrier
provided by a band of peri-implant keratinized mucosa should logically be a prerequisite to ensure
the successful long-term maintenance of peri-implant tissues from both the biological and esthetic
standpoint. A long-term clinical study found that the observed mean radiographic bone loss was
significantly higher in patients with narrower (< 2 mm) as compared to a wider (> 2 mm) zone of
keratinized mucosa (1.72 versus 1.24 mm, respectively) [438]. In addition, the lack of adequate
keratinized mucosa around implant-supported overdentures was associated with higher plaque
accumulation, bleeding on probing, gingival inflammation, and mucosal recession [436].

Gingival Biotype
Patients with a thin, scalloped gingiva have a poorer prognosis than those with a thick, flat
biotype when it comes to soft tissue recession and bone loss [439]. Patients with 2.0 mm or less of
initial gingival thickness show crestal bone loss up to 1.45 mm despite the supracrestal positions
of implant-abutment interfaces [440] (Fig 3.10a). Patients who present with the thick, flat biotype
exhibit broad, keratinized, well-vascularized gingiva, whereas those with thin tissues have a less
vascularized, narrow zone of connective tissue (Fig 3.10b). Clinically, a periodontal probe that can
be seen through the gingival sulcus is an indicator of thin, delicate soft tissues [441]. These patients
display triangular crown shapes and tapered roots as well, which are considered contributing
factors to bone loss due to an unfavorable thin osseous crest and increased papillary shrinkage
after surgery compared with patients with square crowns and broad roots.

a b
Fig 3.10a: Clinical view of thin biotype. Fig 3.10b: Clinical view of thick biotype.

Microbiological Factors
No association was found between bone loss and a single type of microorganism
[440,442,443]. The microflora prior to implant placement determines progression of peri-implant
pocket compositions [444]. Early implant exposure during healing results in more radiographic
bone loss, with the predominant bacteria being Peptostreptococcus species, β-hemolytic
streptococci, and Fusobacterium nucleatum [441].

~ 117 ~
 B forsythus was found in higher quantities in patients with previous periodontal disease.
However, no significant differences were found in microorganism species for single-or two-stage
implants, and all implants remained integrated [441]. This corroborates the findings that
periodontal pathogen presence does not always lead to a destructive process [442]. An increase in
surface roughness and surface free energy facilitates biofilm formation on dental implants and
abutment surfaces. The surface chemistry and design features of implant-abutment connections
are significant in biofilm formation [443].

HIGH RISK FACTORS

Periodontitis
The results of long-term implant therapy in patients with a history of periodontitis have
received much attention in the last years. One study showed that periodontal disease is not a risk
factor for peri-implant mucositis and/or peri-implantitis [444]. It appears that plausible patients
with aggressive periodontitis probably have a higher risk of peri-implant diseases. In a
retrospective study on the efficacy of dental implant therapy in periodontally compromised
patients, Ormianer et al. found that periodontal susceptibility resulted in increased bone loss but
had no effect on implant survival [445].
Certain clinicians are of the opinion that the prognosis of complex periodontal therapy does
not match the high success levels of implant treatment. Consequently, more teeth are extracted on
the assumption that implants perform better than periodontal compromised teeth and that their
longevity is independent of the individual’s susceptibility to periodontitis [446]. To have such an
extended long-term survival rate it is necessary to frequently monitor patients, especially those
who lost teeth due to periodontal disease, and to promptly use adjunctive additional treatment, as
needed. Consequently, implant therapy should not simply be proposed as “definitive”, but be
considered as an important option in the patient’s comprehensive long-term treatment plan.
Chronic periodontitis is a risk factor for SFE implant therapy. Patients with untreated
periodontitis should not receive dental implant treatment or SFE until the successful management
of the periodontitis (Fig 3.11).

Fig 3.11: Chronic periodontitis is considered as a high risk

factor.

Even after treating the periodontitis, there is still a lower survival and/or success rate trend
than in patients who have no history of periodontitis [364]. Consequently, patients with a history
of periodontitis need to be informed that they have an increased risk of peri-implantitis and of
implant failure. Studies on the relationship between chronic or aggressive periodontitis and

~ 118 ~
marginal peri-implant bone loss revealed values from 1.24 to 2.27 mm [447]. Chronically affected
patients are more prone to lower implant survival rates and biologic complications [448]. However,
some studies have reported peri-implant bone remodeling of less than 1.0 mm after 1 and 5 years
in the presence of previous periodontal diseases [449,450]. In fact, patients with generalized
aggressive periodontitis are prone to more bone loss than patients with chronic periodontitis [451-
454]. In addition, clinical findings of bone loss around implants and teeth in patients with
aggressive periodontitis may not follow the same pattern, contrary to what has been reported for
chronic periodontitis patients [455].
Further long-term studies with sufficient power and of carefully selected patients are
needed before any definitive conclusion can be reached about the long-term outcome of implant
treatment in periodontitis-susceptible patients [456]. Numerous cases of tooth loss due to
periodontitis have been followed by the extensive destruction of local bone. The resulting bone
defects and their relationship with the sinus floor are complex. It should also be noted that
extensive (three-dimensional) bone augmentation is required in cases of extreme bone resorption.
Situations of this type often require bone harvesting from extraoral sources such as the iliac crest.

Bone biomarkers
Osseointegration is a biodynamic phenomenon with micro-resorption and micro-
apposition phases. Bone remodeling is regulated by different biomarkers, with alternatively active
osteoblasts and osteoclasts, thus maintaining homeostasis.
Clinical evidence has frequently shown different bone resorption patterns among patients.
The dimensions of peri-implant bone loss are subjected to interindividual variations from implant
to implant and from variations from patient to patient [457]. This interindividual variability seems
to be strictly correlated to individual bone patterns.
Several biomarkers have been found to be involved in bone resorption. Alterations of any
one of the biomarkers within its physiological range could elicit different responses to implant
insertions. Although the data at hand is preliminary, bone resorption levels seem to be directly
correlated to biglycans and indirectly correlated to tumor necrosis factor α (TNF-α) [458].

Acute sinusitis
Acute sinusitis is a high-risk factor for SFE. Dental factors are the cause of sinusitis in 10%
to 12% of cases [459]. Teeth with periapical lesions or cysts have been implicated. Patients with a
periapical disease have a 3.6 greater chance of contracting sinusitis compared to controls [459].
When there is a suspected communication between a sinus and apical tooth segment, an adequate
healing period is needed between tooth extraction and SFE to minimize the risk of perforating the
Schneiderian membrane (Fig 3.12a,b).

~ 119 ~
 a b
3.12a,b: CT scans showing maxillary sinusitis of dental origin – notice the teeth with periapical lesions of cysts with suspected
communication between the apical tooth segment and the sinus.

Significant difficulties are probable outcomes when there is less-than-ideal postsurgical

healing of soft and hard tissues. Communication between the extraction socket and the maxillary
sinus increases membrane perforation risk and by doing so increases the surgical risk as well. This
needs to be carefully evaluated.

Use of bisphosphonates
In 2003, osteonecrosis of the jaw (ONJ) in patients treated with bisphosphonates was first
described with a series of case reports by Marx and Mijliorati [460, 461]. The highest incidence of
ONJ is contributed to intravenous (IV) dosages with an incidence of 0.7 to 12%. Oral nitrogen-
containing bisphosphonates (N-BPs) where not found to be statistically significant with an
incidence per one hundred thousand person-years of exposure [462]. The suggested risk factors
for ONJ are denture wearing, extraction, and bony prominences lined with thin mucosa such as
exostosis, tori, and mylohyoid ridge. However, ONJ could also happen without any risk factor.
ONJ was found to be more common in the mandible as compared to the maxilla by a 2:1 ratio
[463].
Jeffcoat observed after three years, 100% success rate in the bisphosphonates group
without any complications [464]. Bell and Bell showed the implant survival rate of
bisphosphonated patients to be 95% compared to 96.5% in the control group [465]. Implant
surgery for those taking oral N-BPs is not contraindicated in osteoporotic patients. Short-term
results of implant survival show that there is no higher risk in those who received N-BP therapy
and implant placement may be considered a safe procedure in patients taking oral N-BP for less
than 5 years [466]. Although previous studies have shown either little or insignificant association
of oral bisphosphonate therapy and ONJ, cases of ONJ after implant therapy do exist.
According to the American Association of Oral and Maxillofacial Surgeons’ position paper
in 2009, it was recommended for patients to suspend N-BPs therapy three months prior and three
months post-oral surgery for patients using N-BPs for over three years [467]. The treatment
objectives of patients with ONJ are to control infection, eliminate pain, and minimize bone
necrosis progression and soft tissue dehiscence. The general principle for treating ONJ is complete
resection of the necrotic bone, grinding of bone until fresh blood flows from the native bone,
primary closure, and antibiotic therapy. If any necrotic bone is left after surgery, pain symptoms
and purulent discharge may occur. Both conservative and aggressive methods have been shown to
be effective. However, more studies must be performed to determine the better methodology [468].
It is advisable to eliminate all disease indications during the initial surgery to prevent further

~ 120 ~
complications. It is recommended to place patients with a history of bisphosphonate use on a
periodic follow-up schedule after implant surgery.
Several sets of guidelines have been published for the use of bisphosphonates and
bisphosphonate-related osteonecrosis of the jaws (BRONJ) [469-473]. Although the exact
pathological mechanism remains unclear [474], bisphosphonates are thought to promote apoptotic
signals in both osteoclasts and keratinocytes that reduce and destroy the immune keratinocytes
barriers within oral mucosa [475].
Recent findings indicate that bone loss risk after implant placement is greater in patients
taking intravenous bisphosphonates. On the other hand, patients using intraoral forms for less than
five years can receive dental implants because no adverse effects have been seen in short-term
implant survival rates [465].

FACTORS INVOLVING A MODERATE RISK

Bruxism
Bruxism is a motor activity that potentially causes damage to the stomatognathic structures
and is a risk factor for dental implant survival [476, 477]. In spite of the increasing knowledge on
its etiology, diagnosis, and management [478], evidence of bruxism’s effects as a cause of dental
implant complication or failure is still lacking [479]. Therefore, practical management guidelines
for bruxism patients undergoing dental implant restoration are mostly based on expert opinions
rather than on scientifically sound information [480]. The common fear is that bruxism causes
overloading that may affect osseointegration and/or compromise the integrity of the mechanical
components. Bruxism is a catch-all term that includes different motor muscle activities with
different etiologies [481,482]. In these cases, dental implant complications are related to biological
or mechanical damage [2]. There is not enough evidence suggesting that bruxism is a risk factor
for biological dental implant complications. More likely, bruxism is a risk factor for mechanical
complications. Bruxism includes various motor activities such as grinding and clenching that can
potentially and differently affect the stomatognathic structure due to the different forces that they
exert and the loads that they transmit [483].
Occlusion’s role as a force transmitter to teeth and dental implants should be assessed as
well [484]. The influence of factors such as the occlusal design of non-axial loads on implant-
supported rehabilitations should be underestimated as risk factors for implant complications in
bruxism patients. Although sufficient evidence for a relationship between bruxism and implant
failure is lacking [479], relevant precautions should be taken for implants placed in the posterior
maxilla following SFE. All biomechanical aspects relating to the design and span of the prosthesis
should be carefully considered. Depending on the clinical situation, the usual recommendation is
to select as many implants as possible and that they should be of the greatest length possible. An
extended healing period before loading the implants helps minimizing the risk. If bone height is
inadequate and not enough implants can be placed, it is preferable to use an implant supported
removable overdenture, so that the mucosa will be able to dissipate some of the load. In addition,
a night guard (occlusal splint) is recommended [485].

Smoking
Smoking’s adverse effects on oral wound healing were noted almost half a century ago
[486]. Since then, several reports have been published associating smoking with dental implant
failure [311,385,487,488] and, more specifically, with the failure of implants placed in augmented

~ 121 ~
sinuses [489,490]. Some suggested that implant failure in smokers is not due to poor healing or
lack of osseointegration, but of the exposure of peri-implant tissues to tobacco smoke [311].
Although many reports have documented the detrimental effects of smoking on dental implants,
there was one study that concluded that smokers and nonsmokers have the same implant survival
rates [491]. Tobacco smoke contains several noxious substances, including carbon monoxide,
nicotine, and hydrogen cyanide [492,493]. Nicotine has a few toxic effects on peripheral
circulation and immune responses. It reduces the proliferation of red blood cells, macrophages,
and fibroblasts, and increases platelet adhesiveness thus elevating the risk of microclots, reduces
microperfusion, and causes cutaneous vasoconstriction. Nicotine promotes the release of
epinephrine and norepinephrine, resulting in vasoconstriction and decreases tissue perfusion.
Carbon monoxide reduces the blood’s oxygen-carrying capacity, and hydrogen cyanide inhibits
the enzyme systems necessary for oxidative metabolism [492,493]..
Ischemia is an important pathophysiologic factor in impaired wound healing. A number of
reports on dental implant procedures highlight the need to maintain strict oral hygiene, particularly
in smokers [490], and in addition, the use of antibiotics perioperatively [326,503]. According to
Peleg et al. [494], smokers who abstain from smoking prior to surgery and for 10 days afterward
can avoid complications that are frequently found in smokers. Tobacco smoking as a risk factor is
a well-established. It decreases local vascularization, as well as having adverse impacts on
inflammatory, immune, and healing responses in periodontal and peri-implants [495-498].
Tobacco smoking can negatively modify bone filling, bone-to-implant contact, and bone density
due to smoking’s constraining effect on the proliferation of precursor cells and vascularization of
the implant site [495-498].
Two systemic reviews assessed implant failure in smoking patients, and the findings
support the determination that tobacco smoking causes implants to fail at higher rates [499,500].
Smoking was clearly demonstrated to detrimentally impact survival in sites with sinus floor
augmentation. Smokers undergoing elevation of the maxillary sinus floor have an increased risk
of implant failure. This study is in agreement with previous systematic reviews assessing implant
outcomes in smokers at non-grafted sites [499,500]. Whether temporarily stopping smoking before
and after the surgical procedures has any beneficial effect has yet to be resolved. In a recent
systematic review, the implant failure rates in grafted sites were shown to be almost double in
smokers compared to non-smokers [501]. Concerning SFE procedures, even though the difference
was not statistically significant, caution should be exercised when considering smokers for SFE.
It should be noted that smoking together with a history of treated periodontitis is clearly seen as a
risk factor both for implant survival and for biological complications in general [374].
Despite individual variability, the number of cigarettes smoked and the risk of bone loss
has been shown to be positively correlated [502]. Smokers have greater marginal bone loss around
implants than nonsmokers [503]. However, certain long-term studies did not find a consistent
association between bone loss and smoking [504]. The available data indicates that patients
smoking more than 20 cigarettes per day increase the risk of peri-implant bone loss by 31%, and
this loss is aggravated by alcohol intake [505,506]. In an analysis of implants with a history of
"progressive" bone loss (i.e., purulence, soft tissue peri-implant recession, and pocket probing
depths of 6 mm or greater), smokers had a larger number of affected implants as compared to
nonsmokers [507,508]. Smokers were shown to have a higher annual failure rate (3.54%)
compared with 1.86% for non-smokers [501].

~ 122 ~
 Mucosal Thickening of the Sinus Membrane
Mucosal thickening of the sinus membrane is classified according to appearance and
height. Appearance is classified as normal, irregular, rounded, circumferential and complete.

Fig 3.13: CT scan demonstrate mucosal thickening up to 5mm. Fig 3.14: CT slices show mucosal thickening, up to 7mm. This
is considered a relative risk factor.

Fig 3.15: CT scan showing mucosal thickening up to 12mm Fig 3.16: CT scan showing mucosal thickening up to 12mm
combined with severe ridge resorption. combined with severe ridge resorption.

Fig 3.17a: CT scan showing mucosal thickening up to 8mm Fig 3.17b: CT scan showing mucosal thickening up to 12mm
due to infected teeth due to infected teeth

~ 123 ~
 Fig 3.18: Mucosal thickening up to 15 mm. examination of the Fig 3.19: Mucosal thickening is clearly demonstrated. Note the
osteomeatal complex is essential. course of the PSAA.

Abnormalities of the sinus membrane (e.g. hypertrophy) do not contraindicate SFE but
should be considered a relative risk (Fig 3.13, Fig 3.14). Hypertrophy of the Schneiderian
membrane can be caused by allergies, a chronic sinus infection, radicular cysts, developmental
cysts, benign tumors, or fibrous dysplasia. Diagnosis of infective causes of membrane thickening
are based on an examination that includes dental symptoms (e.g. dull pain, periradicular
pneumatization) and the patient's medical history [458]. SFE can generally be safely conducted
when there is mild membrane thickening or if the hypertrophy is not caused by infection. Situations
of aberrant site healing following extraction increase the risk of sinus perforation. Therefore, one
should allow sufficient time for healing and restitution of the sinus membrane [510]. Any
abnormalities of the alveolar mucosa caused by infection, bullous disease, or aberrant healing
increases the risk of postsurgical soft tissue dehiscence. Any of these conditions need to be treated
and resolved prior to SFE procedures.

Pathologic Alterations
Pathological alterations of the maxillary sinus are of considerable importance. These
include: discontinuity of the sinus wall, radicular cyst of odontogenic origin, bone thickening,
polypoid lesions (mucus retention cyst and/or antrochoanal polyp), air–fluid level, antrolith, sinus
opacification, foreign bodies, and sinusitis (Fig 3.20a,b-Fig 24a-i) [28]. Pathological alterations
may alter the surgical sinus floor augmentation and consequently the healing process after surgery.

a b
Fig 3.20a: Discontinuity of the lateral wall due to a traumatic Fig 3.20b: Discontinuity of the lateral wall due to extracted teeth
tooth extraction. with radicular cyst.

~ 124 ~
 a b
Fig 3.21a: CT scan showing huge radicular cyst of dental origin. Fig 3.21b: After tooth extraction the cyst was fenestrated and is
clearly demonstrated.

c d
Fig 3.21c: Enuculation of a huge radicular cyst. Fig 3.21d: Bone augmentation after cyst enuculation.

Fig 3.22a: Bone distruction due to radicular cyst. Fig 3.22a: Lateral wall destruction due to a radicular cyst.

a b
Fig 3.23a: CT scan showing the destruction of the bone due to a Fig 3.23b: CT slices demonstrate the intact lateral sinus wall
residual cyst extending from teeth 24 to 26. despite the extended residual cyst.

~ 125 ~
 c d
Fig 3.23c: Full thickness flap elevation. Fig 3.23d: The residual cyst is well exposed.

e f
Fig 3.23e: After flap elevation the cyst was totally enucleated. Fig 3.23f: The empty space was filled with grafting material.

g h
Fig 3.23g: The grafted area was covered with a collagen Fig 3.23h: Wound closure.
membrane.

b
a
Fig 3.24a: Panoramic radiograph showing radicular cyst 16. Fig 3.24b: Panoramic radiograph of CT showing the extension
of the radicular cyst.

~ 126 ~
Fig 3.24c: CT slices showing the volume and extension of the cyst.

d e
c
Fig 3.24d: Extraction of tooth 16-notice the connection of the radix Fig 3.24e: Enucleation of the radicular cyst with removal of right
with the cyst. upper first molar.

f g
Fig 3.24f: Enucleation of the radicular cyst-notice the appearance Fig 3.24g: An enucleated radicular cyst with tooth radices.
of the cyst’s containment.

~ 127 ~
 h i
Fig 3.24h: Clinical view of the destructed lateral wall of the sinus Fig 3.24i: Wound closure with iodoform strip.
after cyst enucleation.

Secondary sinus cavities

Any secondary cavity identified in presurgical CT scans should be assessed for its
complexity. Non-complex secondary cavities can be usually managed at a moderate risk of
perforation.

Unfavorable interarch relations

Thelikelihood of encountering unfavorable interarch relations in the posterior maxilla
increases with specific three-dimensional patterns of bone resorption in the molar areas. Both
vertical augmentation of the sinus floor and horizontal bone augmentation may be needed to
optimize the restorative outcome. The use of autogenous block grafts is indicated in these cases.
When bone height is inadequate for implant placement due to a combination of vertical resorption
of the alveolar bone and sinus pneumatization, the surgeon should explore the option of vertical
bone augmentation at the crest.

The condition of the adjacent teeth

The condition of the teeth (e.g. remaining tooth structure or pulp status) adjacent to the
proposed SFE should be considered prior to treatment planning. This will minimize any
unexpected tooth-related complications that otherwise can persist and eventually affect the long-
term outcome of the grafted area.

Oral hygiene
A review showed that smokers with poor oral hygiene have greater marginal bone loss
around implants than patients with satisfactory oral hygiene [511]. Similarly, patients how have
healthy peri-implant environments present low plaque scores and less periodontal bleeding on
probing [512]. However, the long-term effects of supportive implant therapy have not been
thoroughly studied on recall intervals or specific hygiene treatments [513] (Fig 3.25a,b, Fig 3.26).

~ 128 ~
 a b
Fig 3.25a: Inflammatory process around implants due to lack Fig 3.25b: Inflammatory process around implants due to
of oral hygiene. denture pressure as well.

Fig 3.26: Removal of infected implant – notice the attached

calculus on the implant surface.

RADIOGRAPHIC EXAMINATION
Radiographic techniques
It is essential to select an appropriate radiographic technique based on the individual patient
history and the clinical examination. The imaging modality selected for diagnostic purposes should
be determined for the expected diagnostic yield and in accordance with the ALARA (as low as
reasonably achievable) principle, the radiation safety principle for minimizing radiation [514]. The
efficacy, benefits, and risks of available alternative technique having the same objective but
involving less or no radiation exposure should be taken into consideration.

Intraoral periapical radiographs

The intraoral technique provides preliminary information and high spatial resolution
imaging of teeth and potentially associated pathologies. In addition to mesio-distal (horizontal)
and crestal-apical (vertical) measurements, it will provide useful information on bone structure
and density of the resorption pattern following tooth extraction.
In terms of the objectives of presurgical imaging, periapical radiography is:
 A useful high-yield modality for ruling out local bone or dental disease.
 Has limited value in determining quantity because the image is magnified, may be
distorted, and does not depict the third dimension of bone width.
 Has limited value in determining bone density or mineralization.

~ 129 ~
  Of value in identifying critical structures.

Periapical radiographs provide information about the mesial and distal aspect of an implant
but the buccal/lingual aspect cannot be assessed. They are therefore unable to display cancellous
bone defects overlapped by existing cortical bone unless the bone loss exceeds a threshold or the
cortical bone is involved in the process [515,516]. Because of the Mach-band effect, i.e.
radiolucent areas in zones of contrasting radiographic densities, peri-implant radiolucences may
occasionally be noted despite successful osseointegration (Fig 3.27a-f).

a b c

d e f
Fig 3.27a-f: Periapical radiographs reveal peri-implant bone conditions for routine longitudinal examination

Digital periapical radiographs are a valid and reliable method for detecting circumferential
peri-implant bone defects and performs significantly better than cone beam computed tomography
(CBCT) which should not be used routinely as a replacement for periapical radiographs for the
diagnosis of peri-implant bone conditions [517]. Intraoperative periapical radiographs are helpful
whenever variations are detected between the panoramic radiographs and CT scans or when
implants are placed near the maxillary sinus. A periapical radiograph is routinely recommended at
the conclusion of an implant placement before the patient is dismissed, during the healing period,
at follow-up visits and any time the patient reports unexpected pain or discomfort or if soft tissue
conditions worsen. The crestal bone level (i.e. the distance from the level of the abutment-implant
junction to the first bone to-implant contact) can be measured. The known distance between
implant threads is used for purposes of calibration and determination of the exact magnification of
the images (Fig 3.28, Fig 3.29a,b).

~ 130 ~
 a b
Fig. 3.28: Intraoral radiograph reveals Fig 3.29a,b: Periapical radiographs showing marginal bone levels.
peri-implant conditions five years after
a simultaneous SFE approach.

Lateral (profile) radiography

Lateral profile radiography may be useful for providing an assessment of the relation
between the upper and lower jaw, for obtaining an estimate of the angulation of the frontal parts
of the jaws and of the widths of the jawbones in their mid-sagittal regions (Fig 3.30a,b).

a b
Fig 3.30a,b: Lateral (profile) radiograph

Panoramic radiographs
In the past, panoramic radiology was the gold standard for dental implant treatment
planning, along with periapical radiographs. However, these imaging techniques have many
drawbacks. The inherent deformation and two-dimensional nature of panoramic radiographs
jeopardize their interpretation and quantitative measurements, thus panoramic radiographs
underscore the mesiodistal distance of available bone, particular in the upper premolar region. The
most significant drawback of these radiographs is that they are two-dimensional. Panoramic
radiographs can only be used for bone height measurements and do not allow for volume
measurements.
Panoramic radiography is a curved plane tomographic radiographic technique used to
depict the maxilla and the mandible. Information about the maxillary sinus form, the alveolar bone
relative to the sinus floor, and any pathological processes that may affect implant treatment can

~ 131 ~
also be seen. The panoramic radiograph can provide a sufficient view of the residual crest height
under the sinus floor (Fig 3.31, Fig 3.32) and of anatomical features such as the anterior and
posterior wall, the septa of the sinus, the palatal curvature, and the pterygoid process.
One must consider that panoramic image quality is highly dependent of the radiologist’s
skill and remains a two-dimensional image of a three-dimensional volume with superimposition
of anatomical structures, real or ghost structures, and shadows of soft tissue and air that may make
the assessment of the true anatomical situation surrounding the sinus cavity unclear. Panoramic
radiographs have an inherent horizontal magnification, particularly in the upper premolar region,
which makes planning more haphazard and less reliable because of a variable degrees of overlap.
The posterior maxillary regions are generally the least distorted regions of a panoramic radiograph.
Traditional panoramic radiography is a high-yield technique for demonstrating dental and
bone disease, does not demonstrate bone quality or mineralization, is misleading quantitatively
because of magnification and due to lacking a third-dimension the cross-sectional view is not
demonstrated. Panoramic radiographs can still be used to provide a quick estimate of the bone
height by taking the magnification into account. The magnification varies between different types
of panoramic machines. Some units permit various types of panoramic images to be taken at
different magnifications. It is thus important that one makes certain of the actual magnification in
the image to be evaluated. The spatial resolution is sufficient for many purposes but inferior to that
obtained by intraoral radiography. Implant companies often market magnified overlays with a
preset 25% magnification for the evaluation of an implant size that is placed on a panoramic film
for comparison with vital structure position.

Fig 3.31: Panoramic radiograph prior to SFE in the posterior Fig 3.32: Panoramic radiograph showing the pneumatized sinus
segment. It's difficult to appreciate the extent of a secondary and the sinus septa.
cavity and to define the height and form of the septum.

A consistent 20% magnification error was found for the posterior maxilla. Because the
concept of standardized magnification is impossible and unreliable, most clinical studies have
observed the inaccuracies of direct measurements of panoramic radiographs. Previously published
recommendations on imaging procedures for preoperative assessment of implant treatment suggest
determining the true magnification factor for implant site calibration, which allows for a more
precise selection of the proper implant size compared with a standard calibration factor [518].
Quantification of regional magnification on panoramic radiographs has been studied using a
variety of radiopaque objects of known dimensions such as acrylic resin stents, metal pins, balls
and implants. Using the implant length as a reference object on postoperative panoramic
radiographs is a simple and effective evaluation method to estimate a panoramic unit's vertical
magnification factor (MF). According to Vazquez et al. [519], the accuracy of the manufacturer’s

~ 132 ~
MF has been verified. In addition, the inter- and intraobserver reliability of the MF confirms that
a panoramic radiograph can be used for preoperative implant length evaluation in the premolar
and molar segments of the mandible. Therefore, the implant length, measured on the routine
postoperative radiograph, can be optimally utilized to quantify the MF similar to other reference
objects on preoperative panoramic radiographs.
The use of a panoramic exam for oral implant planning in severely resorbed maxillae overestimates
the need for a sinus augmentation procedure when compared with the use of both three-
dimensional planning software and strategic implant placement on small remaining bone volume.
Panoramic radiographs also are obtained after second-stage surgery, after the prostheses
placement. However, present pathologies in the maxillary sinus are frequently overprojected and
distorted, such that three-dimensional imaging modalities are found to be superior for evaluating
changes in the maxillary sinus (Fig 3.33a,b).

a b
Fig 3.33a: Distortion of panoramic imaging can lead to Fig 3.33b: A repeated panoramic radiograph clearly
misinterpreting the right diagnosis. A projected implant may demonstrate that there is no implant migration in the sinus
lead to understanding that an implant has migrated in the sinus cavity.
cavity.

CBCT-generated panoramic views can be considered as an alternative to conventional

panoramic imaging [520] (Fig 3.34a-f). Comparing these two modalities, Mischkowski et al. [520]
found that subjective image quality was ranked higher in panoramic radiographs than in CBCT
panoramic views due to noise, poor contrast, and artifacts caused mainly by metallic dental
restorations in the CBCT images. Furthermore, CBCT panoramic views were superior to
panoramic radiographs for identifying the mandibular canal [521]. CBCT should not replace
digital panoramic images in all situations since a CBCT examination gives a higher radiation dose
(4-20 times greater) than panoramic radiography. Which imaging modality to select for diagnostic
purposes should be determined for the diagnostic yield expected and in accordance with the
ALARA (As Low as Reasonably Achievable) principle [514].

a b

~ 133 ~
 c d

e f
Fig 3.34a-f: CBCT panoramic views are considered superior to traditional panoramic radiographs in identification of anatomical
structures.

Computed tomography
Tomography can be used to obtain cross-sectional images, that is, images which are
perpendicular to the curvature of the jaw-bones in the intended implant site. Three main groups of
tomographic techniques are used for peri-implant tomography: motion (conventional)
tomography, CT, and CBCT. For simplicity, in this book the term "computed tomography" will
be used to encompass first generation CT scanners, spiral (helical) CT scanners, and multislice CT
scanners. One important advantage of spiral CT over other methods is the possibility of
reconstructing images in multiple projections from just one acquisition, with an undoubted
reduction in the radiation dose absorbed by the patient. Tomography is the only method by which
reliable estimates of the bone width in intended implant sites can be obtained. Tomography also
displays the angulation and shape of the jawbone and the alveolar process. Computed tomography
has also evolved to become faster, more sensitive, more accessible, and adjustable for dental
diagnostic tasks. Computed tomography (CT) should be used when planning implants in the
atrophic jaws particularly in the posterior maxilla. CT offers diagnostic in site of the maxillary
bone that is not attainable by panoramic radiograph (Fig 3.35).

Fig. 3.35: conventional CT scan. The large field of view reveals

the symmetry of the maxillary sinuses and allows examination
of a wide surgical field.

~ 134 ~
 Computed tomography enables differentiation and quantification of soft and hard tissues.
CT images are inherently three-dimensional digital images, typically 512X512 pixels with a
thickness determined by the slice spacing of the imaging technique. The individual element of the
CT images is called a voxel, which has a value, referred to in Hounsfield units, that describes the
density of the CT images at that point. CT enables identification of disease, determination of bone
quantity, determination of bone quality, identification of critical structures at the proposal region
and determination of the position and orientation of the dental implants. In the past, panoramic
radiology was the gold standard for dental implant treatment planning. For more complex cases or
when accurate representation and location of vital structures was needed, CT was always
integrated into the pre-treatment imaging process. Today, no radiographic modality gives more
information of the paranasal sinuses than CT, which is the gold standard for viewing the osseous
structures and evaluating pathology in the sinuses. This type of radiography, in comparison,
provides much more detailed information regarding prevalence and position of septa, maxillary
sinus anatomy, and detection of sinus pathology. CT scans have to be obtained for SFE patients to
determine the osseous structure and to exclude any pathology of the sinuses such as inflammation,
cysts, tumors, or fractures. However, due to medico-legal reasons, annual CT scans should to be
avoided due to radiation exposure. Previous studies have demonstrated that conventional and
computerized cross-sectional tomography are superior to intraoral and panoramic images
regarding visualization of the mandibular canal, the marginal bone crest, and estimation of the
dimensions of various anatomical structures [522]. In general, implants planned on tomographies
are longer rather than shorter when compared with those planned on panoramic radiographs
particularly in the posterior maxilla.

Cone beam computed tomogrraphy (CBCT)

CBCT is a medical imaging modality, which has been applied in different fields of
medicine. For dentomaxillofacial use, CBCT scanners were developed in the late 1990s, and since
then, the technique has gained great popularity in dentistry. Today, CBCT is a "catch-all" term for
a technology comprising a variety of machines differing from each other in many respects. The
principle behind the technique, as its name implies, is a cone-shaped X-ray beam with the X-ray
source and detector (image intensifier or flat panel detector) rotating around a point of interest in
the patient. The technique has the potential to clearly identify anatomic structures and boundaries,
shape of the jaw-bone, bone structure, and density and jaw pathology, including small periapical
inflammatory lesions. Cone beam CT and CT offer the potential to reformat image data, create
virtual models of the jaws, and provide distinct advantage of accurate measurement in any
dimension or along a curved line [523]. In general, CBCT units can be categorized into large,
medium, and small volume units based on the size of field of view (FOV). Some units allow the
FOV to be selected to suit the purpose of the examination, ranging from small fields for dental
imaging to large fields for maxillofacial examinations. The soft tissue contrast resolution produced
by current CBCT units used in dentistry is poor [524]. CT scans produce much better soft tissue
contrast resolution [524], allowing an evaluation of various soft tissue changes related to bony
lesions. It should be noted that many soft tissue lesions are best examined with magnetic resonance
imaging (MRI). CBCT for dental radiology generally offers higher spatial resolution at a
considerably lower dose than that available from CT. The term “spatial resolution” means the
ability of the system to differentiate two high-contrast objects that are close together. For instance,
a good special resolution has the ability to visualize a black spot (the canal) between two white
spots (bone around canal). According to the Nyquist sampling theorem [525], the best chance to

~ 135 ~
identify a small object is when the pixel size of the radiographic system is half the size of the
object. That is, our best chance to identify a canal of 0.5 mm is with a voxel size of a maximum
size of 0.25mm otherwise, partial volume averaging effect may make the canal vanish from the
image. CBCT imaging is recommended for visualizing anatomical structures such as the
prevalence, width, length, and position of the bony canal (artery) in the lateral sinus wall and to
explore the prevalence, width and length of another (newly detected) bony canal at the palatal
aspect of the upper canine (Fig 3.36, Fig 3.37, Fig 3.38a,b).

Fig. 3.36a,b: Multislice computed tomography of the bony canal Fig. 3.37: Bony canal in the palatal of the canine.
in the lateral wall of the maxillary sinus [541].

a b
Fig 3.38a,b: Bony canal in the canine area.

CBCT is recommended for sinus augmentation procedures to improve the surgeon's confidence
and the accuracy of the sinus augmentation technique. It has been established that panoramic views
of the posterior maxilla will underestimate the amount of bone available for implant placement
and, if relied on, will overestimate the number of clinical situations requiring a sinus augmentation
[528]. CBCT can overcome this problem as it provides more accurate measurements of the
available bone volume and, in some border-line cases, will show that implants can be placed
without sinus grafting surgery. CBCT can also provide information on the presence, and extent of
any septa, as well as the health of the sinus such as absence of sinus membrane thickening, polyps,
or fluid levels. Because cross-sectional imaging offers improved diagnostic efficacy, it is the
preferred method for preoperative assessment for sinus augmentation surgery. In some clinical
situations, when there is evidence of sinus pathology, or it is the clinician's opinion that sinus
drainage is impaired and may jeopardize the outcome of the procedure to be undertaken, there may
be a justification to extend the scan to include the whole of the sinus including the osteo-meatal
complex.

~ 136 ~
 In relation to radiation emission, CBCT has a mean absorbed radiation of 12 mSV or 0.62
mGy [111]. This dosage is 25% of a conventional panoramic radiography. In addition, a medical
CT-scan generates radiation 40-60 times more than CBCT. In CBCT, distortion and magnification
are minimal, with errors of less than 0.1mm [518]. CBCT is reliable as a preoperative tool for
implant treatment planning to assess atrophic posterior maxilla density and microarchitecture
[526]. Reduced radiographic dose and cost are among the other benefits of CBCT over
conventional CT [527] (Fig 3.39a-f).

a b

c d

e f
Fig 3. 39a-f: CBCT slices as a preoperative tool to assess atrophic posterior maxilla density and microarchitecture besides sinus
pathology.

Microcomputed tomography
Microcomputed tomography (MCT), initially described by Feldkamp et al. in 1989 [528],
is a nondestructive, radiographic technique to attain 3D information about bony structure. In recent

~ 137 ~
years, continuous development has made it possible to achieve images with a resolution of up to
less that 10 µm2 voxel size [529,530]. Thomsen et al. [531] compared morphometric abilities of
classical µCT histology for cancellous bone and concluded that µCT could be used as a substitute
for conventional histologic analysis for bone structural evaluation because of the high correlations
of morphometric data evaluation [531]. Micro-computed tomography (micro-CT) is now widely
used for observing and analyzing the internal structure of hard tissue because it is quick,
reproducible, and non-destructive [528]. Many studies have used micro-CT to obtain high-
resolution images and to assess the trabecular structure of human bone quantitatively in three
dimensions [532]. Interest in micro-CT in the field of dental implants is increasing. Micro-CT is
increasingly employed to evaluate peri-implant bone [533] and has been validated using
histomorphometric results [534]. This method also allows evaluation of the three-dimensional
(3D) architecture of grafted bone after a period of bone healing [535]. However, only a few studies
[536] assessed the bone formation in autogenous bone graft by micro-CT and none of these studies
examined the difference in the 3D trabecular structure and bone mineral density (BMD) of
autogenous bone grafts as compared with native bone after maxillary sinus augmentation. Micro-
CT has become the “gold-standard” for evaluation of bone morphology and micro-structure. It
uses data from attenuated X-ray projections in multiple angles to reconstruct a 3D representation
of the model which characterizes the spatial distribution of the material density. It allows the study
of structures of a few micrometers such as bone trabeculae. Architectural metric parameters such
as bone volume (BV), tisular of total volume (TV), and bone surface can be directly determined
from the 3D images without assuming the geometric model, in contrast to classical
histomorphometry [111].

Clinical application of CT images in maxillary sinus surgery

Diagnostic imaging has an indispensable role in presurgical planning. Computed
tomography (CT) has become standard for assessing the feasibility of implant surgery [538-540].
Three-dimensional diagnostic assessements have a decisive value in presurgical treatment
planning, especially in situations in which the alveolar process has pronounced resorption, and
therefore insufficient bone volume for placing dental implants. These situations, which once
limited the placement of implants in the posterior maxilla, can now be overcome via maxillary
sinus augmentation procedures [541-543]. The initial information required from diagnostic
procedures is the volume of the maxillary sinus, especially the area of residual bone. Anatomical
information, the presence of septa and the presence of alterations in mucosa caused by ongoing
orosinus pathologies are important. Correct identification of the position and patency of the
maxillary sinus ostium, together with the presence of any additional ostiae are required.
CT allows accurate calculations of the recipient site for maxillary sinus augmentation.
Three-dimensional reconstructions are an accurate and reliable method for calculating the amount
of bone tissue needed to obtain adequate reconstruction of the alveolar process, allowing the
placement of dental implants.
CT has considerably improved diagnostic assessment of the local situation. Axial images,
with sub-millimeter thickness are very important in local diagnostic capacities. Analysis of the
planned surgical site becomes relatively simple, and the densitometric information available for
areas of interest ensures much higher diagnostic confidence compared with conventional
radiologic assessment. The substantial inclusion of information technology in the diagnostic field
has made electronic reconstructions possible. Three-dimensional reconstructions using volume

~ 138 ~
rendering images have today reached much higher diagnostic levels than early 3D reconstructions,
which used the surface technique, which is now obsolete.
In particular cases, such as the analysis of maxillary sinus lumen morphology, it may be
useful to use virtual endoscopy, which can simulate and help the planning of sinoscopy operations.
The identification of the maxillary sinus ostium, in particular the integrity of the anatomic
structure, known as the ostiomeatal complex, is a key role in planning sinus augmentation. This is
the morphofunctional unit used for drainage and aeration of the anterior ethmoidal cells, the
maxillary sinuses and the frontal sinuses. CT allows precise evaluation of its numerous
components, and can reveal any irregularities in development (e.g. concha bullae, septum
deviation, presence of inflammation that involves the maxillary sinus ostium). Determining the
position of the ostium and its patency is important when planning sinus elevation operations.
Respecting this structure is essential for a successful operation.
The first fundamental step involves presurgical assessment of the implant site. This is best
accomplished with a diagnostic guide or scanning appliance used in combination with three-
dimensional imaging. It is important that the radiographic stents (scanning appliances) contain the
locations of the teeth. This generally is accomplished by using hollow metal cylinders incorporated
into the radiographic stent (scanning appliance) into the location of the desired teeth. The scanning
appliance then replicates the anatomical crowns of the teeth to be replaced. This allows the
clinician to see cross-sectional images that include the location of the teeth and the amount and
location of available bone in the edentulous segments [537]. The apical portions of the metal tubes
should be located at the cementoenamel junctions of the implant restorations. The axis of the tubes
should be parallel to the axis of the implant restorations. Ideally, implants should be three-
dimensional extensions of the implant restorations, but the angles may be changed depending on
whether screw or cement retention is used.
CT images are reconstructed from the digital data developed by the scanning unit. They
are stored, handled, printed, and transmitted in standard digital imaging and communications in
medicine format (DICOM). DICOM data provide the basis to reproduce the anatomical features
to be studied. The virtual environment thus created can be used to plan implant locations using
simulation software, which will readily disclose the need for SFE or any other bone augmentation
procedures. It will also supply information about the augmentation volume required for an ideal
outcome and about implant parameters such as ideal length, number, and positioning. This
approach offers significant advantages, especially in anatomically complex posterior segments of
the maxilla. Simulation software will also yield vital information such as considering alternatives
to SFE. A series of cases are presented in which implants were placed in the premolar and molar
areas according to different treatment modalities to avoid SFE. The sequence of procedures
involving the use of simulation software includes: Initial diagnosis, fabrication of a scanning stent,
CT scanning, treatment planning, construction of a jaw model, surgery.
Software-based simulation based on CT data can be readily implemented and is an effective
tool for managing the posterior maxilla. However, given the rapid development in software
applications and fabrication technologies for surgical stents, all new processes and systems should
always be carefully verified.
Ekestubbe et al. [544] and Sakakura et al. [545] were concerned with the selection criteria
for imaging tests. Their results revealed that most participants did not use sectional images at the
planning stage of implant therapy, despite scientific recommendation by the American Academy
of Oral and Maxillofacial Radiology [546]. Many anatomical boundaries can be identified during
the surgical procedure. It is important to realize that errors can occur when transferring information

~ 139 ~
from a cross-sectional computer image to the surgical situation. The surgeon should be aware of
this possibility and be careful to allow adequate “safty margins” in all cases. For instance, 13% of
sinus mucosa hypertrophy could be detected on CBCT that was not seen on the panoramic x-ray
[547]. Mengel et al. [548] compared the accuracy and quality of peri-implant defect representation
by intraoral radiography, panoramic radiography, conventional CT and CBCT. They found that
CBCT and conventional CT were able to measure all the bone defects to a high level of accuracy
and periapical radiographs could only detect the defects in the mesial/distal and craniocaudal
planes. CBCt showed the best imaging quality and was superior to conventional CT because it is
less susceptible to scatter artifacts.
From a cost-benefit point of view, different opinions exist on whether the additional
information on the bucco-lingual dimension, through conventional tomograms or CBCT, is indeed
needed for implant treatment planning when a panoramic image is already available. Therefore, it
is still pertinent to evaluate the need of cross-sectional imaging during preoperative implant
treatment planning, which does not mean that conventional tomography is better than panoramics,
or vice versa, for implant size planning. Therefore, implant selection should not be based solely
on CT scans or panoramics, but both types of images should be used to achieve information on all
three-dimensions of the alveolar process. A preoperative CT scan to evaluate the anatomy of the
maxillary sinus is therefore strongly recommended [485]. Nonetheless, it is impossible to evaluate
the entire maxillofacial complex, including the ostium of the maxillary sinus, the other paranasal
cavities and the nose in each patient planned for sinus floor augmentation.

Evaluation of bone density

The density of the edentulous jaw bone is extremely variable [170-173,413]. Assessment
of bone quality and the degree of mineralization of the bone prior to implant surgery is
indispensable for establishing a treatment plan. Most techniques previously used to determine bone
density were generally performed during or after surgery [163, 170-173]. In 1985 Lekholm and
Zarb [163] classified bone density into four types (O1, O2, O3, O4) based on the amount of cortical
versus cancellous bone. Misch [170] defined four bone density classes based on the tactile sense
of the clinician placing the implant. Bone density today is typically estimated from radiographs or
at the time of implant site preparation. It is noteworthy to emphasize that the bone density
classification of Misch [170] is slightly different from Lekholm and Zarb's [162] in two points:
1. According to Misch, D3 bone has fine trabeculae and is 47% to 68% weaker than D2 trabeculae,
and 20% stronger than D4 trabeculae, whereas Lekohlm and Zarb stated that Q3 bone has
favorable-strength trabeculae similar to Q2.
2. The Lekholm and Zarb bone quality only evaluates bone in the anterior maxilla and mandible.
The Misch bone density scale also evaluates the posterior molar regions of the jaws. As a result,
the primary difference between D3 and D4 bone is also the presence of cortical bone in D3, which
increases its overall strength and elasticity.

Evaluation of bone density using CT-Images

Computed tomography is currently the only diagnostically justifiable imaging technique
that can evaluate the density and structure of the jaw bones [527]. Bone density is evaluated using
Hounsfield units (HU) for implant placement and the results are considered site specific, objective,
and quantitative. The Misch classification system is still the system that is most widely used to
assess bone quality in clinical situations. Using this system, the surgeon grades the bone from D1

~ 140 ~
(hard) to D4 (soft) based on the way it feels during drilling. Another method for an objective
quantitative classification of bone density was recently proposed by Norton and Gamble [172].
This method uses CT assessment of bone density in Hounsfield units (HU). It is site-specific,
quantitative and more objective, since there is less dependence on subjective operator experience.
CBCT is a reliable tool for preoperative estimation of density values to objectively determine bone
density. This tool allows the clinician to presurgically determine which areas of the maxillary
bones correspond to the highest density osseous micro-structure by radiographic bone density, and
so to know which areas are better suited to place dental implants. We recommend using the tactile
sense of drilling and HU units. Both methods are equally good [173, 175].The great majority of
patients have posterior maxilla shapes corresponding to D or E in the Lekholm and Zarb
classification of bone quantity and type III or V of bone quality. Shapurian et al. [175] reported
that the mean bone density in the posterior maxilla is 333 HU. The average bone density of the
maxilla is less than half of the mandible, with the posterior maxilla showing the lowest bone
mineral density of all jaw regions. Therefore, a time span of at least 3 months isnecessary to obtain
the desired integration of implants placed in the posterior maxilla. Bone density can be obtained
in HU when helical CT is used. For CBCT, however, there is no standard unit such as HU because
no calibration has been conducted as yet. Density values obtained by CBCT were confirmed to
correspond reasonably with those estimated using helical CT [549]. Several studies have also
reported a high level of correlation between the CBCT density values and multi-slice CT HU [550-
552]. With CBCT, the dimensional accuracy is also comparable with CT, but unlike CT, the gray
density value of the CBCT images (voxel value [VV]) are not absolute [553]. CT can be calibrated
using a reference of air density values (-1000 HU) and pure water (0 HU). Otherwise, CBCT can
be only calibrated based on gray scale differences presat by the manufacturer. In a resent study
aimed at determining the relationship between CT- and CBCT-based gray density values, Arisan
et al. [553] revealed gray density values ranging from 167 to 989 HU and from 229 to 1042 VV.
According to Cassetta et al. [554], a conversion ratio between the two gray values was determined
and defined equalling to 0.7. Therefore, to convert CBCT gray values into CT values, it is
necessary to multiply the CBCT values by 0.7. Whether CT or CBCT values are truer to
corresponding histological bone densities, remains to be seen.

Evaluation of bone density during implant site preparation

Evaluation of bone density by drilling resistance is performed by the Misch method [170],
previously proposed by Lekholm and Zarb [163]. The presence and thickness of a crestal plate and
the density of transalveolar bone are easily determined during implant site preparation. The density
of bone is determined by the initial bone drill until the final implant site preparation. For preparing
the implant site in different bone densities of the posterior maxilla, a physiodispenser with copious
cooled sterile saline irrigation is used during the bone preparation (Fig 3.40).

~ 141 ~
 Fig 3.40: Physiodispenser with cooled sterile saline for irrigation.

There is a great difference in the tactile sensation during implant site preparation in different bone
densities. According to Misch, implant site preparation in D3 bone is similar to drilling into
compressed balsa wood, D4 bone is similar to drilling into a compressed Styrofoam or a light balsa
wood. It is difficult to feel the difference between D3 and D4 bone. In D4 bone, the drill is inserted
to the full depth without the drill rotating. This means that the drill acts as a bone condenser and
not as a bone drill. D3 bone is very easy to prepare, but requires the drill to rotate with slight
pressure to the final position. Using this tactile method for bone density estimation can lead to
modifying the surgical protocol and treatment plan according to the resulting tactile sense during
implant site preparation.

Evaluation of implant stability (IS)

Primary stability was always considered a fundamental prerequisite to acquiring
osseointegration and it is now even more important, whenever clinicians want to use immediate
loading protocols. Implant stability as an indirect indication of osseointegration, is a measure of
the clinical immobility of an implant [555]. It is achieved at two levels: primary mechanical and
secondary biological stability. Biologically, quantifying stability allows the clinician to determine
whether an implant should be immediately loaded or submerged for a period of healing. Several
factors influence primary implant stability: a) The stiffness of the implant bone interface, b) the
stiffness of the bone itself, and c) the stiffness of the implant components (geometry, surface
micromorphology, material composition and tightness).
To enhance bone density and with it implant stability, different surgical techniques have
been described such as: underdimensioned drilling, step-back, and lateral condensation. Primary
implant stability depends on two factors: the shearing strength of the bone and the thread geometry.
Primary stability is a mechanical property related to local bone quality and volume, implant design,
and surgical technique. Secondary stability is biological stability through bone regeneration and
remodeling. Table 3 presents the constant and the variable factors that influence implant stability.

~ 142 ~
 Table 3: Factors that influence implant stability
Constants Variables
Implant length Bone quality
Implant diameter Bone quantity
Implant geometry (implant system)
Implant surface characteristics
Implant position
Abutment length

Merheb et al. found a very good correlation between primary stability and cortical
thickness, which is in agreement with the conclusion of several clinical papers on the
preponderance of cortical thickness as a determining factor in implant dentistry [555] . Primary
implant stability seems to be mainly influenced by bone-related factors, namely bone density of
the spongious part of the osteotomy site and the cortical plate’s thickness. Among the different
bone and implant related factors, the preoperative evaluation of the cortical thickness and the HU
of the spongious part of the osteotomy site is considered to be the most reliable for predicting
implant stability. In this regard, they could serve as a guide for surgeon to evaluate potential
osteotomy sites and selec the regions of highest primary stability. Rodrigo et al. stated that
attaining primary implant stability is not a prerequisite for osseointegration and long-term implant
survival [556]. Cehreli et al. concluded that conventional placement leads to higher implant
stability than the combination of drilling and the osteotome technique [557].

Evaluation of primary stability via the tapping test

The “tapping” test (percussion of the implant with a mirror handle) is the simplest
noninvasive test method of primary stability. It only allows the detection of mobile or poorly
osseointegrated implants. According to Coutant et al. [558], primary stability in a conical implant
with a double-lead thread design seems to be bone density-dependent, regardless of the anatomical
location. For nearly parallel-wall implants with a classical thread design, the primary stability
seems to be anatomical dependent. Diameter and length of the implants do not seem to influence
primary stability [559]. At the time of implant placement, implant stability is based solely on the
mechanical component. During the healing period, mechanical stability decreases, whereas
biologic stability increases [560]. More precisely, implant stability increases during healing only
in implants with low primary stability, whereas in implants with high primary stability, a decrease
in stability is observed [560]. In cases of a slow increase in biologic stability and a rapid decrease
in mechanical stability, a transient decrease in overall stability during healing occurs. This
phenomenom has been termed a “dip” (or “drop” or “gap”) in stability.

Evaluation of primary stability via insertion torque (IT)

Torque is the force expressed in Ncm needed to rotate a screw-shaped implant around a
predefined axis. Insertion torque (IT) measurement is a noninvasive clinical test method to gauge
implant stability which can provide valuable information about local bone densities during the
taping process, which correlate to bone-implant contact. A possible correlation between primary
stability and implant insertion torque has been suggested [561]. Researchers have attempted to

~ 143 ~
identify a minimum insertion torque value that would indicate adequate stability for loading by
using insertion torque values for quantifying primary implant stability. Implants placed with an
average insertion torque of higher than 35 Ncm are associated with success. The maximal insertion
torque is an indicator of primary stability. An increase of the insertion torque of 9.8 Ncm has been
shown to reduce the potential risk of implant loss by 20% [562]. Excessive tightening which can
create impression forces in the surrounding bone that may disturb the microcirculation and lead to
bone resorption should be avoided. We recommend using an average insertion torque ≥ 25 Ncm
as an indicator of primary stability in conjunction with underdimensioned implant bed preparation.
High insertion torque can be achieved due to the tapered implant design, the slightly wider implant
diameter and the absence of bone tapping. The documentation of insertion torque for scientific
purposes has been proposed by many different groups due to its indicative values. A threshold of
> 32 Ncm for a self-tapping implant designed for soft bone in the posterior maxilla has been
established [563]. However, an upper limit for primary stability has never been definitively
established. The insertion torque can be recorded during implant placement with the help of a
simple insertion ratchet torque driver with a fixture-mount attached to the implant at 25 Ncm, or
by using a torque gauge incorporated within the drilling unit, which is used to measure implant
torque in Ncm. High implant insertion torque produces compression and distortion of the peri-
implant bone (Fig 3.41a,b).

a b
Fig 3.41a: Implant incertion with torque driver Fig 3.41b: Torque driver

A speed of 15 RPM with a torque of 25 Ncm should be used for insertion of implants. The
machine-driver insertion should be discontinued prior to the last three threads, followed by a
manual final placement using a ratchet with a torque driver. It should be noted that no gold standard
for the evaluation of implant stability exists which can be used for comparison.

Evaluation of implant stability using periotest device

The periotest is a unit to assess the osseointegration of dental implants (Fig 3.43a). The
unit indicates the damping characteristic of the bone surrounding the implants, and indirectly
measures implant mobility as an optical and acoustical periotest-value (PTV). The periotest has
been thoroughly studied and is considered a reliable method to determine stability. The periotest
instrument was originally designed to objectively measure movement of a tooth within the
periodontal ligament. The manufacturer has suggested the following ranges for a natural tooth:
firm = -8 to +9; palpable mobility = 10 to 19; visible mobility = 20 to 29; and mobility in response
to tongue and lip pressure = 30 to 50. The periotest uses an electromagnetically driven and
electronically controlled tapping metallic rod in a headpiece. Response to a striking or "barking"

~ 144 ~
is measured by a small accelerometer incorporated into the head. Contact time between the test
object and the tapping rod is measured on the time axis as a signal for analysis. The signals are
then converted to a unique value called the Periotest value (PTV), which depends on the damping
characteristics of tissues surrounding the implants [564-566]. The Periotest uses a transient
impulse as an excitation force and analysis is conducted on the time axis. The dynamic range used
for measuring implant mobility is very limited. The Periotest measurement is made in a mid buccal
direction and during measurement the periotest hand piece should always held perpendicular to
the tooth axis (Fig 3.42b). Long-term data on Periotest have shown that it is an objective clinical
measurement of bone implant anchorage stability [555, 562, 564].

a b
Fig. 3.42a: Periotest® S device Medizintechnik Gulden, Fig. 3.42b: The Periotest measurement is made in a mid buccal
Germany. direction and during measurement, the periotest hand piece
should always be held perpendicular to the tooth axis,

Despite a wide variation in host factors such as bone density, normal PTV of an
osseointegration implant falls in a relatively narrow zone (- 5 to +5) within a wide scale (-8 to
+50). The measurements should be repeated until the same value is recorded twice and then this
measurement is taken as the PTV for the implant. The implant stability should be measured with
the periotest at the abutment close to the implant edge when the prostheses are removed for
cleaning or for checking of the abutment screws during the follow-up examinations. The Periotest
value (PTV) is given in form of an implant stability degree to allow comparison in the follow-up
examination and between different study groups. The sensitivity of the periotest instrument has
been defined as 90%, and the specificity has been defined as 95%.

Meaning of the Periotest values

Periotest values range from -8 to +50. An osseointegrated implant falls in a relatively narrow zone
(-5 to +5). Smaller PTVs show greater stability damping effects. The indicated PTV provides the
following information:
 A negative PTV of less than 0 is generally good, meaning that the implant is well
osseointegrated.

 A PTV of 0 to +9 indicates that a clinical examination is necessary (the values measured

in the posterior maxilla are generally higher than in other jaw regions).
 PTV≥ +10 is an indicator that the implant is not sufficiently osseointegrated.
 A PTV of -5 and lower indicates implant stability sufficient to allow loading.

~ 145 ~
Usually, the values decrease in the first year by 1 to 2 PTV (ossification of the surrounding bone)
if the PTV gets worse in comparison with the initial value (deviation of the device +/- 1) the reasons
could be destabilization of the implant, loosening of a screw, overloading, or infection.

RFA and insertion torque represent two different features of primary stability, the first indicating
the resistance to bending load, with the later indicating the resistance to shear forces [567]. A PTV
of greater than 5 at stage II surgery is highly predictive of an implant that will not be successful
one year after occlusal loading. Implants may not be osseointegrated but are not clinically mobile.
The manufacturer of the Periotest instrument considered this situation to be possible in the PTV
range of +4 to +9. Clinical studies have suggested that PTVs of 5 or greater indicate a potential
problem and lack of osseointegration [568]. Olive and Aparicio [568] reported that periotest
measurements taken after stage II surgery can be very useful clinical parameter to identify implants
that are clinicaly immobile but not stable enough for clinical loading. They speculate that leaving
such implant temporarily unloaded or submerged could allow the formation of a mature bone-
implant interface for later use. Periotest values may be susceptible to changes in the direction of
the force applied to the implant components. Periotest values may vary depending on the quality
of the bone (type 1 to 4).

Evaluation of implant stability using an Osstell device (implant stability quotient ISQ)
More than 20 years ago, two scientists shared the frustration of not being able to determine
osseointegration accurately, objectively, and consistently, beyond their own dexterity and tactile
skills. The concept of resonance frequency analysis (RFA) was developed and formed in 1999 in
Gothenburg Sweden. Today, major clinicians all over the world use the Osstell device ISQ in
addition to the Periotest device. RFA implies a resonance frequency measurement of a transducer
connected to the implant fixture or abutment. The value, implant stability quotient (ISQ), reflects
the stability of the implant as a function of interface stiffness and is influenced by the distance
from the transducer to the first contact of supportive marginal bone. This means that bone support
can be also assessed in buccal-lingual aspects. RFA is sensitive to changes in the marginal bone
level and is usually used as a complement to intraoral radiographs.
Osseointegration is a dynamic and biological process that should be monitored to develop
predictable loading protocols customized for each of the implant patients. Torque is a one-time,
static measurement of mechanical stability, shear forces and friction. Through monitoring
osseointegration, the practitioner will often be able to reduce treatment time and avoid premature
loading. In addition, the practitioner will also be able to treat risk patients in a more predictable
way.
The Osstell ISQ (Fig 3.44) aids in successfully treating risk patients and helps prevent early
loading.

~ 146 ~
 Fig 3.44: The Osstell ISQ Device

The Osstell ISQ is a complete diagnostic system for determining implant stability and
osseointegration. It provides the treating dentist with the accurate, consistent and reliable stability
measurements needed to make informed decisions about which surgical and prosthetic protocols
to use. As part of a quality assurance system, it also makes it easier to explain treatment planning
to both patients and colleagues. ISQ at placement appears to be more predictive of implant loss
than torque measurement. In contrast, the EAO consensus conference stated that ”the lack of
normative values and the ranges of reported values for stable implants and those with increased
potential to fail indicate that there is currently no justification for routine clinical use of PTVs and
RFA” [569].

The ISQ Scale – a global standard

ISQS (implant stability quotient scale) is a clinically useful measurement scale (from 1-100 ISQ)
for use with the RFA (resonance frequency analysis) method of determining implant stability and
osseointegration. The ISQ scale correlates perfectly with micromotion with a higher ISQ score
corresponding to a more stable implant (Fig 3.45). ISQ measurements can be used as an additional
parameter for diagnosing implant stability and decision-making during implant treatment and
follow-up. The green zone is the high stability implant zone with primary ISQ values from about
70 and above. The red zone indicates low stability implants with an ISQ value below about 55.
The yellow zone represents medium stability implants with an ISQ from 55 to 70.

~ 147 ~
 Fig 3.45: The ISQ scale makes it possible to establish a standard clinical range
of 1-100.

The Osstell ISQ instrument stimulates a “SmartPeg” mounted on the implant, by emitting
magnetic pulses. These cause the SmartPeg to resonate at certain frequencies depending on the
stability of the implant. The ISQ system is a wireless non-invasive and completely objective
technique. The SmartPegs have been calibrated in such a way that they all show comparable values
for the same degree of stability. If the ISQ value at day to load is < 65, an additional healing period
is recommended. The ISQ value is measured again three weeks later or until the required level is
reached. This approach is practical and well understood by patients. Buser proposed at the Osstell
Scientific Symposium of the EAO 2010 a threshold ≥ 70 ISQ for single teeth and early loading,
otherwise an additional wait period of three weeks is reccomended. One-stage placement of
implants with ISQ values greater than 66 can be performed. Implants with ISQ values of less than
or equal to 66 should be placed using the two-stage protocol, which shows a higher survival rate.
The computed ISQ = 66 cut-off value used to select between one-stage and two-stage placement
has been validated [570]. Early loading of implants with ISQ values of greater than 64 can be
performed. Implants with ISQ values of less than 64 should utilize traditional loading, which
shows a higher survival rate. The computed ISQ = 64 cut-off value used to select between early
and traditional loading has been validated in some studies [570]. Higher ISQ values at
osseointegration correlate with higher survival rates.
RFA measurements have confirmed that firm stability is achieved at implant placement
with a mean ISQ value of 67, which is regarded as a high degree of stability and even considered
as sufficient for immediate loading [571-573]. The technique measures lateral stability and is
sensitive to the density of the bone at the marginal portion of the implant. According Friberg and
colleagues [574], the higher results found in the grafted sites could be explained by the nature of
RFA technique, where the crestal third of the implant site seems to be the most important for
determining the ISQ values at least in machined parallel-walled implants. Degidi and colleagues
[575] reported a statistically significant positive correlation between RFA values and implant
length and diameter. After 6 to 12 months of observation, this correlation is not significant
anymore. Huwiler and colleagues [576] studied the RFA changes during the early phase of
osseointegration. The authors reported a progressive decrease of the mean ISQ value to a minimum
after 3 to 4 weeks followed by a subsequent progressive increase during the following 8 to 9 weeks
of observation.

~ 148 ~
 Differences in ISQ values should not be misinterpreted as differences in stability or degree
of osseointegration. One study on immediate loading [577] found that the majority of failed
implants were located in the posterior maxilla and all exhibited below the desired ISQ values.
Based on the preliminary data of Glauser and colleagues [578], immediate loading should be
possible where the ISQ is greater than 60 at implant placement. Type I bone has the highest primary
stability but shows the highest decrease in ISQ in the first 30 days [579]. The implant modulation
of the bone-implant stability “set point” depends upon bone quality, implant location, thread
design, and surgical technique [579]. Implants placed with high levels of primary stability do not
reach the initial level of stability. However, implants in bones with lower levels of primary stability
can return to or exceed the initial level of stability [579]. Implants with an initial ISQ <60 have
shown an increase of stability while implants with an initial ISQ >60 have had their stability
decrease for 8 weeks before stabilizing or increasing to ther initial value [580]. It seems that the
initial decrease in commonly reported ISQ values from implants installed with good primary
stability may be attributed to an increase remodeling of the surrounding bone. Berglundh et al.
[581] reported that by increasing the press fit of an implant, the resulting initial bone remodeling
increases compared with an implant with a large contact-free surface, which, in turn may have a
shorter osseointegration phase.
The Osstell ISQ is especially valuable when treating higher risk patients and implants at
risk of failure due to poor integration. Osstell gives an early warning, as a decreased ISQ value, of
osseointegration isn’t progressing as expected. It can help avoid the cost of implant failure or
redoing a crown due to premature loading.
If the initial mechanical stability is high enough, a one-stage approach is often used
together with immediate or early loading. Measuring again before the final restoration, and
comparing that value to the baseline value taken at placement, makes the decision whether to
proceed quick and easy.

Micromotion
In past orthopedic literature there was a common belief that implant failure was due to bone
resorption on the interface, caused by excessive loading [582]. It has been demonstrated that
resorption is caused by implant micromotion, even when a minimum load is applied [582].
The basic working hypothesis of the “strain” theory is that tissue cannot be produced under
strain conditions that exceed the elongation of rupture of the given tissue element, such as cells
[582]. It has been hypothesized that the fulcrum of the implant oscillation is the bone crest.
According to Trisi et al. [171], increasing the peak insertion torque can reduce the extent of
micromotion between the implant and the bone when submitted to lateral forces in vitro. Primary
stability is not only dependant on insertion torque and host bone density but also on implant
geometry and surface features. For this reason, different implants can show different micromotion
when placed in similar bone densities and using similar torques. Therefore, further studies are
necessary to show which factors affect the micromotion of different implants.
Avoiding micromotion by correctly assessing implant stability and osseointegration is important
in predicting treatment outcomes. The Osstell ISQ accurately and objectively assesses implant
stability and also describes the relationship between ISQ and other factors such as micromobility
and BIC. The Osstell ISQ can be integrated with other implant diagnostics to provide the best
quality treatment plans and care for patients. Results show a high dependence between the
observed micromotion and the ISQ values, indicating that micromotion decreases with increasing
ISQ values [583]. Even though the instruments used to measure the implant osseointegration have

~ 149 ~
been widely mentioned in the literature, they have never been used for directly measuring implant
micromotion, which represents the only direct measurement of the initial stability. Therefore, they
must be considered as approximate measurements.

Evaluation of secondary (biologic) stability via reverse torque test (RTT)

The reverse torque test (RTT) developed by Johansson and Albrektsson [584] measures
the "critical" torque threshold where bone-implant contact (BIC) is destroyed. This indirectly
provides information on the degree of BIC in a given implant. After implant exposure, reverse
torque is applied to the implant-mount screw. If the implant rotates, it is assumed that the insertion
torque is lower than initially proposed. Removal torque value (RTV) as an indirect measurement
of BIC or clinical osseointegration was reported to range from 45 to 48 Ncm [585]. An RTV of
greater than 20 Ncm may be acceptable as a criterion for a successful osseointegration. The
threshold RTV may be lower in type IV bone. Hence, an RTV of greater than 20 Ncm may result
in a shearing of the BIC interface and can lead to implant failure. RTV can only provide
information about whether there was a successful osseointegration or not. It cannot quantify degree
of osseointegration. To determine the implant stability (secondary stability) in the bone bed, RTT
should be measured at the time of second stage surgery with a hand torque wrench by unscrewing
the implants with 20 Ncm. If interfacial failure occurs, the implant is considered as failed.

~ 150 ~
 4. IMPLANT PLACEMENT IN THE ATROPHIED POSTERIOR MAXILLA
THROUGH LATERAL WINDOW SINUS FLOOR AUGMENTATION

Successful and predictable rehabilitation with osseointegrated implants has been reported
in sites with normal bone volume and density. Posterior maxillary bone atrophy in combination
with pneumatization of the sinus may result in inadequate pre-treatment bone height between the
alveolar ridge crest and the floor of the sinus [586,587,305]. When the pre-treatment bone height
is less than 10mm, conventional implant techniques may not provide adequate stabilization for
implants of standard diameter and length [587].
Several strategies have been promoted to restore the posterior maxilla and address the
deficiency of bone volume and poor bone quality to allow the placement of implants of more than
10mm in length. These strategies include maxillary sinus elevation surgery to increase the height
of bone available for implant placement [309,588-591], transcrestal sinus elevation with graft
material and simultaneous implant placement [489], onlay bone grafting, cortical split osteotomy
[310,314], horizontal osteotomy, and interpositional bone grafting [317,592-594].
During the past 35 years, sinus augmentation procedures have been developed with the aim
of increasing the local bone volume, in situations where the lack of bone volume is related to an
enlarged maxillary sinus. Sinus grafting aims to restore the resorbed posterior maxilla with dental
implant through the dynamic process of osseointegration as originally defined by Branemark et al.
[183] and revised by Schenk and Buser [595]. Introduced by Dr. Hilt Tatum in 1975 [596], the
sinus augmentation has gradually gained proponents over the years, and a consensus conference
on sinus grafts in 1996 organized by the academy of osseointegration found sinus grafting to be a
highly predictable and effective therapeutic modality [489]. The maxillary sinus graft procedure
is a well-established technique for increasing bone volume in preparation for implant placement.
When executed properly on the appropriate patient, this surgical procedure is one of the most
successful bone-grafting procedures performed today. Numerous studies of maxillary sinus
grafting, both prospective and retrospective, have repoted long-term success. This is remarkable
given the wide assortment of graft materials being used.
Among the variety of techniques that have been described, the three that are the most
widely used are:
1. The one-step lateral approach sinus elevation [354,597].
2. The two-step lateral approach sinus elevation [598,599].
3. The osteotome technique (crestal approach) [601,602].
The most commonly utilized method for sinus augmentation is the lateral approach
technique.
The one-stage (simultaneous) lateral antrostomy accomplishes sinus grafting and implant
placement in one appointment, which minimizes the cost and the number of surgical procedures
for the patient. The two-stage (delayed) lateral antrostomy involves grafting the sinus first,
allowing several months for graft maturation and followed by a second surgical procedure to place
the implants [590, 599]. These techniques are supplemented with bone graft materials, or their
substitutes, with the goal of providing space for and accelerating bone formation [608]. The
introduction of new graft materials (ie, allograft, xenograft and alloplastic materials) have provided
alternatives to autogenous bone which is considered as the gold standard.
The pretreatment bone height is frequently the primary predictor for determining the
technique used to modify and reduce the sinus cavity [93] In addition to host factors, surgical
experience, and clinical traditions [601,602]. The high survival rate of implants placed in

~ 151 ~
augmentation sinus has been extensively reported in systematic reviews [597,603]. Besides the
various techniques utilized for an SFE, there are many other variables that may alter the outcome
of this procedure such as: simultaneous or delayed implant placement, use of barrier membranes
(resorbable vs. non-resorbable) over the lateral window, the use of different grafting materials, and
the use of different implants with varying length, width, and surface characteristics. The outcome
of lateral wall sinus elevation surgery, as measured by implant survival in evidence-based reviews,
has been shown to be highly predictable [5917,604,605] (Fig 4.1- Fig 4.7).

a b
Fig 4.1a: Baseline panoramic radiograph showing bone loss at Fig 4.1b: Panoramic radiograph demonstrating the stable
teeth sites 26,27 with limited subantral bone height. implants in an augmented left sinus after 5 years of function.

a b
Fig 4.2a: Panoramic radiograph showing residual bone height of Fig 4.2b: Panoramic radiograph demonstrate four stable implants
5 mm at sites 15-18. in an augmented left sinus.

a b
Fig 4.3a: Baseline panoramic radiograph showing inadequate Fig 4.3b: Panoramic radiograph taken 15 years after sinus
residual bone height on the left side. augmentation and delayed implant placement – notice the stable
implants and the bone maintenance.

~ 152 ~
 a b
Fig 4.4a: Panoramic radiograph showing severe bone resorption Fig 4.4b: Panoramic radiograph 3 years post loading shows the
in the posterior segment of the maxilla. stable implants and graft.

a b
Fig 4.5a,b: Panoramic radiograph illustrates implants condition inserted in augmented sinuses after 15 years of function – notice the
stable marginal bone.

a b

c d

~ 153 ~
 e f
Fig 4.6a-f: Panoramic radiographs showing implants condition in augmented sinuses after several years of function – this surgery
has been shown to be highly predictable.

a b
Fig 4.7a: Panoramic radiograph demonstrating different Fig 4.7b: Panoramic radiograph post surgery showing different
subantral bone resorption on both sides of the maxilla. treatment modalities. On the right side, transcrestal sinus floor
elevation with grafting material and on the left side, lateral wall
sinus floor augmentation with delayed implant placement were
performed.

History of maxillary sinus grafting

Augmentation of the maxillary sinus was first introduced by Tatum at the annual meeting
of the Alabama Implant Study Group in 1977 and by Geiger and Pesch [606] and later on published
by Boyne & James [351] and Tatum Jr. [607]. The use of bone grafting of the maxillary sinus to
increase the bone volume for prosthodontic purposes was first proposed in the 1960s by Boyne
(US Navy Dental School Lectures to postgraduates, 1965-1968). Grafting of the maxillary sinus
was used at that time to increase the bone volume for subsequent maxillary posterior ridge
reduction for optimal prosthodontic interarch distance allowing the establishment of complete
mandibular and maxillary dentures. Some patients presenting for conventional complete maxillary
and mandibular prostheses had bulbous or enlarged tuberosities that made it impossible to
construct appropriate functional prostheses. Removal of bone from the maxillary tuberosity was
the obvious option. However, some of these patients presented with large, pneumatized sinuses
that bone removal would not achieve the necessary interarch accommodation. To resolve this
situation, sinus augmentation was undertaken. Three months later, the bone of the enlarged
tuberosity could be reduced without the risk of penetrating the sinus, which is now protected by
the additional grafted bone. This unique surgical treatment enabled many patients to have
conventional prostheses. In essence, the first sinus elevation bone graft procedure was undertaken
for placing a conventional denture.

~ 154 ~
 During the late 1970s, grafting of the maxillary sinus as described for conventional
prostheses was undertaken for patients who had large, pneumatized sinuses. This was in
preparation for blade implant placement to enable construction of fixed, semi fixed, or removable
prostheses for the posterior maxilla [603]. Autogenous particulate iliac bone was usually used as
the grafting material. In 1980, Boyne and James [351] published the first report detailing the
surgical technique and the results of three such cases. The same report also described successful
results for 11 additional cases of sinus grafting for the construction of conventional prostheses. In
the early 1970s, Tatum also began augmenting the posterior maxilla with onlay autogenous rib
bone to increase vertical bone for implant support [296,607]. He found that onlay grafts below the
existing alveolar crest would decrease the posterior interocclusal distance, and a very limited bone
height would be gained. Therefore, in 1974, Tatum developed a modified Caldwell-Luc procedure
for elevating the sinus membrane subantual augmentation [296,607]. Access to the sinus was
initially achieved through the crest of the ridge [351]. After modification of the surgical procedure,
access was accomplished through the lateral wall of the maxilla [351]. The crestal ridge of the
maxilla was infractured and used to elevate the maxillary sinus membrane. Autogenous bone was
then added in the previously occupied inferior third of the sinus. Six months later, implants were
inserted in the grafted bone. After an additional six months, the implants were then loaded with
the final prostheses.
In 1975, Tatum developed a lateral approach surgical technique that allowed the elevation
of the sinus membrane with bone graft and implant placement simultaneously. Ceramic implant
and a transmucosal post were used. The results with this technique were unpredictable because
ceramic implants were not adequately designed for this procedure. In 1980, Tatum expanded the
use of synthetic bone as substitution material through a lateral approach. Most of data published
in the 1980s, were based on very small sample sites. In 1981, Tatum developed a submerged
titanium implant for use in the posterior maxilla. The advantage of submerged healing together
with the use of titanium as a biomaterial along with an improved surgical technique and improved
biomechanics made this implant modality more predictable. The primary graft material for the
sinus graft was autologous bone [355].
In 1987 Misch developed a treatment concept for the posterior maxilla based on residual
bone between the alveolar crest and the sinus floor. In 1989, he expanded the treatment approach
to include the available bone width related to surgical approach and implant design [581]. In 1989,
Kent and Block presented a modified lateral maxillary wall infracture technique for sinus floor
elevation and simultaneous placement of hydroxyapatite-coated implants [608]. In 1997,
Daelemans et al. reported a success rate of 93.4%, similar to Misch, for the single-stage sinus
augmentation procedure using the corticocancellous iliac bone [609].
In 1999, Khoury reported on 216 sinus graft procedures in 216 patients [589]. The initial
bone height at the implant site was between 1 and 5 mm. the maxillary sinus was augmented with
block bone grafts harvested from the retromolar, ramus, or symphysis areas of the mandible. Peleg
et al. assessed the efficacy of performing a one-stage procedure in patients whose available
alveolar bone height in the posterior maxilla was between 3 and 5 mm prior to grafting [589].
Since then, modifications regarding surgical technique and the graft materials were proposed. A
variety of augmentation procedures, depending on the location and site of defect, have been
introduced to provide bone support necessary to permit placement of implants.
Entrance to the antrum was made from three anatomic sites:
 The classic superior position of the Caldwell-Luc opening, located just anterior to the
zygomatic buttress [610].

~ 155 ~
  A mid-maxillary position, between the level of the crest of the alveolar ridge and level of
the zygomatic buttress [314, 610].
 A low position along the anterior surface of maxilla, very near the level of the existing
alveolar ridge [310,314].
The third entrance site has become quite popular but it also poses a problem in cases of
infection, hematoma or sinus disease. The resulting necessary drainage in such a case tends to
produce an oroantral fistula. Thus, the midposition access and the high classic Caldwell luc
opening are the ones recommended by most oral and maxillofacial surgeon [314, 610]. Today,
most clinicians use a modified Caldwell-Luc approach which involves preparation of a buccal
window to gain access to the sinus cavity and then elevation of the Schneiderian membrane to
create a compartment for the augmentation material.
Various types of grafting materials have been successfully utilized for sinus augmentation
including, autologous bone, xenogeneic bone and composite grafts. All of these have been
associated with high success rates. Autogenous bone is considered the gold standard because of its
high biocompatibility, osteoinductive potential and good clinical outcome [68,354,611]. The
collection of enough autogenous bone tissue requires an extra surgical site for bone harvesting
which increases the risk of morbidity and discomfort. To minimize donor site morbidity without
losing the osteoinductive potential of autogenous bone, the use of bone substitutes in combination
with autogenous bone has been recommended [489, 611]. Several surgical techniques were
designed to enter the antrum, elevate the sinus membrane, and place a bone graft of one type or
another. Three major differences in technical approaches to the surgical procedure were reported:
 The technique used for the lateral wall antrostomy [314, 610]
 The amount of sinus membrane elevation [314]
 The type of graft material used [68,504, 610]
The most significant factor in the overall success of implants placed in grafted sinuses is the
physiologic bony sinus floor repair phenomena.

Indications for sinus augmentation

The main indication for maxillary sinus floor augmentation utilizing a lateral approach is
reduced residual bone height that does not allow standard implant placement or placement of
implants in combination with minor sinus floor elevation using the transcrestal approach.
In the posterior maxilla, adequate bone volume is often unavailable because of severe post
extraction alveolar crest resorption coupled with age-linked sinus pneumatization. Therefore, in
these situations, sinus floor grafting and the placement of implants in the reconstructed bone have
frequently been proposed as the best treatment option. This technique enables a greater volume of
augmentation material to be placed in the appropriate position and placed to maximum density,
because it allows a direct view of the sinus (Fig 4.8a,b – Fig 4.10a,b).
The surgical technique chosen may depend on the residual ridge bone height, the implant
length and the amount of bone grafting required. In the one step procedure, the maxillary sinus is
augmented and dental implants are placed simultaneously into the grafted site. Empirically, the
general consensus has been that one step procedure should be reserved for patients who have at
least 4mm of alveolar bone in the posterior maxilla to ensure implant stabilization and parallelism.
An approach of this type is considered if primary stability of the implant is attainable in the residual
subantral bone. Bone at least 4 to 5mm thick is necessary to sufficiently secure implant stability.
Primary stability is, however, influenced by several other factors as well. Bone density has a
significant role. It is considered insufficient if there is less than 4mm of available host bone to
~ 156 ~
mechanically obtain adequate primary stability, and thus the two step procedure has been
recommended in these patients.
Local sinus lifts are made to replace a premolar or a molar tooth. Patients are treated with
maxillary single-tooth implant supported restorations with simultaneous sinus augmentation if
their remaining teeth are intact, and the adjacent teeth show signs of periodontal bone resorption
precluding the restoration of fixed partial dentures. Surrounding dentition and the possibility of
reduced occlusal loading of the single implants in the augmented regions may represent a
protective factor for single-tooth implants in posterior regions and may be beneficial for the long-
term success of single-tooth implants placed with sinus augmentation. Different amounts of
residual bone before sinus-grafting procedures and, in particular, the bone resorption pattern of the
edentulous maxilla may considerably influence both the type of grafting procedure and the final
outcome of implants placed in the grafted areas.
The majority of publications suggest sinus floor elevation procedures (SFEPs) when the
residual bone between the crest and the maxillary sinus floor is <8-10mm and they do not
differentiate whether the insufficient bone height is related to sinus pneumatization or resorption
of the alveolar ridge. It has been demonstrated that atrophy of the edentulous maxilla develops
tridimensionally, and it is not just dependant on sinus pneumatization [612]. Therefore, an
insufficient bone height may also be related to a vertical resorption of the alveolar ridge or a
combination of both factors. In the first situation, an SFEP may be indicated, whereas in the second
one (vertical atrophy) it may be that the sinus does not need to be grafted. Instead, a vertical
reconstruction to recreate an adequate interarch distance may be the treatment of choice. Moreover,
bone resorption of the edentulous ridge may lead to a horizontal discrepancy between the maxilla
and the mandible. If a sinus floor elevation alone is performed, implants will be placed in a palatal
position, with a less than ideal prosthetic rehabilitation. Therefore, the atrophic posterior maxilla
should be elevated and classified not only as far as the residual bone height and width is concerned.
Consequently, sinus floor elevation may represent only a part of the reconstruction necessary to
re-establish adequate bone volumes and intermaxillary relationships to optimize implant
placement and final prosthetic results from a functional and esthetic point of view.

a b
Fig 4.8a: Clinical view of the lateral window. Fig 4.8b: Elevated sinus membrane with grafting materials.

~ 157 ~
 a b
Fig 4.9a: Clinical view of the trapped door lateral window. Fig 4.9b: Grafted sinus

a b
Fig 4.10a: Clinical view of lateral wall sinus floor Fig 4.10b: Grafted sinus with vertical GBR.
augmentation with vertical reconstruction to recreate an
adequate interarch distance.

It must be stressed that the success rates of the reconstruction procedures and implant
placed in the grafted areas differ according to the class of atrophy, showing lower success rates in
classes presenting with more severe atrophy. The condition of native bone in the atrophic maxilla
is likely to influence the condition of the adjacent grafted bone. Three meta-analyses evaluated the
implant survival rate of reports in the literature and they varied from 61.2% to 100 % for the lateral
window technique, with an average of 91.8% [597,6]. In LSFEs in which the lateral window was
covered with a barrier membrane, the implant survival was 93.6% and in the cases without a
membrane it was 88.7%. The membrane raises the implant survival by 4.9% according to the meta-
analysis. The second meta-analysis showed similar implant survival rates, with an overall implant
survival rate of more than 92% [613]. A better survival rate was observed for the use of bone
substitute material (95.8%) rather than autogenous bone (87.7%). The data presented by Tetsch et
al. [614] shows a survival rate of 97.4% for bovine bone substitute material, which agrees with the
findings of Del Fabbro et al. [613].
However, the importance of RBH is not exclusively related to implant stability and implant
success/survival rates. The success of any bone grafting procedure, including maxillary sinus
augmentation, relies of the provision of adequate angiogenesis and migration of osteogenic cells
from native bone [615]. Therefore, it has been suggested that residual bone, as a foundational
source of cells and blood supply, may play an important role in the consolidation and maturation
of maxillary sinus graft. Tadjdoedin et al. [616] showed that bone growth primarily originates from
the preexisting native bone surfaces of the maxillary sinus, particularly from the residual alveolar
bone. This concept has been recently confirmed by Busenlechner et al. [615], who demonstrated

~ 158 ~
that bone formation is significantly higher in the interface of native bone with different grafting
materials, than in deeper areas. Del Fabbro et al. [613] showed that residual bone crestal height is
one of most critical factors influencing implant survival rate (Fig 4.11a-d).

a b

c d
Fig 4.11a-d: Panoramic radiographs showing different subantral bone heights all indicating the need of sinus floor augmentation
surgery. It is noteworthy that residual bone is the foundational source of cells and blood supply and may play an important role in
the consolidation and maturation of maxillary sinus graft.

Contraindications for sinus augmentation

Since the maxilla comprises a variety of anatomic structures, including the maxillary sinus,
lateral nasal wall, pterygoid plates, associated vasculature, and teeth, understanding these
structures and their functions is a prerequisite for successful sinus floor augmentation [617]. A
properly functioning maxillary sinus depends on a delicate balance between mucus production,
transport by ciliated epithelium, sinus ventilation, and sustainable drainage through the ostium. In
addition, there are communicating ethmoid and frontal sinuses that affect the maxillary sinus if
they are unhealthy or chronically inflamed. These conditions can arise unilaterally or bilaterally
and any factor interfering with one of these functions will compromise maxillary sinus health. A
grafting procedure generally does not interfere with sinus function when performed on a healthy
sinus [376,510,617-621]. However, when performed on an unhealthy sinus, the same procedure
will contribute to fluid stagnation and bacterial overgrowth, leading to an exacerbated sinusitis.
It is important to understand maxillary sinus function and how it is affected by the sinus
augmentation procedure. There are limits to this treatment modality. There are several
contraindications for SFE, which include any impairment of the maxillary sinus drainage pathways
(e.g., septal deviation, paradoxical bending of the middle turbinate, and concha bullosa),
inflammatory conditions (e.g., acute viral or bacterial sinusitis), sinus polyposis, foreign bodies,

~ 159 ~
oroantral fistula, or benign nasosinus neoplasms that impair the maxillary drainage pathways
[607].
Implant treatment and augmentation procedures in the posterior maxilla are contraindicated
in full-dose irradiated patients, and i.v. administration of bisphosphonate. Medical and surgical
risk factors should always be addressed before a decision is made to proceed with surgery. Risks
and benefits are important and should be considered and discussed with the patient.
Contraindications should be carefully considered to avoid possible complications. Patients have to
meet the following requirements of a strict selection protocol (Table 3).

Table 3: Criteria Used for Patient Selection

Indications

Presence of at least 1 mm residual bone height (RBH)

Good general health and patients with controlled medical conditions
Stable mental health condition

Willingness to provide signed informed consent

Contraindications

Uncontrolled diabetes
Evidence of sinus pathology e.g., chronic or acute sinusitis, cysts, tumors
Presence of immunodeficiency
Use of immunosuppressive
Use of bisphosphonate
Radiation therapy in head and neck included the maxilla
Chemotherapy in the 12-month period prior to proposed therapy
Heavy smokers more than 20 cigarettes/day

Diagnosis and treatment planning

Following a thorough review of medical histories, patients are considered suitable or not
suitable to receive augmentation therapy. Initially, each patient receives a comprehensive dental
and periodontal examination, including probing depth, recession, clinical attachment level,
bleeding on probing, tooth mobility, furcation involvement, and plaque scores, and radiographic
evidence of alveolar bone loss. Stone models should be obtained from upper and lower alginate
impressions and the casts should be mounted on a semi-adjustable articulator. Cheek-bite
registration, diagnostic wax-ups, and surgical templates should also be prepared.
A complete examination of oral hard and soft tissues should be carried out for each patient
prior to the formulation of an overall treatment plan. Each candidate should undergo a radiographic
examination, including periapical radiographs, panoramic and computed tomography (CT) scans
or cone-beam computed tomography (CBCT) scans. To obtain the average residual alveolar bone
height, three sagittal cuts should be selected from the mid portion of the sinus from the CT-scans
of the patients. One week prior to surgery, smokers should reduce their cigarette consumption 2 to
5 cigarettes per day. They are required to stop smoking completely one day before the surgery.

~ 160 ~
Treatment planned for sinus augmentation surgery should be free of contraindications. Following
the detailed examination including all the radiographs, the final treatment plan should be based on
the best scientific evidence available.

Importance of ENT assessment in stratifying candidates for sinus floor elevation

Anatomical relationships exist between the maxillary floor and the overlaying maxillary
sinus. In addition, surgical procedures can lead to transient inflammatory reactions. Therefore, the
possibility of post-augmentation infection sequelae should be considered. In particular, sinus floor
elevation may impair physiological maxillary drainage into the middle meatus by inducing
transient inflammatory periosteal swelling or other mechanisms predisposing to acute maxillary
sinusitis. It is important to note that “sinus compliance” depends on the sinus’s baseline
anatomical-physiological condition. In general, the better the starting condition, the lower the risk
of complications.
A medical history questionnaire should be taken determining symptoms indicative of a
probable sinus disease such as impaired nose breathing, consistent postnasal drip (retronasal
secretion), or swelling of the eyelids. Clinical examination should consist of visual inspection of
the nose to evaluate position of the vomer and possible swelling of the middle and inferior conchae.
Pathological findings suggestive of sinus infection such as secretion from the nasal sinus, mucosal
swelling, and increased vascularization of the infundibulum mucosa have to be examined and the
patient should be referred to an ENT specialist. The most frequent complication is maxillary
sinusitis, which has been reported in up to 27% of the cases [584]. For this reason, it is
recommended that candidates for maxillary sinus floor elevation with any radiological or
anamnestic evidence suggesting impaired maxillary sinus conditions undergo an ENT evaluation
that may include nasal endoscopy and, possibly, CT of the maxillo-facial complex covering the
upper dental arch, the maxillary sinus in toto and region of the ostiomeatal complex region [607].
Patients judged as potentially reversible contraindication (PREC) caries should be treated
pharmacologically or surgically before the sinus floor elevation to re-establish the physiological
maxillary drainage and ventilation, and reduce the risk of post-lifting maxillary sinusitis, which
may spread the infection to the noble structures.
As previously stated, any surgical treatment of the maxillary sinus activates cellular
inflammatory mediators and promotes transient sinusitis [607]. This occurs because the traumatic
lifting of Schneider’s membrane may temporarily inhibit ciliary activity [622], thus predisposing
the area to an altered mucosal composition and bacterial infection [586]. However, it is well known
that sinus mucosa recovers well after surgery, and previous studies have shown that the maxillary
mucosa can promptly return to homeostasis after sinus floor elevation, especially if sinus drainage
is good [623]. In unfavorable situations, post-lifting maxillary homeostasis cannot occur, which
leads to bacterial sinusitis. The preoperative detection, and, whenever possible, correction, of all
the conditions impairing maxillary ventilation and clearance are necessary in reducing the risk of
sinus floor elevation-related morbidity. This means that a preoperative ENT assessment is very
important for stratifying candidates for sinus floor elevation.
Patients who have previously undergone dental treatments deserve a particularly careful
elevation to exclude a possible silent maxillary sinusitis of dental origin, which has to be
completely resolved before performing sinus floor elevation. Common anatomical alterations,
such as mild septal deviation or the presence of small concha bullosae or paradoxical middle
turbinates not associated with history or evidence of sinus disease, should not be considered ENT

~ 161 ~
contraindications to sinus floor elevation and thus do not require any pre-lifting surgical correction
(Fig 4.12, Fig 4.13).

Fig 4.12: A CT-scan demonstrates a concha bullosa. Fig 4.13: Polyposis or mases obstructing the medio-meatal
region.

In such cases, particular attention should be paid to maximize the sinus compliance
properly treating any possibly associated naso-sinusal minor disease. Similarly allergic rhinitis and
non-allergic nasal hyper-reactivity without chronic sinusitis are not contraindication per se,
although patients with these conditions should be prepared with topical nasal steroids and
irrigations. Sinus floor elevation should be avoided during the seasonal exacerbations of allergic
rhinitis to reduce ostial edema and improve sino-nasal drainage [622]. The presence of an antral
cyst on the sinus floor is also not considered a PREC. However, if judged large enough to obstruct
the natural ostium of the maxillary sinus when lifted with the sinus floor, we advised the oral
surgeon to evacuate it, using a fine needle, before detaching the schneider’s membrane through
the vestibular window (Fig 4.14a,b , Fig 4.15a-c).

a b
Fig 4.14a: Clinical view of evacuated antral cyst. Fig 4.14b: Evacuated fluid of an antral cyst.

~ 162 ~
 a b
Fig 4.15 a: Healthy symmetric bilateral sinuses. Fig 4.15 b: Foreign body in the left sinus compromising the
osteom drainage.

Fig 4.14 c: The following sinus abnormalities were

identified: 1) a large pneumatized bulla ethmoidalis; 2)
stenosis of the ethmoid infundibulum due to edema of the
mucosa; and 3) a basal maxillary sinus cyst. Note also the
c edema of the maxillary sinus mucosa on the right side.

Appraisal of needed bone volume

Deatiled knowledge of bone volume needed prior to augmentation surgery is needed to
minimize the extent of the surgical procedure, to reduce the potential for complications and to
reduce costs and expenses.
Since 1993, various software tools that enable pre-implant planning and perform volume
measurements have been developed, combining CT images with computer design. However,
studies found in the literature such as those published by Uchida et al. [624] or more recently by
Krennmair et al. [625], do not rely on these software tools to measure the volume of bone graft
needed for maxillary sinus lifting. Recently, improved programs have emerged that have been
designed for pre-implant diagnostic evaluation, to be used in pre-operative planning, offering new
and better possibilities. During preoperative evaluation, the use of these diagnostic tools can help
in calculating the necessary volume for the graft thus reduced surgical time, cost, and
complications. Grafted volumes may vary considerably in shape and volume due to
repneumatization of the maxillary sinuses (Fig 4.16a,b).

~ 163 ~
 a b
Fig 4.16a: Apical bone reshaping after Fig 4.16b: Bilaterally sinus floor augmentation, left lateral wall sinus floor
simultaneous sinus floor augmentation and right transcrestal sinus floor elevation.
augmentation.

For that reason, precise determination of the behavior of the augmented bone is one of the
most important factors for successful implant treatment, as loss of graft height and width might
affect the long-term success of implants inserted into the grafted maxilla. The expected behavior
of the planned augmentation should be considered in the appraisal of needed volume (Fig 4.17a,b).

Fig 4.17a: Panoramic radiograph demonstrate apical bone loss Fig 4.17b: Panoramic radiograph demonstrates apical bone
and bone reshaping due to repneumatization. loss and bone reshaping due to repneumatization.

Conventional panoramic radiographs should be taken along with a dental CT from which
CT cross-sectional scans are prepared. The amount of bone needed to augment the sinus for placing
an implant of the desired length is calculated with the help of vertical reference lines, which are
superimposed on the scans.
The total height of the residual bone plus the amount of bone which is necessary to be
grafted for a 13mm-long implant calculated via the 15mm vertical reference line which includes a
2mm safety zone. In addition, 2mm of augmentation height are added when calculating the
augmentation volume in an attempt to compensate for the possibility of graft reduction. The
defined size calculated by all the 1mm cross sectional scans is done using the determined anterior-
posterior distance. This produces the overall volume which is necessary for augmentation. In
general, it is necessary to increase the bone volume of the antral floor by 3 to 5 cm3. Volume
calculation is also performed for planned sinus elevation procedures with adequate consideration
of residual alveolar ridge height (Fig 4.18).

~ 164 ~
 13mm

Fig 4.18: bone volume calculation

needed for sinus grafting is calculated
to include adequate consideration of
residual bone height plus the amount of
bone necessary for 13-mm long
implant.

Maxillary sinus floor augmentation by lateral access and simultaneous implant placement
It is generally acknowledged that the alveolar ridge should be at 4 to 5 mm in height to
effectively immobilize the implant and to ensure adequate implant stabilization and parallelism
during the period when the sinus bone graft is maturing. When residual bone height is less than 4
mm, a two-stage procedure with delayed implant placement is traditionally advocated.

Fig 4.19: Alveolar bone height of 4 to 5mm

can be seen in the areas requiring
augmentation with simultaneous implantation
in the CT-scan.

Empirically, for sinus floor augmentation and simultaneous implant placement, a minimum
of 5mm of residual crestal bone height has been recommended to achieve sufficient implant
stability [586]. However, 5 mm of residual crestal bone height as a relevant threshold for
simultaneous implant placement and sinus floor augmentation is controversial [626,627]. Residual
alveolar bone height (RBH) is a critical anatomical factor that should be carefully considered when
planning a maxillary sinus augmentation procedure. Given its direct influence on primary implant
stability, RBH is commonly used to determine the implant placement protocol of choice, either
simultaneous or delayed. Abundant and compact residual alveolar bone favors primary implant

~ 165 ~
stability. In the vast majority of maxillary sinus augmentation protocols, the cut-off value deciding
between simultaneous or delayed implant placements is in the range of 4 to 6 mm of RBH [628].
High implant survival rates have been extensively reported in challenging clinical scenarios, where
implant were simultaneously placed with <5mm of RBH [601,602,629,630] (Fig 4.20a-c). The
impact of RBH on implant stability and survival has been the subject of intense investigation
[166,631,632].

a b c
Fig 4.20a-c: unilateral atrophy of the maxilla augmented with simultaneous implant placement.

Appropriate spacing and angulation are critical for prosthetic restorability. However,
achieving these goals can be particularly challenging when minimal residual crestal bone is
available because mastication can cause the implants to move during the graft maturation period.
Initial axial and lateral implant stability can be achieved by meticulously condensing the
particulate graft material around the implant, thus optimizing the direct bone-to-implant contact
and increasing cellular density. The greater the cellular density of the transplanted osteocompetent
cells, the greater the potential for new bone formation [619]. Meticulous condensation will
eventually lead to the formation of type 2 or type 3 bone rather than the type 4 bone normally
found in the posterior maxilla (Fig 4.21a-j).

a b
Fig 4.21a: Bilaterally augmented sinus with implants and final Fig 4.21b: Unilateral augmented sinus with implants and final
restoration. restoration.

c d
Fig 4.21c: Bilaterally augmented sinus with delayed Fig 4.21d: Bilaterally augmented sinus 10 years after final
implantation in one stage procedure. restoration.

~ 166 ~
 e f
Fig 4.21e: Augmented left sinus with implants and final Fig 4.21f: Three implants in augmented right sinus after 7 years.
restoration.

g h
Fig 4.21g: Functional implants in augmented left sinus after 12 Fig 4.21h: Functional implants in augmented left sinus after 15
years years.

i j
Fig 4.21i: Bilaterally augmented sinus with delayed implants Fig 4.21j: Right sinus augmentation with implants in function
and connected abutments. after 8 years.

A study published by Peleg et al. in 1998 involving a limited number of patients

demonstrated the validity of a treatment protocol that combined simultaneous implant placement
with maxillary sinus augmentation in a one-stage procedure when the alveolar bone height was 1
to 2 mm [601]. Many studies demonstrated a high survival rate for simultaneous implant placement
with grafting of the maxillary sinus [109,601]. A large-scale prospective study with long-term
follow-up to evaluate simultaneous implant placement in different alveolar bone heights with the
same surgical technique, implant types, graft material, and surgeons has not been reported.
Achieving stable implants can be particularly challenging when minimal residual crestal bone is

~ 167 ~
available because mastication can cause the implants to move during the graft maturation period
(Fig 4.22a-h - Fig 4.26a-d).

a b
Fig 4.22a: Flap elevation – see the already placed implant. Fig 4.22b: Preparation of the lateral window.

c d
Fig 4.22c: Elevated membrane. Fig 4.22d: Implant site preparation.

e f
Fig 4.22e: Grafting the sinus with simultaneous implant Fig 4.22f: Implants in situ – notice the implants in partly grafted
placement. sinus.

~ 168 ~
 g h
Fig 4.22g: Additional grafting. Fig 4.22h: Wound closure.

a b
Fig 4.23a: Implant placement after membrane elevation. Fig 4.23b: The removed window was used to seal the perforated
membrane.

a b
Fig 4.24a: Clinical view of a complete antrostomy. Fig 4.24b: Clinical view of lateral wall sinus floor augmentation
with simultaneous implant placement. Implant placement in
region 16 was performed using a staged approach due to
inadequate primary stability.

~ 169 ~
 a b
Fig 4.25a: Panoramic view of CT scan showing healthy sinus Fig 4.25b: Flap elevation – note the radix 14.
and implant in site 15, RBH 3-5 mm.

c d
Fig 4.25c: extracted tooth 14 and immediate implant placement. Fig 4.25d: lateral window preparation.

e f
Fig 4.25e: Grafting the sinus with implant site preparation. Fig 4.25f: Implant placement.

g h
Fig 4.25g: Additional grafting of the sinus. Fig 4.25h: Membrane coverage.

~ 170 ~
 a b
Fig 4.26a: Flap elevation. Fig 4.26b: Prepared lateral window.

d
c
Fig 4.26c: Elevated membrane – notice the elevated trapped Fig 4.26d: Sinus augmentation with simultaneous implant
door with the attached sinus membrane. placement.

Maxillary sinus floor augmentation by lateral access and delayed implant placement
The two-stage (delayed) lateral antrostomy requires grafting the sinus first, then allowing
a period of 4 to 6 months for healing of the graft material before the implants are placed. This
delayed approach is recommended when the residual crestal bone height is less than 3 to 5mm and
primary stability cannot be assured [633]. Achieving initial implant stability and maintaining
parallelism are major concerns in implant placement especially when implants are placed in less
than 5 mm of bone.

Fig. 4.27: CT-slices demonstrate the residual bone height.

~ 171 ~
 a b
Fig 4.28a: Full thickness flap elevation. Fig 4.28b: Rectangular lateral window preparation.

c d
Fig 4.28c: Grafting the sinus with DBBM. Fig 4.28d: Collagen membrane coverage.

a b
Fig 4.29a,b: CT sacn showing the malposition of two implants.

c d
Fig 4.29c: Clinical view of two implants in malposition. Fig 4.29d: Removed implants.

~ 172 ~
 e f
Fig 4.29e: Clinical view of alveolar ridge after implant removal. Fig 4.29f: Preparation of lateral window.

g h
Fig 4.29g: grafting the sinus. Fig 4.29h: Membrane coverage.

a b
Fig 4.30a: Panoramic view of CT scandemonstrating the egg- Fig 4.30b: CT slices showing the extension of the antral cyst –
like antral cyst. note the healthy sinus.

c d
Fig 4.30c: Lateral window preparation. Fig 4.30d: Aspiration of antral cyst through the SM.

~ 173 ~
 e f
Fig 4.30e: Aspiration fluid of the antral cyst. Fig 4.30f: Note the perforated membrane.

g h
Fig 4.30g: perforation repair with collagen membrane. Fig 4.30h: Grafting the sinus.

i
j
Fig 4.30i: Collagen membrane coverage. Fig 4.30i: Wound closure.

a b
Fig 4.31a: Lateral window preparation after flap elevation. Fig 4.31b: Elevated membrane – notice the communication
between the window and the extraction site.

~ 174 ~
 c d
Fig 4.31c: Collagen membrane repair. Fig 4.31d: Grafting the sinus.

e f
Fig 4.31e: Membrane coverage. Fig 4.31f: Wound closure.

a b
Fig 4.32a: Lateral window preparation with membrane elevation Fig 4.32b: Grafting the sinus.
- note the extraction socket with the surrounding bone
destruction.

c d
Fig 4.32c: GBR of the extraction socket and the destructed area. Fig 4.32d: Collagen membrane coverage.

~ 175 ~
 According to the consensus conference held in 1996 on sinus lifting [489], when residual
bone height is between 1 and 3mm, a lateral approach involving bone grafting material and a two
step implant placement (also called staged SFE) is recommended whenever adequate primary
stability cannot be obtained. The implants should be placed following a healing time of 4 to 9
months following sinus augmentation. The Academy of Osseointegration Sinus Consensus
Conference Failure Analysis Section reported that simultaneous placement in the severely atrophic
maxilla (i.e., in less than 2mm of bone) is more prone to implant loss than a delayed technique
unless blocks of bone are used to stabilize the implants. Depending on the augmentation volume,
sinus anatomy, and grafting protocol, a waiting period of 3 to 4 months is appropriate in single
tooth gaps if the sinus anatomy is narrow and an autogenous bone graft in combination with bone
substitute is used for augmentation. A total of 6 months of graft consolidation is needed before
implant insertion, if an expanded "eggshell" sinus floor is augmented with bone substitute alone
(Fig 4.27- Fig 4.32).
This protocol has yielded a cumulative success rate from 91% to 100% in 9 to 46 months
follow up as reported by Tong et al. [633]. In 1990, Jensen et al. rehabilitated severely atrophic
maxillae using bilateral sinus bone grafting and delayed placement of dental implants four months
later [634]. Nine of the 36 implants placed in the grafted bone failed. Hallman et al performed 44
maxillary sinus elevations in 22 patients using particulate bone and cancellous marrow with
delayed implant placement [635]. Though the sinus floor was less than 3mm thick, a 90% implant
success rate was observed after five years of follow-up. In 2002, Hallman et al. evaluated the
survival rate of implants placed in delayed fashion into 30 maxillary sinuses augmented with a
mixture of 80% bovine hydroxyapatite and 20% autogenous bone mixed with fibrin glue [598].
The mean alveolar bone height was 3.8mm. After 6 months of primary healing, 108 implants were
placed and followed for one year. Implant survival rate was 90.8%. In 2004, Hallman and Nordin
retrospectively evaluated a mixture of bovine hydroxyapatite and fibrin glue as grafting material
using a delayed placement with nonsubmerged implants after graft consolidation [510]. A total of
71 maxillary sinuses were augmented and the grafts were allowed to consolidate for 8 months. A
total of 218 implants were placed, and a mean of 10 weeks of healing was allowed before loading.
In this study, there was a 94.5% implant survival rate after 20 months of occlusal function.
The primary disadvantage associated with the 2-stage procedure is the amount of time it
adds to the overall treatment. Another disadvantage relative to the 1-stage procedure is the
difficulty of assessing the amount and position of graft material that will be required for a future
implant. Implant angulation and position have been showed to be more predictable and ideal in a
staged approach, decreasing the need for angled abutments, which encourage nonaxial loading
(Fig 4.33- Fig 4.42).

a b
Fig 4.33a: Panoramic radiograph showing RBH prior to sinus Fig 4.33b: Augmented left sinus six months after sinus
augmentation. augmentation.

~ 176 ~
 Fig 4.33c: Implants placed in site 25,26,27 six months after
sinus augmentation.
c

a b
Fig 4.34a: Panoramic radiograph showing tooth 26 with a Fig 4.34b: Panoramic radiograph showing the augmented sinus.
periapical lesion.

c d
Fig 4.34c: CT slices showing the bone destruction due to Fig 4.34d: Panoramic radiograph showing the augmented sinus
periapical lesion 3 months after tooth extraction 26.

e f
Fig 4.34e: Flapless implant placement six months after sinus Fig 4.34f: One stage implant placement with healing cap.
augmentation.

~ 177 ~
 a b
Fig 4.35a: Clinical view of second stage surgery. Fig 4.35b: Implant placement 6 months after sinus
augmentation.

a b

Fig 4.36a: Panoramic radiograph obtained after teeth extraction Fig 4.36b: Panoramic radiograph showing augmented left sinus.
25,26,27.

c d
Fig 4.36c: Implant placement six months after sinus Fig 4.36d: Final restoration.
augmentaton.

a b
Fig 4.37a: Panoramic radiograph prior extraction and sinus Fig 4.37b: Panoramic radiograph after bilaterally sinus
augmentation. augmentation.

~ 178 ~
 Fig 4.37c: Implant placement six months after sinus
augmentation.
c

a b
Fig 4.38a: Preoperative radiograph. Fig 4.38b: Staged sinus augmentation with delayed implant
placement and final restoration.

a b
Fig 4.39a: Panoramic radiograph showing extracted tooth 26. Fig 4.39b: Augmented left sinus.

c d
Fig 4.39c: Implants in augmented sinus. Fig 4.39d: Final restoration.

~ 179 ~
 a b
Fig 4.40a: Preoperative radiograph. Fig 4.40b: Bilateral augmentation of maxillary sinuses – note
implant placed in site 14 through transcrestal sinus elevation.

Fig 4.40c: Staged sinus augmentation with delayed implant

c placement and final restoration.

a b
Fig 4.41a: Augmentation of the right sinus. Fig 4.41b: Implant placement six months after sinus
augmentation.

c d
Fig 4.41c: Bilateral augmentation of the maxillary sinus. Fig 4.41d: Implants placement six months after sinus
augmentation.

~ 180 ~
 a b
Fig 4.42a: Augmentation of the right maxillary sinus. Fig 4.42b: Implants placement six months after sinus
augmentation.

c
Fig 4.42c: Staged sinus augmentation with delayed implant
placement and final restoration.

Surgical approach and techniques

A detailed description of the surgical techniques used for lateral sinus floor elevation and
grafting procedure is presented here based on my knowledge and experience and those of several
other experienced clinicians.
Initially, certain anatomical structures such as the location of sinus floor septi, spines,
exostosis, arteries, lateral alveolar canal and the surgical entry site have to be identified. Patients
should then be given prophylactic antibiotic coverage. Patients should receive 1.5g oral
clavulanate-potentiated amoxicillin one hour before surgical procedure. Penicillin-allergic patients
should be given 450mg clindamycin. The antibiotics should be continued for 10 days postsurgery.
Immediately before surgery, patients must undergo a 3-minute mouth rinse with 0.2%
chlorhexidine gluconate. All patients must undergo this appropriate antibiotic prophylaxis and
analgesic anti-inflammatory therapy.
There are four choices of anesthesia for sinus surgery as well as implant placement surgery:
local anesthesia (LA) only, LA in conjunction with oral sedation, LA in conjunction with
intravenous (IV) sedation, or general anesthesia (GA).
After choosing an appropriate LA containing adrenalin for vasoconstriction, a crestal
incision slightly offset from the palatine level is made throughout the entire length of the
edentulous area. At the level of the proximal aspect of the tooth that mesially bordered the
edentulous area, an anterior releasing incision is made. Posteriorly, the releasing incision is located
in front of the tuberosity. A full thickness flap is reflected to expose the lateral wall of the sinus.
The mucoperiosteal flap is reflected superiorly to the level of the molar buttress to expose the

~ 181 ~
complete lateral wall of the maxilla. Elevation of the periosteum adjacent to the implant site is
minimized to preserve the blood supply to the alveolar crest. The periosteum is reflected superiorly
to the anticipated height of the lateral maxillary wall infracturing. The soft tissues overlaying the
cortical bone of the buccofacial wall of the maxillary sinuses are removed entirely to reveal the
bony surface in the region of interest. The buccofacial sinus wall has to be managed cautiously.
It is obligatory to estimate the thickness of the buccofacial wall of the maxillary sinus to
minimize the occurrence of a mucoperiosteal perforation during the antrostomy. Extra precautions
are required on thick buccofacial wall to keep the mucoperiosteum of the sinus wall intact. Care
should also be taken not to make the hinge (superior margin of the window) during the window
opening procedure deeper than the inferior margin, which may lead to a mucoperiosteum
perforation. To ensure that the outlined bone had been penetrated all around the osteotomy, it
should be tapped gently with a blunt instrument until movement is visible, creating a rectangular
window with rounded or elliptically shaped angles ensuring that the inferior border is at least 2 to
3mm superior to the sinus floor. The advantage of entering through the lateral antral septum is that
it protects the tissue integrity in the region of the implant [109]. With this combination of
augmentation and implant insertion, the possibilities for osseous implants can be expanded to
allow adequate treatment even under unfavorable circumstances.

Antrostomy techniques of the lateral wall

Certain anatomic factors determining the morphology of the antrostomy can be detected
preoperatively on CT scans. One anatomical factor that should be considered is the position and
the course of the vascular anastomosis between the posterior superior alveolar artery and the
infraorbital artery inside the buccal wall of the sinus. The handling of the lateral cortical plate,
which represents the lateral window of the sinus, varies with the surgical technique. Many
surgeons eliminate this plate using a bur to thin the cortical plate prior to elevating the sinus
membrane. Others use the infractured cortical plate as a superior limit to the window, leaving it
attached to the mucosa. Other surgeons remove the infractured cortical plate and replace it on the
lateral surface as a graft to cover the graft material used at the end of the procedure. It was
demonstrated that the lateral window will heal with the apposition of the bone without the use of
a cortical bone window graft [354]. In the presence of the septa with multiple sinus compartments,
surgeons prepare two or three separated windows to access the sinus. The surgical technique
applied can vary between patients i.e. the surgeon can perform a complete antrostomy or a
repositioning antrostomy.

Elevated antrostomy
A superior hinge or an infracturing “trap-door” technique is indicated when the thickness
of the lateral wall allows reflection < 2 mm. A maxillary sinus floor elevation is performed
according to Tatum's top hinge "trap door" technique [614] (Fig 4.43a,b). A curved bone
preparation with a round steel bur or a round diamond drill should be used to carefully cut through
the bone to the sinus membrane without perforating it. At the end of the curved preparation a
fracture line is made inferior to the infraorbital nerve. The buccal bone window is fractured into
the sinus cavity to form a roof for the graft. The elevated "trap door" is rotated inward and upward
along the upper horizontal axis into a horizontal position. The most frequently used technique is
the “trap-door technique” or in-fracturing of the cortical bony plate like a trap-door and using it as
the superior border of the sinus compartment leaving it attached to the underlying Schneiderian
membrane.
~ 182 ~
 a b
Fig 4.43a: The sinus window is outlined and infractured into the Fig 4.43b: The elevated trapped door is rotated inward and
sinus cavity using it as the superior border of the sinus upward into a horizontal position.
compartment.

c d
Fig 4.43c: Clinical view demonstrate the “trap door technique” Fig 4.43d: Clinical view demonstrate the infractured cortical
or infracturing technique. bony plate attached to the elevated sinus membrane.

e f
Fig 4.43e: The curved bone preparation with the outlined buccal Fig 4.43f: The elevated “trap door” is rotated medially and
bone window.. superiorly.

Complete antrostomy
The second surgical technique that we discuss is the preparation of an access hole by
removing the entire buccal bone plate before the elevation of the sinus membrane. Many surgeons
eliminate the lateral cortical plate totally through a curved bone preparation with a round steel bur
or a round diamond drill or by using piezosurgery, going carefully through the bone and taking
care not to tear the sinus membrane. When the sinus antrum is narrow, it will not be possible to

~ 183 ~
rotate the window inwards and upwards turning it into a horizontal position. In these situations, a
complete osteotomy technique (removal of the lateral bone window) should be used [636].
This antrostomy opening measures in average about 6mm in vertical dimension and 15mm
in the mesiodistal dimension depending on several parameters: size of the sinus, the latero-medial
angle, lateral wall thickness, septi, and other factors. The antrostomy is outlined with a number 5
or 6 round bur in a straight hand piece at 2000 rpm under copious external irrigation. Once the
access is delineated, the bur is used to continue outlining the osteotomy until a bluish hue is
observed all around the access windows, indicating the approaching underlying Schneiderian
membrane (Fig 4.44- Fig 4.46).
This technique is the most widely used. Some bone walls can be removed and utilized for
bone grafting and others are left as is, based on window size and configuration.

a b
Fig 4.44a: Panoramic radiograph showing pneumatized left Fig 4.44b: Flap elevation.
sinus combined with ridge resorption.

c d
Fig 4.44c: Lateral window preparation – complete antrostomy. Fig 4.44d: Grafting the sinus.

e Fig 4.44e: Membrane coverage.

~ 184 ~
 a b
Fig 4.45a: Flap elevation. Fig 4.45b: Rectangular lateral window preparation.

c d
Fig 4.45c: Grafting the sinus. Fig 4.45d: Collagen membrane coverage.

a b
Fig 4.46a: Papilla saving incision with releasing incisions. Fig 4.46b: Flap elevation.

c
c d
Fig 4.46c: Lateral window preparation. Fig 4.46d: Removal of the lateral bony window.

~ 185 ~
 e f
Fig 4.46e: Membrane elevation. Fig 4.46f: Grafting the sinus.

g h
Fig 4.46g: Grafting the sinus. Fig 4.46h: Membrane coverage.

Repositioning antrostomy
The repositioning antrostomy also called the outfracture osteotomy or “off the wall”
technique for sinus floor augmentation is indicated when a thick vestibular wall ≥2 mm or septa is
present in which a complete 360-degree osteotomy is performed. The lateral window bone segment
is totally separated from the sinus membrane. It is placed in normal saline during sinus grafting
and is replaced to its original position after grafting and implant placement (Fig 4.47-Fig 4.53).
The repositioning antrostomy sinus grafting technique is advantageous in the following
situations:
1. In cases with both height and width problems.
2. When the sinus septa resisting infracture of the bony window.
3. In situations when a thick lateral sinus wall is accompanied by intrabony bleeding.

a b
Fig 4.47a: Panoramic radiograph prior to sinus augmentation. Fig 4.47b: Panoramic view of CT prior to sinus augmentation.

~ 186 ~
 c d
Fig 4.47c: Lateral window preparation with piezosurgical saw. Fig 4.47d: Lateral bony window removal.

e f
Fig 4.47e: Clinical view of the course of the PSAA in the lateral Fig 4.47f: Removed lateral window – note the impression of the
wall (intrabony) and in the SM (intramembranous). artery.

g h
Fig 4.47g: Repositioned lateral window. Fig 4.47h: Panoramic radiograph immediatly after sinus
augmentation.

a b
Fig 4.48a: Repositioing of the lateral window preperation. Fig 4.48b: The removed lateral bony window is placed in normal
saline.

~ 187 ~
 c d
Fig 4.48c: SM is exposed after lateral window removal. Fig 4.48d Membrane elevation.

e f
Fig 4.48e: gafting the sinus. Fig 4.48f: Lateral bony window is repositioned.

a b
Fig 4.49a: Repositioning the lateral window preparation. Fig 4.49b: Removal of the bony lateral window.

c d
Fig 4.49c: Membrane elevation. Fig 4.49d: Elevated membrane.

~ 188 ~
 e f
Fig 4.49e: Grafting the sinus. Fig 4.49f: Lateral bony window is repositioned.

The creation of a pair of holes with a small diameter round bur should be performed just over
and below the inferior margin of the rectangle. This maneuver should allow the replacement of the
window in the right position and allow stabilization of a bony window at the end of the surgical
procedure with resorbable sutures if needed (Fig 4.50).

a b
Fig 4.50a: A rectangular bony window is outlined with Fig 4.50b: Removed repositioning lateral window.
piezoelectric saw according to the principles described for sinus
augmentation procedure, taking care to maintain the integrity of
the Schneiderian membrane. Two holes just over and below the
inferior margin of the rectangle bony window are created with
surgical round bur for replacement and stabilization

c d
Fig 4.50c: After membrane elevation, grafting the sinus is Fig 4.50d: The bony window is repositioned after grafting the
accomplished. sinus. No stabilization is needed to hold the bony window in
place.

~ 189 ~
 a b
Fig 4.51a: Lateral window preparation with piezosurgical saw. Fig 4.51b: Prepared repositioning window.

c d
Fig 4.51c: SM is exposed after lateral window removal. d 4.51d: Membrane elevation.
Fig

e f
Fig 4.51e: Grafting the sinus. Fig 4.51f: Lateral bony window is repositioned.

a b
Fig 4.52a: CT slices prior to sinus augmentation – note the thick Fig 4.52b: Flap elevation.
buccofacial wall.

~ 190 ~
 c d
Fig 4.52c: Lateral window preparation. Fig 4.52d: Removal of the lateral window – notice the thickness
of the lateral bony window.

e f
Fig 4.52e: Removed lateral bony window. Fig 4.52f: Exposed SM.

g h
Fig 4.52g: Membrane elevation. Fig 4.52h: Grafting the sinus.

i j
Fig 4.52i: Repositioning the bony window. Fig 4.52j: Wound closure.

~ 191 ~
a b
Fig 4.53b: Lateral window preparation. Fig 4.53c: Exposed sinus membrane.

c d
Fig 4.53d: Membrane elevation – notice the perforation. Fig 4.53e: Perforation repair using a collagen membrane.

e f
Fig 4.53f: Grafting the sinus. Fig 4.53g: The bony window is repositioned.

a b
Fig 4.54a: Lateral window preparation using a piezoelectic saw. Fig 4.54b: Rectangular bony window.

~ 192 ~
 c d
Fig 4.54c: Bony window removal. Fig 4.54d: Removed lateral bony window.

e f
Fig 4.54e: Exposed sinus membrane. Fig 4.54f: Elevated sinus membrane.

g h
Fig 4.54g: Grafting the sinus. Fig 4.54h: Repositioned lateral bony window.

Double window antrostomy

A double window antrostomy is indicated when septa with multiple sinus compartments
are present. Since bone growth starts from the bony walls surrounding a cavity and progresses
toward the center, the lateral osteotomy site is one of the last areas to mineralize [510]. The
reconstruction of the external cortical plates of the lateral maxillary wall has proven to be very
predictable when related to the survival or failure of implants [510,54]. As a consequence, it is
recommended to preserve the lateral wall as much as possible (Fig 4.55- Fig 4.58).

~ 193 ~
 a b
Fig 4.55a: Double window antrostomy combined with implant Fig 4.55b: Double window antrostomy and elevated sinus
placement. membrane.

c d
Fig 4.55c: After elevating the sinus membrane, the surrounding Fig 4.55d: Double window antrostomy- notice the preserved
sinus walls are clearly visible. lateral wall.

a b
Fig 4.56a: Double window antrostomy with different sizes. Fig 4.56b: grafting the sinus.

c Fig 4.56a-c: Collagen membrane coverage.

~ 194 ~
 a b
Fig 4.57a: Full thickness flap elevation. Fig 4.57b: Preparing the first lateral window.

c d
Fig 4.57c: Sinus membrane elevation. Fig 4.57d: Preparing the second window.

e f
Fig 4.57e: The communication between the two windows is well Fig 4.57f: Schneiderian membrane elevation.
demonstrated.

g h
Fig 4.57f: Grafting the first window. Fig 4.57h: Grafting the second window.

~ 195 ~
 i j
Fig 4.57i: Collagen membrane coverage. Fig 4.57j: Wound closure.

a b
Fig 4.58a: Full thickness flap elevation. Fig 4.58b: Double window preparation.

c d
Fig 4.58c: Grafting the sinus. Fig 4.58d: Collagen membrane coverage.

Size and location of the lateral window

When indicated, the creation of a large window offers two advantages. First, it allows
exposure and elevation of the sinus membrane from all sinus bony walls (the medial wall of the
sinus, the lateral wall of the nasal cavity, the maxillary tuberosity, and inferiorly to the floor and
to the posterior wall of the maxillary sinus) to create a large compartment, which is crucial for
bone graft consolidation during phase one bone formation. Second, it provided access to the lateral
wall of the nasal cavity. The location of the lateral window and its size clearly affects the clinician's
ability to elevate the membrane safely. Having the window in a location that gives the best access
to areas where instrument angulation and hence membrane elevation is difficult, has a great effect
on the operator's ability to keep the hand instruments directly on the bone surface. Changes in

~ 196 ~
instrument angulation are required to go across the floor and up the anterior and medial walls.
From the author's point of view, it is recommended to create a window just large enough to achieve
proper access to the sinus cavity. A large window weakens the lateral wall and endangers the
success of the procedure. The size of the lateral window is determined by the number of implants
to be installed with a consideration to minimize the size of the lateral window as possible (Fig
4.59- Fig 4.67).

a b c
Fig 4.59a-c: Window size and position are determined in accordance with anatomical conditions.

a b
Fig 4.60a,b: Clinical view of a small lateral window – a large Fig 4.60b: It is recommended to create a window just large
window may weaken the lateral wall. enough to achieve adequate access to the sinus cavity.

Fig 4.61a: Clinical view of a medium size lateral window. Fig 4.61b: Clinical view of a medium size lateral window.

~ 197 ~
 a b
Fig 4.62a: Huge lateral window due to an overpneumatized Fig 4.61b: A large lateral window.
sinus.

a b c
Fig 4.63a-c: The buccal mucoperiosteal flap is reflected in a full-thickness manner.

a b c
Fig 4.64a-c: Demonstrating the antrostomy with a straight hand piece with a no 5 or 6 round bur.

a b c
Fig 4.65a-c: Demonstrate the complete antrostomy technique for sinus grafts, in which a complete 360-degree osteotomy was
performed.

~ 198 ~
 a b c
Fig 4.66a-c: Some bone walls are removed and utilized for bone grafting and other are left as is, based on window size and
configuration.

a b c
Fig 4.67a-c: The ideal location for the window is appreciated 3mm superior the sinus floor and 3mm distal to the sloping anterior
wall.

The maxillary sinus is a pyramid-shape cavity. It is believed that the narrow form is often
found in the anterior region of the sinus [54,56]. Obtaining adequate access to this region, which
is frequently the site of perforation, is difficult and may require a larger window than initially
thought. The ideal location for the window is approximately 3mm superior the sinus floor and
3mm distal to the sloping anterior wall, which allows a controlled membrane elevation to be
accomplished while keeping the elevating instruments on the bone surface at all time avoiding
membrane perforation. The shape of the lateral window in the superior extent of a sloping anterior
wall is trapezoidal with the superior osteotomy being longer and more anterior than the inferior
osteotomy, always keeping the window within 3mm of the anterior wall. The anterior wall is an
extension of the sinus floor and the best predictable way to reach it is by following the floor in an
anterior and superior direction. When bone scrapers are used to perform the lateral antrostomy, the
lateral wall of the sinus is scraped and provides autogenous bone grafts. Working directly against
the membrane should be avoided to decrease the risk of membrane perforation (Fig 4.68).

a b
Fig 4.68a: Full thickness flap. Fig 4.68b: Lateral window preparation.

~ 199 ~
 c d
Fig 4.68c: window height for the residual bone is determined Fig 4.68d: Implant site preparation should be accomplished prior
based on the desired length and the lateral wall arteries. to sinus grafting.

e f
Fig 4.68e: Implants are inserted half way. Fig 4.68f: Implants fully inserted – notice implants body within
grafting material.

g h
Fig 4.68g: Implants placed with simultaneous lateral window Fig 4.68h: Wound closure.
SFE. Implants are anchored within residual bone.

Presence of an artery
In the presence of an artery, any osteotomy created in the lateral wall will increase the risk
of hemorrhage during and after surgery [63]. A detailed presurgical analysis, including a CT scan,
is mandatory to identify any blood vessels in the lateral wall [54] (Fig 4.69- Fig 4.74).

~ 200 ~
Fig 4.69: CT scan demonstrates the course of the intrabony Fig 4.70: Mucosal thickening is clearly demonstrated, note the
PSAA. course of the PSAA.

a b
Fig 4.71a: Full thickness flap. Fig 4.71b: Lateral window preparation – notice, the PSAA has
been dissected from the lateral wall.

c d
Fig 4.71c: Grafting the inferior complartment which is formed Fig 4.71d: Grafting the superior complartment which is formed
by the PSAA. by the PSAA.

a b
Fig 4.72a: Clinical view of clearly visible dissected PSAA using Fig 4.72b: Using a piezoelectric device used to dissect the PSAA.
a piezosurgical device.

~ 201 ~
 a b
Fig 4.73a: Lateral wall preparation – notice the PSAA is Fig 4.73b: Sinus membrane elevation.
dissected using a piezoelectric saw.

c d
Fig 4.73c: Elevated sinus membrane – notice the medial wall of Fig 4.73d: Grafting the sinus.
the sinus is visible.

e f
Fig 4.73e: Collagen membrane coverage. Fig 4.73f: Closed flap with barrier membrane underneath.

a b
Fig 4.74a: CT-scan demonstrates the course of the PSAA. Fig 4.74b: Rectangular window preparation for staged sinus
augmentation outlined with piezoelectric saw.

~ 202 ~
 c d
Fig 4.74c: A piezoelectric saw.

e f

g h
Fig 4.74d-h: Removal of the repositioning lateral window taking h
care to maintain the integrity of the PSAA and the sinus
membrane.

i j
h 4.74i: The removed lateral bony window – note the Fig
Fig h 4. 74j: The PSAA course is well demonstrated.
impression of the PSAA.

~ 203 ~
 k l
h 4.74k: Elevated membrane – notice the small perforation.
Fig h 4.74l: Small perforation covered with collagen membrane
Fig
prior to grafting.

m n
h 4.74m: Sinus cavity filled with graft material.
Fig h 4.74n:The removed window is positioned over the graft
Fig
material
h – no fixation is required.

Piezosurgery for sinus augmentation

Piezosurgery, a concept of bone surgery, developed by Vercellotti and specially adapted
for sinus elevation surgery uses low frequency ultrasonic vibrations (range of 24-32 KHZ) to
perform cutting (osteotomy) and grinding (osteoplasty) procedures. This low frequency, selective
cutting procedure is safe for soft tissues and blood vessels or the Schneiderian membrane. An
ultrasonic generator is used to create the osteotomy. The ultrasounds generated at the active tip of
the device facilitate the opening of the bony window. The osteotomy line can be easily made by
cutting the osseous table in a progressive, precise, and controlled way [637] (Fig 4.75a,b- Fig
4.76).

a b
h 4.75a,b: A piezosurgical device is used to create and enlarge a proper
Fig h access to the sinus cavity.

~ 204 ~
 Another interesting property of the ultrasonic device is that it provides greater tactile
control and minimizes the damage on surrounding soft tissue, effectively reducing the risks of
perforating the Schneiderian membrane. In addition, visualization of the surgical area is improved
because of the cleaning effect of the irrigation liquid under the action of the ultrasound. In fact,
the latter transforms the liquid jet into a low-pressure aerosol that facilitates the cleaning of the
area, reducing the risks of subcutaneous emphysema. The thin cutting provided by the ultrasonic
device facilitates the removal and the posterior reinsertion of the bone window after a slight
adjustment.

a b
Figh4.76a: A piezosurgical saw. h 4.76b: Clinical view of a piezosurgical instrument being
Fig
used to open the lateral sinus wall.

Piezoelectric surgery has been used successfully to avoid soft tissue complications (Fig
4.77a,b). The selective cutting action (bone cutting only) allows us in some cases to dissect the
posterior superior alveolar artery from the bony window area, leaving it completely intact.
Piezoelectric surgery has minimized and in many cases prevented bleeding during the preparation
of the lateral window. In cases where piezoelectric surgery is performed, decreased membrane
perforation rates were observed [638]. This is due to the fact that piezoelectric inserts do not cut
soft tissue.

a b
h 4.77b: Rectangular bony window.
Fig 4.77a: Rectangular window preparation for staged sinus Fig
augmentation outlined with a piezoelectric saw.

~ 205 ~
 c d
Fig 4.77c: Exposed sinus membrane. Fig 4.77d: Membrane elevation.

e f
Fig 4.77e: Grafting the sinus. Fig 4.77f: The bony window is repositioned.

Piezoelectric and conventional rotary surgical techniques are performed depending on the
thickness and shape of the lateral sinus wall. In cases where the window is thin, a diamond insert
is used to make a superior hinge or a free-floating bone island attached to the membrane, which is
then elevated horizontally. In cases where the lateral wall is thick or it is convex in the molar
eminence area, the entire lateral wall window is eliminated via osteoplasty exposing the
Schneiderian membrane which is then elevated with manual elevators. Care is taken to guard
against the sharp edges of the elevated bony window which may cause a laceration of the
membrane. It is this surgeon’s experience that using conventional rotative instruments instead of
piezoelectric surgery increases the chances of perforations and consequential outcomes (Fig 4.78a-
j).
However, according to Rickert et al., piezoelectric bone surgery shows no advantage over
conventional rotative instruments with respect to bone healing, operation time, and complication
pre/postsurgery [639].

a b
Fig 4.78a: Lateral window preparation using a piezoelectric saw. Fig 4.78b: Rectangular bony window.

~ 206 ~
 c d
Fig 4.78c: Bony window removal. Fig 4.78d: Elevating the sinus membrane.

e f
Fig 4.78e: Elevated sinus – notice membrane perforation. Fig 4.78f: Elevated sinus membrane.

g h
Fig 4.78g: Perforation repair using a collagen membrane. Fig 4.78h: Grafting the sinus.

i j
Fig 4.78i: Addition of grafting the sinus. Fig 4.78j: Repositioned lateral bony window.

~ 207 ~
 Membrane elevation
Once the lateral window is created, the sinus membrane is carefully peeled back with
curettes of different shapes from the sinus floor and medial sinus wall until it became completely
detached from the lateral and inferior walls of the sinuses. A compartment for grafting material is
created and an absorbable surgical pad soaked in lidocaine 2% with 1:100,000 epinephrine is
applied to promote hemostasis if bleeding occurs. Once there is sufficient exposure, the membrane
is examined for perforations. If no visible perforations are observed, the space is filled with saline,
and the patient is asked to gently perform the Valsalva maneuver. Air bubbles indicate the presence
of a perforation. An overlapping resorbable collagen membrane should be used to repair
perforations. Some practitioners used minimal elevation of the sinus membrane, others elevated
all of the sinus membrane, while still others elevated the membrane only from the lower half of
the antral cavity. It is advisable that the membrane be elevated to the medial wall of the maxillary
sinus for the following reasons: First, the grafts can gain additional blood supply from the medial
wall. The posterior lateral nasal artery that is located on the medial wall provides another source
of blood supply to the grafts [56, 63]. Second, by lifting the membrane to the medial wall, the
tension in the membrane can be sufficiently relieved. Reduced membrane tension is beneficial in
decreasing the incidence of membrane perforation [640]. Third, reaching the medial wall ensures
that the implants are totally surrounded by regenerated bone once the bone grafts are integrated.
Without proper membrane elevation to the medial wall, a void can still be present between the
medial wall and the grafted sinus, which could compromise implant survival [641] (Fig 4.79a,b –
Fig 4.84a,b).

a b
Fig 4.79a: Clinical view of exposed the sinus membrane. Fig 4.79b: Elevated sinus membrane.

a b
Fig 4.80a: Clinical views of the exposed sinus membrane. Fig 4.80b: elevated sinus membrane - note the integrity of the
sinus membrane and the exposed medial wall.

~ 208 ~
 a b
Fig 4.81a: Clinical view of an elevated perforated membrane. Fig 4.81b: The membrane should be elevated to the medial wall
of the maxillary sinus to gain blood supply from the medial wall.

a b
Fig 4.82b: Lateral window preparation. Fig 4.82b: Elevated trapped door with the attached Schneiderian
membrane.

a b
Fig 4.83a,b: Clinical view of exposed sinus membrane – note the Fig 4.83b: Elevated intact membrane.
overextended lateral wall access

Pommer et al. explored the force needed to cause membrane perforation using isolated
samples of human maxillary sinus floors and facial walls. The burst tension of the sinus membrane
ranged from 5.9 ± 2.5 to 8.6 ± 5.1 N/mm2 [115].

~ 209 ~
 a b
Fig 4.84a: Clinical view of complete antrostomy using Fig 4.84b: Clinical view of elevated membrane – note the
piezosurgical device – note the PSAA. attached PSAA to the membrane.

Implant site preparation and implant installation

After the sinus membrane is elevated until it becomes completely detached from the lateral
and inferior walls of the sinus, preparation of the implant sites can proceed. The implant sites
should be marked using a surgical template and then drilled in the desired positions under cool (4
to 5°c) sterile saline irrigation. In order to increase primary stability, osteotomes are performed
using narrower drills for underdimensional preparation. This allows implant insertion that avoids
buccal bone fractures. Care is taken to protect the elevated membrane with a hand instrument in
position to avoid laceration of the drills. Residual bone height can be then assessed using a
modified probe with a small hood. Implants are placed from the crestal bone and extended into the
space, with primary stabilization provided by the residual alveolar bones. The shortest implant
should be no less than 10mm. Dental implant insertions are performed simultaneous to the sinus
grafting by using standardized preparation techniques, initially using a round burr followed by
spiral drills up to 3.2mm. If the initial stability of 15 Ncm is not obtained by torque gauge, the
implant should be replaced with a larger diameter implant. Initial axial and lateral implant stability
is ensured by meticulous condensation of the particulate bone graft around the implants, thus
optimizing direct bone-to-implant contact. The root-shaped implant used should have full length
sandblasted and acid-etched surfaces. In the coronal zone, mini-threads are present to better
distribute stress and achieve a better primary stability, while the apical portion presents with an
oval design. The implant body is placed to half of its total length and the remaining sinus space
around the implant is completely packed with graft material (Fig 4.85a-d – Fig 4.89a,b).
It is generally preferable to insert longer implants. The impact of implant length on implant
prognosis was described by Ferrigno et al. [642] as well as by Herrmann et al. [643]. They reported
that maxillary implants longer than 10 mm have better prognosis than those that are 10 mm or
shorter. There is a tendency toward greater implant length in augmented areas of the sinus floor.
Implants are placed with a minimum torque value >20N.
However, whether sinus floor augmentation is preferable to implantation in the
unaugmented posterior maxilla has not yet completely determined. When there is unfavorable bone
quality in the posterior maxilla, a higher loss rate may result and some authors postulate that a
minimal implant length of 10 mm is required in this region. The predominant use of long and wide
implants in the maxillary molar area should provide for an optimal implant-crown ratio, which can
improve long-term success without complications [642,643].

~ 210 ~
 a b
Fig 4.85a: Clinical view of exposed alveolar ridge and elevated Fig 4.845: Preparing the implant site. The exact position of the
sinus membrane. implant site is first marked with small round bur, then widened
with burs of two sizes to a diameter approximately 0.5 mm
smaller than the proposed implant diameter – note that the
membrane is elevated and protected

c d
Fig 4.85c: Implants placed with simultaneous SFE half way with Fig 4.85d: Implants in situ – final position. Note the visible
grafting the sinus. implants inside the sinus cavity.

e f
Fig 4.85e: The sinus is filled with grafting material. Fig 4.85f: Closed flap with barrier membrane underneath.

~ 211 ~
 a b
Fig 4.86a: Preparing the implant site. Fig 4.86b: Implants placed with simultaneous SFE half way with
grafting the sinus.

c d
Fig 4.86c: The sinus is filled with grafting material combined Fig 4.86d: Collagen membrane coverage above the grafting
with GBR. material.

a b
Fig 4.87a: Six months after sinus grafting, the implant site is Fig 4.87b: Implant placement in a standard surgical procedure.
prepared for implant placement. Excellent primary stability was obtained.

a b
Fig 4.88a: Implant site preparation. Fig 4.88b: implant placement after staged sinus augmentation.

~ 212 ~
 a b
Fig 4.89a: Implant site preparation. Fig 4.89b: implant placement after staged sinus augmentation.

Grafting the sinus

After a complete sinus membrane elevation followed by an implant site preparation, a
minimum of 3 cm2 grafting material from different sources alone or mixed with autogenous bone
collected from the surgical area is mixed with sterile saline solution or the patients’ blood and
carefully packed into the sinus cavity. The material is packed especially posteriorly and anteriorly
and against the medial aspect of the cavity below the elevated membrane and at the superior aspect
of the sinus (Fig 4.90 – Fig 4.93). In some cases, liquid antibiotic (Clindamycin 150 mg/ml) can
be added to the bone graft to minimize the incidence of postoperative infection, using a ratio of
one ml antibiotic to two ml of grafting material. After the implants are placed in their final position,
care is taken to pack the graft material around the apices of the implants to cover the entire implant
body. Mesiodistal parallelism of the long-axis orientation of the implants is achieved by matching
the distance between the apices of the implants with that between the implant necks. Further graft
condensation increases the primary stabilization of the implants in cases of incomplete
stabilization. The distance between the buccal plate and the implants apices is measured to
determine the correct buccopalatal implant position. Care is taken to meticulously condense and
to pack the graft material to the entire implant body without dislodging the implant’s axial position.

a b
Fig 4.90a,b: Grafting the sinus. Fig 4.90b: note the channels and concavities of the grafted
material.

Autologous cortical bone from the anterior maxillary wall, the zygomaticomaxillary
buttress and the maxillary tuberosity can be harvested with a bone scraper to reduce the lateral
bone thickness, allowing an easy access to the sinus membrane.

~ 213 ~
 a b
Fig 4.91a: The sharp bone scraper enables harvesting autogenous Fig 4.91b: A piezoelectric device enables harvesting autogenous
bone. bone from the lateral wall.

c d
Fig 4.91c: A sharp chisel is used to collect autograft chips from Fig 4.91d: The bone scraper enables the harvesting and
the alveolar ridge. collecting of autogenous bone partially from the buccal wall of
the maxillary sinus.

a b
Fig 4.92a,b: Bone mill with autogenous bone.

~ 214 ~
 a b
Fig 4.93a,b: The collected autograft chips mixed with DBBM particles, the composite graft is applied in the created compartment
after elevation of the membrane.

Barrier membrane over the lateral window

After completion of the sinus augmentation, resorbable collagen membrane is then
trimmed and adapted to cover the lateral window, three mm at least beyond the osteotomy lines in
accordance with the principle of guided bone regeneration. To avoid the proliferation of the
connective tissue into the sinus cavity (encleftation). It is not necessary to stabilize the membrane.
In some cases after bone grafting is completed, the detached lateral window can be repositioned
with the application of gentle pressure to the grafted area. In these cases, no rigid fixation with
plates is required and a barrier membrane is not used (Fig 4.94- Fig 4.96).

a b

c d

~ 215 ~
 e f
Fig 4.94a-f: Different cases of grafted sinuses with collagen membrane coverage which is supposed to promote vital bone formation
and to avoid soft tissue encleftation.

a b
Fig 4.95a,b: A double layer collagen membrane was adapted over the grafted material.

a b
Fig 4.96a,b: Following GBR principles, the graft material was covered with a double layer of collagen membrane.

In the scientific literature, these still controversy over the need to use a barrier concurrently
with a graft both in guided bone regeneration and sinus augmentation procedures. Although the
use of membranes could have some advantages such as preventing connective tissue invasion of
the graft, possible increased bone formation, and containment of particulate graft material, a
criticism that has arisen is that the exclusion of the buccal flap could decrease vascular supply to
the graft, compromising the formation of vital bone. According to Barone et al. [644], the
percentage of vital bone in patients where a membrane was used was 30.7 % +- 15.5%, while in
the absence of membrane the amount of vital bone was 28.1%+- 19.4%. Barone et al. [644] found
that the re-absorption rate in sites without a membrane is greater than in sites with a membrane. It
is plausible that the blood supply of maxillary sinus plays a role. In fact, vascularization is derived
primarily from the maxillary artery and to a lesser degree, from the anterior ethmoidal and superior

~ 216 ~
labial arteries. A study showed that a significant greater amount of new vital bone was produced
in the human maxillary sinus when nonresorbable membrane was used, compared to the no-
membrane side.
The theoretical function of the barrier membrane covering the lateral window of the grafted
sinus is to inhibit graft particle displacement and to prevent proliferation of connective tissue into
the maxillary sinus. By excluding the nonosteogenic connective tissue that competes with the
osteogenic cells, bone formation inside the sinus may become more favorable for graft maturation.
The direct contact between the connective tissue and the graft particles allows immediate tissue
proliferation and infiltration into the anorganic bovine graft resulting in soft tissue adherence to
the graft particles. The resorbable membrane has the additional effect of stabilizing the graft
particles.
A recent meta-analysis of the literature [597] concludes that implant survival rate is higher
when a membrane is placed over the lateral window in sinus augmentation. Choi et al. [645]
concluded that the placement of a resorbable membrane over an augmented sinus does not present
any additional risks. While the resorbable membrane had no effect on the amount of new bone
formation within the sinus grafted with anorganic bovine material, it significantly reduces the
amount of soft tissue formed in grafted human maxillary sinuses. As a consequence, the reduction
of blood supply due to the membrane’s area may explain such a delay in the reabsorption of the
biomaterial. The use of the membrane may slightly increase the amount of vital bone over a period
of six months. The mucoperiosteal flap is then replaced over the grafts and the implants and is
sutured using 3-0 with vertical mattress sutures at the level of the crestal incision. For one-stage
implants, the healing abutments on the implants are left exposed and the wound is closed. For two-
stage implants the mucoperiosteal flap is then replaced over the grafts and implants and is sutured
with vertical mattress sutures at the level of the crestal incision (Fig 4.97).

Fig 4.97: Wound closure with interrupted sutures.

Surgical technique for two-stage sinus augmentation

To avoid repetitions, a brief description of the surgical techniques, two-stage sinus
augmentation is presented. The lateral wall sinus augmentation is performed according to a
previously described detailed protocol. The surgical procedures are always carried out with a low
trauma surgical technique. Following a crestal incision and releasing incisions, a full thickness flap
is elevated to expose the lateral wall of the sinus. The size of the lateral window is determined by
the size of the sinus space to be augmented, and considering few anatomic factors such as the
Underwood septa and the position of the course of the vascular anastomosis inside the lateral wall

~ 217 ~
of the sinus. The lateral window, oval in shape, is free of sharp edges to avoid membrane
perforation during the membrane elevation. The handling of the lateral cortical plate, which
represents the lateral window of the sinus, varies with the surgical technique as previously
mentioned. In most cases, the bony window is completely removed with distinct bur drilling or
with Piezosurgery. The Schneiderian membrane is carefully reflected to the desired extent in all
directions. Care is taken not to perforate the membrane during its mobilization from the inner bone
surface to secure blood supply for the grafting material. In case of membrane perforation, a
resorbable collagen membrane is used to protect sinus membrane during the grafting procedure.
Mostly composite grafts are mixed with fresh blood from the wound, and then applied into the
created space following elevation of the membrane. The graft material is first placed in the
posterior and anterior recesses and is not compacted too densely to ensure the vascular neogenesis
that is necessary for bone formation. The amount of grafting material used at each site varies
according to the extent of maxillary sinus and the anatomy. Care is taken not to obstruct the middle
nasal meatus to allow free sinus drainage. When necessary, other surgical procedures can be
performed simultaneously to increase the width of the residual alveolar ridge, such as cortical split
osteotomy and guided bone regeneration (GBR). The grafted area, including the horizontal
augmented area if indicated is then covered with a bioresorbable collagen membrane. The flap is
closed tension free and if necessary, periosteal releasing incisions are made to help achieve passive
closure (Fig 4.98).

a b
Fig 4.98a: Panoramic radiograph demonstrating teeth 25,26,27 Fig 4.98b: Lateral window preparation after teeth extraction.
with periapical lesions - note maxillary left sinus
pneumatization.

c d
Fig 4.98c: Grafting the sinus. Fig 4.98d: Collagen membrane coverage.

~ 218 ~
 e f
Fig 4.98e: Panoramic radiograph demonstrating left sinus six Fig 4.98F: Full thickness flap elevation.
months after augmentation.

g h
Fig 4.98g: implant site preparation six months after sinus Fig 4.98h: First implant placement.
augmentation

i j
Fig 4.98i: Second implant placement.. Fig 4.98j: All three implants placed in situ.

Implants are placed in a subsequent surgical phase, 6 to 9 months following either a

submerged or a non-submerged technique (Fig 4.99a-f – Fig 4.102a,b). There are instances where
the bone graft appears soft and cannot provide primary stability during implant placement.
Implants are placed using a standardized surgical procedure, with the coronal border of the implant
approximating the alveolar bone crest. Details of surgical techniques and postoperative treatments
have been reported in previous chapters.

~ 219 ~
 a b
Fig 4.99a: Surgical field after elevation. Full thickness Fig 4.99b: Clinical view after implant placement.
mucoperiosteal flap six months after sinus grafting.

c d
Fig 4.99c: Surgical field after elevation. Full thickness Fig 4.99d: Clinical view after implant placement.
mucoperiosteal flap six months after sinus grafting.

e f
Fig 4.99e: Surgical field after elevation. Full thickness Fig 4.99f: Clinical view after implants placement.
mucoperiosteal flap six months after sinus grafting.

~ 220 ~
 a b
Fig 4.100a: Surgical field after elevation. Full thickness Fig 4.100b: Clinical view after implants placement – note the
mucoperiosteal flap six months after sinus grafting. augmented bone volume gained after six months.

a b
Fig 4.101a,b: Clinical view of second stage surgery. Fig 4.101b: Additional GBR was needed to achieve adequate
bone surrounding the implants.

a b
Fig 4.102b: Postoperative radiograph six months after bilateral Fig 4.102c Postoperative radiograph three months after
maxillary sinus grafting shows the healthy appearance of the bilateral implant placement.
sinus and the absence of a “gap” between the native bone and
the grafted bone.

Surgical technique for local sinus augmentation

A crestal incision is made in the edentulous area and connected with diverging relaxation
incisions in the vestibule. A circular area over the sinus cavity bone extending to the adjacent roots
is removed to the sinus membrane and if possible the bone is collected with bone scrapers during
the preparation. The sinus membrane is then carefully elevated and the implant is installed through
the crestal bone using a standardized preparation technique (Fig 4.103a-d). Because of the

~ 221 ~
smallness of the access hole, tearing of the sinus membrane is considered a common intra-
operative surgical complication.

a b
Fig 4.103a: Panoramic radiograph demonstrating tooth 16 with Fig 4.103b: Clinical view of an access hole to the maxillary
a periapical lesion. sinus.

c d
Fig 4.103c: The sinus cavity is filled with grafting material for Fig 4.103d: Grafted sinus with implant in situ.
implant site preparation.

The implant should penetrate into the sinus cavity about two or three times the adequate
residual bone volume. Primary stability is a prerequisite for implant installation. The sinus
membrane is thus held up by the implant which acts as a tent pin for the membrane. The implant
is surrounded by the bony walls of the adjacent teeth and at the top of it the sinus mucosa. A cover
screw is adapted and the collected bone material and grafting material is placed around the exposed
part of the implant. The apical part of the implant is completely covered with bone. The flap is
then repositioned with interrupted sutures. Sutures are removed after two weeks and an abutment
connection is made after three months followed by single crown therapy (Fig 4.104a,b , Fig
4.105a,b).

~ 222 ~
 a b
Fig 4.104a: Panoramic radiograph illustrating left local sinus Fig 4.104b: Panoramic radiograph illustrating the inserted
augmentation – note the healthy appearance of the grafted implant with final restoration and the extracted tooth 27.
bone.

a b
Fig 4.105a: Panoramic radiograph illustrating the situation Fig 4.105b: Panoramic radiograph illustrating the augmented
prior sinus grafting. right sinus.

Reentry sinus augmentation

The indications for reentry sinus augmentation procedure may arise due to unsuccessful
previous augmentation surgery that has led to insufficient new bone formation which necessitates
implant placement. Some authors emphasize previous sinus surgery as a contraindication to sinus
augmentation, because scar tissue may risk detachment of the Schneiderian membrane from the
inner bony aspect of the antrum [510,76]. Others recommend that reentry for re-augmentation
should be considered only after a six-month healing period following unsuccessful previous
surgery [152] (Fig 4.106- Fig 4.108).
Failure of the initial surgical procedure for sinus augmentation may modify the
characteristics of the soft and hard tissue involved in the reentry intervention, mainly by creating
adhesions of the Schneiderian membrane facing the previously created osseous lateral window to
the buccal flap (71%). Such changes create a challenging surgical approach i.e. difficulties in
reflecting the buccal flap to overcome the modified site [646]. The characteristics of the
Schneiderian membrane are modified as a result of the previous mucosal elevation failure. Because
of this eventful healing, the flexible nature of the healthy thin membrane becomes a thick fibrotic
nonflexible one. The membrane has less resilience to fold as a regular membrane.
The combination of a high perforation rate and fibrotic changes of the Schneiderian
membrane may lead to a higher postoperative complication rate. It must be kept in mind that the
primary failure might have also affected the bony environment, jeopardizing the ability to create
new bone and consequently osseointegration.

~ 223 ~
 Mardinger et al. concluded that (i) reentry sinus augmentation is predictable despite its
complexity [646]. (ii) Clinicians should be aware of the challenges inherent in the reentry
procedures. It is recommended that the reentry sinus augmentation should be performed only by
highly experienced and well-trained practitioners. (iii) Patients should be informed about lower
rates of implant osseointegration in reentry procedures.

a b
Fig 4.106a: Panoramic radiograph showing bilaterally Fig 4.106b: Clinical view of surgical field six months after sinus
augmented sinuses six months after surgery. augmentation. A limited part of the augmented sinus shows soft
tissue enclefation.

c d
Fig 4.106c: Removal of soft tissue and granulation tissue. Fig 4.106d: Implants in situ.

e f
Fig 4.106e: The fenestration defect was filled with a composite Fig 4.106f: Barrier membrane coverage before closure.
graft.

~ 224 ~
 a b
Fig 4.107a: Panoramic radiograph obtained after surgical Fig 4.107b: Reentry with implant placement and final
intervention of infected augmented right sinus illustrating the restoration.
condition after removal of infected grafting material.

a b
Fig 4.108a: Panoramic view of Ct scan demonstrating healthy Fig 4.108b: Ct scan slices of the right maxillary sinus – notice
looking right maxillary sinus – notice the thin mucosa almost the discontinuity of the lateral wall due to previous multiple
not visible on the view. unsuccessful attempts to augment the sinus.

c d
Fig 4.108c: Clinical view eight months after previous last Fig 4.108d: The incision line was designed taking into
surgical intervention. consideration the previous incisions.

~ 225 ~
 e f
Fig 4.108e: Full thickness flap elevation – notice the scar Fig 4.108f: Fully elevated flap after split thickness incision and
attachment of the flap to the Schneiderian membrane. detachment of the flap from the Schneiderian membrane.

g h
Fig 4.108g: Scar tissue removal and enlarging the lateral wall Fig 4.108h: Extra-large membrane perforation due to thin
access hole. membrane, scar tissue and previous surgery.

i j
Fig 4.108i: Extensive repair of the perforation using multiple Fig 4.108j: Leaving a third of the repair membrane outside the
layer of collagen membrane in different directions. sinus to avoid membrane displacement.

k l
Fig 4.108k: Grafting the sinus while cautiously taking care of Fig 4.108l: Grafted sinus – notice the collagen membrane
the repair membrane. outside the sinus.

~ 226 ~
 m n
Fig 4.108m: Collagen membrane coverage. Fig 4.108n: Panoramic radiograph immediately post surgery
showing the graft material in its proper site.

Sinus augmentation combined with horizontal guided bone regeneration (GBR)

In cases of horizontal deficiency not allowing the placement of standard implants, sinus
augmentation combined with horizontal guided bone regeneration is needed to allow the placement
of standard implants following the principles of sinus augmentation and GBR protocols as
previously comprehensively described.
The following cases demonstrate sinus augmentation combined with horizontal guided bone
regeneration:

a b
Fig 4.109a: Four corner flap incision. Fig 4.109b: Full thickness mucoperiosteal flap elevation.

c d
Fig 4.109c: Sinus membrane elevation – notice the small Fig 4.109d: Collagen repair membrane is used to seal the
perforation. perforation.

~ 227 ~
 e f
Fig 4.109e: Sinus grafting with simultaneous implant placement. Fig 4.109f: Grafting material addition for GBR.

g h
Fig 4.109g: Collagen membrane coverage. Fig 4.109h: Wound closure.

a b
Fig 4.110a: Full thickness mucoperiosteal flap elevation. Fig 4.110b: Exposed sinus membrane - extended pneumatized
sinus cavity and the proper large lateral window.

c d
Fig 4.110c: Elevated sinus membrane. Fig 4.110d: Grafting the sinus.

~ 228 ~
 e f
Fig 4.110e: Additional grafting materials for horizontal GBR. Fig 4.110a-g: Collagen membrane coverage.

a b
Fig 4.111a: Full thickness mucoperiosteal flap elevation. Fig 4.111b: Exposed sinus membrane.

c d
Fig 4.111c: Use of electrocautery to control bleeding. Fig 4.111d: Grafting half the sinus and implant site preparation.

e f
Fig 4.111e: Grafting the sinus with simultaneous implant Fig 4.111f: Implants fully inserted and the addition of grafting
placement. materials for horizontal GBR.

~ 229 ~
 g h
Fig 4.111ag: Collagen membrane coverage. Fig 4.111h: Wound closure.

a b
Fig 4.112a: Panoramic radiograph demonstrating missing 26 Fig 4.112b: Full thickness mucoperiosteal flap elevation.
and pneumatized maxillary sinuses.

c d
Fig 4.112c: Exposed sinus membrane. Fig 4.112a: Elevated sinus membrane.

e f
Fig 4.112e: Grafting the sinus with simultaneous implant Fig 4.112f: Additional bone grafting materials is added for
placement. horizontal GBR and vertical GBR.

~ 230 ~
 g h
Fig 4.112g: Collagen membrane coverage. Fig 4.112h: Wound closure.

a b
Fig 4.113a: Full thickness mucoperiosteal flap elevation. Fig 4.113b: Exposed sinus membrane.

c d
Fig 4.113c: Elevated sinus membrane and implant site Fig 4.113d: Grafting the sinus with simultaneous implant
preparation. placement.

e f
Fig 4.113e: Addition of more grafting materials for horizontal Fig 4.113f: Double layer collagen membrane coverage.
GBR.

~ 231 ~
 a b
Fig 4.114a: Elevated sinus membrane combined with standard Fig 4.114b: Sinus grafting combined with implants placement in
implant placement in site 24. site 25 ,26.

c d
Fig 4.114c: Additional bone grafting materials for horizontal Fig 4.114d: Collagen membrane coverage.
GBR.

a b
Fig 4.115a: Exposed sinus membrane – notice the knife edge Fig 4.115b: Elevated sinus membrane – notice sinus septum.
configuration in site 24,25.

c d
Fig 4.115c: Sinus augmentation combined with horizontal and Fig 4.115d: Double layer collagen membrane coverage.
vertical GBR.

~ 232 ~
 Sinus augmentation combined with vertical augmentation
This procedure is indicated in cases where a vertical bone deficiency exists due to both
pneumatization of the sinus and alveolar ridge resorption. A three dimensional reconstruction is
indispensable to allow placement of implants in adequate length and width. A destruction of the
bone simultaneously with bone augmentation and GBR is indicated.

a b
Fig 4.116a: a rectangular bony window is outlined with Fig 4.116b: Removal of the repositioning lateral window.
piezoelectric saw according to the principles described for sinus
augmentation procedure, taking care to maintain the integrity of
the Schneiderian membrane.

c d
Fig 4.116c: Intact exposed sinus membrane. Fig 4.116d: Elevation of the sinus membrane.

e f
Fig 4.116e: Elevated membrane – note the exposed medial wall.

~ 233 ~
 g h
Fig 4.116f,g: Using a piezoelectric saw, the distraction segment
is outlined keeping the segment attached to the palatal flap.
Fig
i 4.116h-j: Clinical view of destructed alveolar ridge segment
taking care to maintain the integrity of the sinus floor and to
maintain the segment attached to the gingiva.
k 4.116l: The removed bone window is positioned in situ – no
Fig
fixation is required.
~ 234 ~
Fig 4.116h: Vertical distraction of bony segment to compensate
for vertical bone resorption.
j 4.116k: The composite graft (autogenous bone and DBBM)
Fig
is inserted into the sinus cavity and in the created space after
segment destruction.
Fig
l 4.116m: The grafted site is covered with a collagen
membrane. Primary wound closure is achieved after a releasing
incision of the periosteum.
a b

c d

e f

g h

~ 235 ~
 i j
Fig 4.117a-j: Staged repositioning of a lateral window sinus augmentation procedure with vertical GBR – note primary wound
closure is achieved after a releasing incision of the periosteum

a b

c d

e f

~ 236 ~
 g h
Fig 4.118a-f: one implant placed with simultaneous lateral window SFE combined with bone augmentation of simultaneously
extracted tooth 26

a b

c d

e f

~ 237 ~
 Fig 4.119a-i: Staged sinus augmentation combined with standard implant placement in sites 24,25 and vertical GBR using double
window antrostomy technique – note the gained autogenous bone using a sharp chisel.

Sinus augmentation combined with molar extraction

In cases of molar extraction and augmentation, a midcrestal incision is made with a sulcular
incision around the adjacent teeth. Mesial and distal releasing incisions extending well up into the
buccal fold are placed at the mesial aspect of the mesial papilla tissue in the flap extent. The bases
of the buccal releasing incisions are extended approximately 3 to 6mm horizontally. The buccal
mucoperiosteal flap is reflected in a full-thickness manner, with care taken to completely release
the tissue beneath the horizontal releasing incision extensions, thus creating a freely moving buccal
mucoperiosteal flap. Mesial and distal palatal releasing incisions are positioned to coincide with
the buccal releasing incisions and the palatal mucoperiosteal flap is reflected. In cases where a
discontinuity of the lateral wall is known to exist as a result of an aggressive extraction, or due to
inflammatory lesions, a split thickness flap dissection over the site is performed to avoid lacerating
the sinus membrane. The soft tissues overlying the cortical bone of the buccofacial wall of the
maxillary sinuses are removed entirely to reveal the bony surface in the region of interest. The
buccofacial sinus wall has to be cautiously managed.
It is obligatory to estimate the thickness of the buccofacial wall of the maxillary sinus to
minimize the occurrence of a mucoperiosteal perforation during antrostomy. Extra precautions are
required on thick buccofacial wall to keep the mucoperiosteum of the sinus wall intact. Care is
taken not to make the hinge (superior margin of the window) during the window opening procedure
deeper than the inferior margin, which may lead to a mucoperiosteum perforation. To ensure that
the outlined bone had been penetrated all around the osteotomy, it should be tapped gently with a
blunt instrument until movement is visible. A rectangular window is created with rounded or
elliptically shaped angles ensuring that the inferior border is at least 2 to 3mm superior to the sinus
floor. The advantage of entering through the lateral antral septum is in protecting the tissue
integrity in the implant region [109]. With this combination of augmentation and implant insertion,
the spectrum of indication for osseous implants can be expanded to allow adequate treatment even
under unfavorable circumstances. A detailed description of the following steps for completing the
surgical procedure has been previously presented.
The following cases demonstrate lateral wall sinus augmentation combined with molar
extraction:

~ 238 ~
 a b

c d

e f

g h
Fig 4.120a-i: Staged sinus floor augmentation procedure combined with molar extraction – note the communication between
the lateral window and the extraction site showing the discontinuity of the sinus floor. Grafting both the sinus cavity and the
extraction site according to the GBR principles is required. The grafted sites are covered with two layers of collagen membrane.
After a releasing incision of the periosteum is made, primary wound closure can be achieved.

~ 239 ~
 a b

c d

e f
Fig 4.121a-f: Staged sinus augmentation combined with GBR and molar extraction.

a b

~ 240 ~
 c d

e f
Fig 4.122a-e: Staged sinus augmentation combined with multiple molar extraction and GBR – note the bone defects created after
teeth extraction and also the membrane perforation.

a b

c d

~ 241 ~
 e
Fig 4.123a-e: Staged sinus augmentation combined with premolar extraction and GBR – note the communication between the sinus
cavity and the extraction site.

Sinus augmentation combined with standard implantation

In cases of partly sufficient bone available for standard implant placement, a combined
sinus augmentation simultaneous/delayed procedure with standard implant placement can be
performed in the same manner as previously comprehensively described.
The following cases demonstrate sinus augmentation procedure combine with standard
implant placement:

a b

c d

~ 242 ~
 e f
Fig 4.124a-g: Staged sinus augmentation procedure combined with standard implant placement in sites 23-25. Note the small
lateral window needed to accomplish grafting the sinus.

a b

Fig 4.125a-c: Staged sinus augmentation procedure combined

c
with standard implant placement in sites 14,15.

Managing septa
During sinus elevation surgery, the presence of anatomic variations within the maxillary
sinus, such as septa can complicate membrane elevation and increase the risk of sinus membrane
perforation. Knowledge of the septa’s locations and morphology is essential in determining the
surgical approach. The literature indicates that septa and sinus floor irregularities will often go
unnoticed by two-dimensional radiographic assessment [648]. Recent developments in CT
scanning enable surgeons to obtain detailed information about internal sinus anatomy before SFE.
In this way, they can evaluate the various surgical options prior to opening the sinus cavity. The
presence of septa creates a need for increased vestibular access for complication free handling
without creating uncontrolled pressure on the membrane. Careful preparation with hand
instruments while elevating the membrane along anatomical irregularities is necessary to prevent

~ 243 ~
tearing of the mucosal membrane. When high septa are known to be present, it is necessary to
lengthen the window in the anterio-posterior direction so that the window is located both anterior
and posterior to the septum. This is called a double window antrostomy. This allows for a lateral
to medial elevation of the membrane from both sides of the septum. In some cases, it is extremely
difficult to elevate the membrane from a sharp septum in a mesial to distal direction while keeping
elevation on the bony surface at all times. If the two separate windows are decreased in size causing
poor access and visibility, the two windows should be joined at the septum, creating one large
window with improved access to both sides of the septum. In some cases, the shapes of the
instruments determine the need to remove parts of the septa to release the sinus mucosa from the
bone.
Septa with a low height (up to 2mm) do not require further treatment, because the
membrane can be elevated without further procedures. Medium-size septa (2 mm- 5 mm) require
resection because the palatal area of the sinus cavity cannot be reached by the instruments. High
septa (> 5 mm) require the preparation of two or even three cavities because such septa lead to
partial or complete separation of the sinus cavity (Fig 4.126a-h).
The prevalence of septa limits the mobility of the sinus instruments, requiring a need for
increased vestibular access to avoid tearing of the sinus membrane.

a b

c d

~ 244 ~
 e f

g h
Fig 4.126a-h: managing septa during sinus floor augmentation.

The following paragraphs explain how to select the appropriate surgical procedures for
managing septa in the sinus cavity.
When the septum is higher than the length of the planned implants, the sinus cavity may
be separated into two or more compartments. In this situation, it may be impossible to remove the
septum and manage the case by creating one cavity for sinus augmentation. Therefore, opening a
separate window for each compartment is recommended, although opening more than two
windows is not realistic. Complex anatomical conditions like the presence of completely isolated
compartments will render the procedure more difficult.
When the septum is lower than the length of the planned implants, the sinus cavity does
not have to be separated into compartments. In this situation, it is possible to remove the septum
and manage the case as one cavity for sinus augmentation. Depending on the orofacial dimension
of the septum, it may still be advantageous to start out by preparing two separate window openings
until the septum is identified and removed. Depending on the clinical situation, the opposite
procedure may also be an option. When the height of the septum limits the facial aspect, the case
may be approached as a single cavity in terms of initial window opening.
In conclusion, septum surgery in conjunction with SFE requires meticulous and careful
analysis of the underlying anatomy. Appropriate radiographic imaging is essential to increase the
predictability and reduce the complications of septum surgery. Clinicians should be aware that
some cases may be too severely compromised to achieve predictable sinus floor elevation.

Postoperative considerations
Sinus floor augmentation and implant placement procedures increase the risk of
introducing pathogenic bacteria into sinus and nose, and the prophylactic use of antibiotics reduces

~ 245 ~
the risk of infection [621]. Preoperative prophylactic antibiotic therapy, should be continued
postoperatively for 7 to 10 days. The use of high-dose antibiotics preoperatively not only reduces
the incidence of postoperative infection [55] but also significantly reduces implant failure rates
during second stage surgery [621]. Subjects are instructed to take corticosteroids in decreasing
daily doses of 6, 4, and 2 mg starting the day of the surgery. A nasal decongestant, 30 to 60 mg
per day, should be prescribed, and nasal spray should be used on an as-needed basis for nasal
congestion. Patients are instructed not to smoke for 10 days before surgery.
Postoperative considerations for maxillary sinus grafting procedures are similar to those
for most oral surgery and sinus manipulation procedures. After the first week, a chlorhexidine
mouth rinse should be used twice daily for two weeks to reduce the chance of infection. Blowing
the nose, sucking liquid through a straw, and smoking cigarettes, all of which create negative
pressure, should be avoided for at least two weeks after surgery. Coughing or sneezing should be
done with an open mouth to relieve pressure. Pressure at the surgical site, ice, elevation of the
head, and rest are also recommended. Analgesics should be used to control postoperative pain. An
anti-inflammatory medication and an antihistamine can also be used.
Depending on the graft materials and the host osteogenic potential, 3 to 6 months should
be allowed for the bone graft and implants to integrate before the prosthodontic phase begins.
During this period, the patient can wear a conventional prosthesis that has been relined with a soft
material. If an intraoral donor site has been used, it is usually well tolerated and recuperation
normally takes one to two weeks. Patients who wore removable prostheses prior to surgery are
permitted to resume wearing their prostheses immediately after surgery.
Patients who undergo sinus augmentation and lateral bone augmentation are instructed not
to wear their prostheses for 3 weeks after surgery. Dentures should be relined periodically with a
soft tissue conditioner. Sutures are removed after 7 to 10 days following surgery. All patients
should undergo periodic checkups to verify healing. Any adverse reactions, signs of infection,
hematomas or swellings have to be checked.

Second stage procedure and follow-up

Second-stage surgery to expose the implants is performed six months after sinus grafting
and simultaneous implant placement, and three months after delayed implant placement. After
performing a minimal crestal incision just over the area corresponding to the implant, cover screws
are exposed and removed and healing abutments are screwed in.
Since an adequate amount of peri-implant mucosa which is firmly attached to the
underlying periosteum and bone is a factor for the long term success of the dental implant [376],
the surgeon should verify the presence of increased width and thickness (> 1mm) of keratinized
gingiva. A buccally positioned palatal flap is used to ensure sufficient keratinized gingiva at the
buccal side of the implant. Attached keratinized mucosa is left both on the palatal and buccal aspect
around all implants. A minimum of one month is required for the healing of the flap and peri-
implant tissues prior to loading.
After the implants are exposed, they should be assessed for stability and crestal bone loss.
Panoramic and periapical radiographs and in some cases CT-scans should be obtained to assess
bone support of the implants.
Flap surgery should be performed at the second stage surgery to assess new bone formation
rather than using the punch technique, which limits visualization of the implant cover screw.
During the postoperative reentry surgery, interference of surrounding fibrous tissue, epithelial
invaginations and resorption or loss of grafts should be checked.

~ 246 ~
 In general, bone regeneration in the lateral window shows different patterns: complete bone
healing, graft exposure, or residual particles of grafting material. At the repositioning window,
mobility or resorption of the repositioned bony window can be seen. Clinical evaluation criteria at
the time of implant exposure include stability in all directions, eventual crestal bone resorption.
Any reported pain or discomfort should be resolved. Abutments are screwed at 35N and
provisional restorations are seated. Splinted crowns are preferred to allow better occlusal force
distribution. An acrylic resin provisional restoration is placed on all the implants for a minimum
of two months before the final restoration is provided.
After prosthesis delivery, the patients should be annually recalled for a clinical and
radiographic examination. It is recommended to assess the newly formed bone and its interface
with the implants via radiographic examination of the treated area, including panoramic, periapical
radiographs and in some cases CT scans. At subsequent review appointments, the implants are
examined for clinical mobility, adverse symptoms, such as pain, and the presence or absence of
repeated peri-implant infection. Furthermore, all biological complications in the initial healing
phase, as well as during the follow up period including any mobility or radiolucency around the
implants have to be resolved immediately. Based on clinical and radiographic findings, each
implant is then classified as either successful or non-successful or surviving using Zarb’s success
criteria [587].

a b

c
Fig
c 4.127a-c: Implant exposure with healing cap three months after implant placement.

Guidelines for choosing the proper surgical technique

The following guidelines for choosing the proper surgical concepts are recommended: a)
creating a large buccal window, allowing access to a large recipient site if needed; b) using
composite grafts consisting of at least 50% autogenous bone; c) meticulous condensation of the

~ 247 ~
bone graft material; d) placement of long implants; selecting microtextured “rough” implant
surfaces; e) using a membrane to cover the graft and implants; f) antibiotic use and strict oral
hygiene; g) use of interim implants when possible and restricted denture use.
Potential candidates for SFE should be carefully evaluated prior to considering the surgical
technique and grafting protocol to be adopted. A complete medical history (health status,
medication, allergies, smoking, and habits) should be obtained and the patient should be evaluated
for compliance. The goal of this assessment is to identify the presence of any general risk factors.
A thorough clinical examination should be conducted prior to SFE. The parameters of this
examination should include interarch relations, periodontal status, evidence of bruxism, and
distance to the neighboring teeth and the kind of opposing dentition.
A radiographic evaluation should be conducted. This evaluation should include three-
dimensional information about the residual subantral bone (volume and density), the periapical
status of any neighboring teeth, sinus floor anatomy, including the presence of any septa and
secondary cavities, and evidence of sinusitis or any other pathologic alterations in the maxillary
sinus. The purpose of these clinical and radiographic assessments is to identify any local risk
factors.
An overall risk assessment should be performed based on any general and/or local risk
factors that have been identified in this process. If any absolute contraindications to SFE or
associated procedures are present, alternative modalities should be considered. Potential
alternatives in the presence of contraindications to major bone augmentation procedures may
include the placement of short, tilted, palatal positioned, pterygo-maxillary or zygomatic implants.
Tooth-supported fixed restorations or removable dentures should be considered if surgical
procedures as such are contraindicated.
Informed consent should be obtained from each patient based on a risk assessment, and the
clinician should supply explanations about the advantages and disadvantages of the planned
treatment. Two main decisions need to be made for the indications of SFE: 1. timing of implant
placement (simultaneous versus staged approach). Simultaneous implant placement is generally
preferred whenever primary stability can be obtained, reducing the number of surgical procedures
and, hence, morbidity, cost and time. This treatment option is contingent on achieving an ideal
three-dimensional position of the implants from a restorative viewpoint. 2. Grafting protocol
(autogenous bone and/or bone substitute material). Any autogenous bone included in the grafting
protocol will accelerate bone formation compared to protocols using bone substitute materials
alone. Bone substitute materials with a low substitution rate are helpful in maintaining the
augmentation volume.

Marginal bone loss (MBL) in the augmented maxillary sinus

Marginal bone remodeling is defined as the difference in marginal bone level relative to
the bone level at the time of surgery. Peri-implant bone levels can be measured on conventional
periapical, digital periapical and/or panoramic radiographs at the time of implant placement,
loading time, and at any follow-up visits. The measurements are carried out using the threads of
the implants as the internal standard, a technique formally suggested by Haas and associates [648].
A variety of parameters are used to evaluate the health status of dental implants.
Measurement of peri-implant pocket depth and the radiographic controls are important diagnostic
and prognostic procedures that are nowadays standardized in clinical practice [152]. In addition,
to assess peri-implant mucosal health, clinicians use the gingival index (GI), bleeding index (BI),
and the sulcus fluid flow rate (SFFR).

~ 248 ~
 There is insufficient scientific evidence available to establish any theory understanding the
mechanisms of MBL. Different configurations of the implant neck have been suggested to preserve
marginal bone level. The prevalence, incidence, and severity of marginal (crestal) bone loss (MBL)
and peri-implantitis at dental implants were evaluated in a number of clinical studies. In a recent
retrospective study, the mean amount of marginal bone loss occurring in a 5-year period following
loading was 0.2 mm, and the overall mean amount of marginal bone loss during 10 years of
observation is small (0.36 ± 1.4 mm). However, the bone-level reduction is twice as great during
the second five year period as compared to the first 5-year period [648,650].
Progressive bone loss at implants can occur both as an early and as a late complication
during function [650]. In a recent consensus meeting (VIII European Workshop on
Periodontology), it was recommended that for studies on the incidence of peri-implantitis, the
threshold for detectable bone loss at implant sites should be 1-1.5 mm [651,637].
It is currently agreed that most implants demonstrate initial bone loss “to the first thread”,
which is attributed to etiologic factors, including biologic width formation, implant crest module,
the surface characteristics of the implant, and implant-abutment microgaps [652]. This bone loss
can be divided into two different phases. The first is related to the time of implant exposure or
prosthetic connection and can be regarded as ‘early bone loss’. The second is bone loss that occurs
during the time of implant function, and is considered ‘late bone loss’ [415,652-655]. The latter is
believed to be related to an infectious process, i.e., peri-implantitis [448]. However, this “standard
MBL” does not present a risk to implant longevity because of its tendency to stabilize at a certain
level after approximately 12 months [649].
MBL has been associated with occlusal overload, plaque accumulation, smoking,
biocompatibility of transmucosal components, abutment loosening, and biomechanical factors
[649,556,657]. MBL is not related to the amount of preoperative residual bone. It is almost
impossible to isolate the numerous factors that affect MBL around implants [658].
To calculate the marginal bone loss (MBL) around implants placed in the maxillary sinus
grafts, a technique formerly suggested by Haas and associates [648], using the implant threads as
the internal standard is used. Mean values for each measurement are calculated. The number of the
threads not surrounded is counted and the higher number is used to calculate the mesio disto
angular defect. The number of threads not surrounded by bone at implant exposure are subtracted
from the number of threads measured on radiographs (panoramic or intraoral) not surrounded by
bone at the most recent follow-up. To determine the amount of MBL in mm, this result is
multiplied by the implant pitch (in mm). The number of threads is converted to millimeters using
the given millimeter-per-thread information for the implants used. Manufacturers provide
information regarding the pitch of the implant system. These measurements can be either a positive
number (if the crestal bone is coronal to the implants threads), zero (when the crestal bone is
located at the level of the coronal implant threads), or a negative number (if the crestal bone is
located apical to the implants threads). A negative mesio distal peri-implant bone level implies
peri-implant bone loss. A positive mesiodistal implant bone level suggested an increase in crestal
bone levels over time, because the bone continues to remodel throughout the lifetime of the
implant. One to two mm of MBL within the first year of implant restoration and successive annual
mean MBL of 0.2 to 0.5mm during the follow-up period are considered as prerequisites for an
implant to be considered successful [587].
The biological width dimensions appear to be more similar to natural teeth around one-
piece non-submerged implants compared with either two-piece non-submerged or two-piece
submerged implants. A rough surface with microthreads at the implant neck is the most effective

~ 249 ~
design for minimizing marginal bone loss during functional loading [659]. An apical positioning
of dental implants (2mm below the crestal bone) has more influence than a more apically
positioned first bone-to-implant contact [660]. Jung et al. detected minimal crestal bone loss for
implants placed at the crestal bone level or 1 mm above [661].
Although strongly significant, the reason for the MBL differences between systems can be
due to a wide array of subject-related factors such as implant-supporting bone feature (location,
nature, or architecture), microbiologic characteristics, and individual inflammatory profile,
implant-related factors such as surface, macro-, or micro-design, roughness at the cervical portion,
platform switching, and location of the micro-gap [266,662-670]; or surgical-related factors such
as distance between implants and delayed versus immediate placement [658,671,672].
Platform switching is a prosthetic concept accepted in literature that minimizes the post-
restorative peri-implant bone remodeling [673]. Bone resorption is supposed to be strictly
correlated to the so called “biological width re-establishment”, following bacterial invasion of the
implant/abutment interface [674]. This biological process is altered when a wider implant is
restored using a narrower abutment. The horizontal gap resulting from this mismatch seems to
move the infection away from the vital bone, minimizing the effect of “biological width re-
establishment” [675]. Implants placed in sites that receive maxillary sinus augmentation exhibited
more MBL than implants placed in pristine bone [676]. Selecting wider implants reduce peri-
implant bone resorption. The use of the platform switching prosthetic concept may preserved peri-
implant bone from further resorption during the first months of loading [677]. This should
theoretically allow graft material to mature for a longer period.
Smoking and a history of periodontitis negatively influence MBL regardless of the type of
the osseous substrate [676]. Implants with external implant connections are strongly associated
with increased MBL over time [676].
The so called healing adaptation theory or combined factor syndrome attributes crestal
bone loss to a combination of implant factors, clinical handling, and patient factors [678,679].

a b
Fig 4.128a: Panoramic radiographs showing the marginal bone Fig 4.128b: Panoramic radiographs showing the marginal bone
maintenance. loss at site 16 and marginal bone maintenance and site 26.

~ 250 ~
 c d
Fig 4.128c: Panoramic radiographs showing the marginal bone Fig 4.128d: Panoramic radiographs showing the marginal bone
apposition. maintenance.

e f
Fig 4.128e: Panoramic radiographs showing the marginal bone Fig 4.128f: Panoramic radiographs showing the marginal bone
loss. maintenance.

g h
Fig 4.128g: Panoramic radiographs showing the marginal bone. Fig 4.128h: Panoramic radiographs showing papilla like
remodeling of marginal bone.

Apical bone loss (ABL) in the augmented maxillary sinus

It is assumed that after the initial apical bone resorption in augmented maxillary sinus, the
regenerated bone shows the same biological behavior as non-regenerated natural bone and will
remain stable even after 10 years, with only a minimal decrease, comparable with natural bone
resorption [647].
Factors that may influence graft reduction:
 Demographic data (gender, general health, smoking).
 Location (RBH, classification).
 Surgical protocol (simultaneous or delayed implant placement grafting materials).

~ 251 ~
  Complications (membrane perforation, graft migration, sinusitis).
 Implant characteristics (manufacturer, surface, length, width and location).
 Loading protocol.
Bone measurements after implant positioning for the evaluation of alterations in the
augmented bone within maxillary sinuses should be performed from the apex of implants placed
inside the maxillary sinus to the upper-most part of the visible grafted material at two points per
implant.
The length of the implant is used as a reference for measuring bone resorption, which is
expressed as a percentage of the implant length. Grafted bone can be distinguished clearly from
original bone by density and structure. Augmented material should be included in the
measurements only if radiolucency is clearly visible.
Vertical measurements are used to evaluate changes in bone graft height during the follow-
up period and, if detected, whether the reduction in graft height occurred in the initial healing
period or whether it is an ongoing process during the loading time. Maintenance of graft height
should be measured and calculated with the use of a conversion factor that was adjusted for
panoramic radiograph magnification. In each case, the surface of the grafted sinus is marked with
a virtual marking line. Image analysis software can be used to calculate the grafted bone height
changes at the level of implant site by comparing pre-operative and follow-up panoramic
radiographs. In this manner, the intrasinusal peri-implant bone gain is evaluated. The software
calculations have the ability to compensate for eventual radiographic distortion.
Two panoramic radiographs for each graft are used to measure the grafted area. The first
radiograph is taken at implant placement. The second radiograph is taken at the patient's follow-
up visit postoperatively (Fig 4.129a-d). For each patient, the following measurements should be
made on the radiographs:
 The distance between the crestal ridge and the original sinus floor in the area of implants.
 The distance between the original sinus floor and the elevated sinus floor in the area of
implants.
 The distance between the elevated sinus floor and the apex of the implant.

a b
Fig 4.129a: Panoramic radiograph before maxillary sinus floor Fig 4.129b: Panoramic radiograph directly after sinus floor
augmentation augmentation

~ 252 ~
 c d
Fig 4.129c: Panoramic radiograph at the time of implant Fig 4.129d: Panoramic radiograph three year after loading – note
placement. the apical bone remodeling and reshaping.

Dental CT scans can also be obtained to evaluate the reconstruction of the intrasinusal
bone. The most important factors influencing reduction in vertical bone height on the time axis
after sinus augmentation is the grafting material, followed by the presence of a functional implant
[694]. Anorganic bovine bone was found to be superior in graft height maintenance in up to 10
years’ follow up [680]. Dimensional change of the bone grafts was also evaluated, with a mean
decrease of 1.4mm (< 10%) in the height of the bone grafts after 1 year. New bone formation is
best evaluated by histomorphometry [681], while volumetric changes over time can be assessed
using three-dimensional (3D) imaging, i.e., computed tomography (CT) or cone beam computed
tomography (CBCT) [682,683].
Volume changes in sinus augmentations occur as the result of graft consolidation i.e., a
discrepancy between the rate of graft resorption and host bone regeneration and sinus
pneumatization [684]. Progressive pneumatization occurs after augmentation and apical bone level
(ABL) significantly decreases during the first 2-3 years after augmentation, but subsequent
changes are minimal in the following years. Knowledge of these changes can assist in clinical
decision making via (1) preoperative estimation of the required graft volume and appropriate
selection of graft material(s) and/or autologous donor site [682,685,686]; (2) intraoperative use of
an adequate quantity of graft material that accounts for any anticipated remodeling/resorption
[687]; and (3) ensuring postoperative maintenance of bone around single-stage implants, or
formation of adequate bone for stage-two implant placement [109,688,689] (Fig 4.130a-c –
4.132a,b).

a b
Fig 4.130a: Panoramic radiograph before maxillary sinus Fig 4.130b: Panoramic radiograph directly after sinus floor
floor augmentation. augmentation.

~ 253 ~
 c Fig 4.130c: Panoramic radiograph three years after
loading – note the apical bone remodeling and reshaping.

a b
Fig 4.131a: Panoramic radiograph showing apical bone loss at Fig 4.131b: Panoramic radiograph showing resorption and
site 25, 26. repneumatization at site 26.

c d
Fig 4.131c: Panoramic radiograph showing over augmented Fig 4.131d: Panoramic radiograph showing apical bone loss
sinus. obviously developing along the implant length.

e f
Fig 4.1301: Panoramic radiographs showing moderate apical Fig 4.131f: Panoramic radiographs showing moderate apical
bone maintenance. bone maintenance.

~ 254 ~
 a b
Fig 4.132a: Panoramic radiographs showing severe apical bone Fig 4.132b: Panoramic radiographs showing severe apical bone
loss due to repneumatization of extended sinuses. loss – note the over-pneumatized sinus.

Regardless of the material used for grafting, the quality of native bone around the atrophic
sinus plays an important role on the osteogenesis process [690]. Grafted bone can be clearly
distinguished from original bone by density and structure. Several factors are likely to influence
the resorption rate of the grafting materials including: preoperative bone height, surgical technique,
compression, stability and resorptive patterns of the grafting material, composition of the graft,
bone or bone substitute, as well as air pressure. Block et al. found no significant correlation
between resorption, native bone height and amount of augmented bone height [691]. Hatano et al.
suggested that implant loading promotes osteogenesis in the long term [692]. Implant loading may
exert a stabilizing effect on the maintenance of bone graft [692]. Studies have suggested that
dimensional height reductions of autogenous or composite sinus grafts of approximately 20%
occur primarily during the initial postoperative phase (up to two years), with little or no change in
subsequent years [317,692,693].
The current evidence does not indicate whether volume loss is a continuous phenomenon
or whether it is limited to the initial postoperative period. Nevertheless, “overaugmentation” of
the sinus floor, regardless of the choice of graft material, may be beneficial to compensate for
expected volume reduction [694]. When autografts or demineralized allografts are utilized, there
is a tendency for both a volumetric resorption in the order of 25% and a transformation of the
graft density towards that which would normally be found in the posterior maxilla. The result is
an implant receptor site with a typical type 3 or 4 bone density. These volume reductions do not
adversely influence implant survival. It is unclear whether simultaneous implant placement
contributes to longer volume loss or better stability of sinus augmentation compared to a staged
procedure [694] (Fig 4.133a,b).

a b
Fig 4.133a: Panoramic radiographs showing apical bone Fig 4.133a: Panoramic radiographs showing apical bone
shrinkage. reshaping due to repneumatization (slumping).

~ 255 ~
 a b
Fig 4.134a,b: CT radiographs showing apical bone loss due to repneumatization.

Bone grafting materials (BGM)

Modern bone tissue engineering techniques aim to obtain a bone substitute with ideal
structural and biological properties. Biologically, this material should have the same features of
autogenous bone, such as osteogenic, osteoconductive, and even osteoinductive properties
[695,696]. The evidence regarding bone grafting materials now appears to be quite clear. A
structured, unbiased evaluation of sinus grafting materials may be found in published evidence-
based reviews. The reviews select studies to obtain a larger database and thereby achieve more
statistical power. The Sinus Lift Consensus Conference of 1996 [489] reported on the results
obtained by experienced clinicians, and while accurate, is somewhat dated due to the dramatic
increase in published reports on various grafting procedures since 1996. More recently, several
exhaustive evidence-based literature reviews were conducted [597,605,613]. This chapter will rely
heavily on the results from these evidence-based reviews. It is noteworthy to mention that
observations of several animal studies indicate that the amount of bone formation following
maxillary sinus floor grafting may be due in part to the intrinsic capacity of the surgical procedure
and subsequent implant loading and not to the load-bearing capacity of the sinus-grafted bone.
A variety of grafting materials, either alone or in combination, have been validated for
effective use in sinus augmentation: autogenous (AB) (e.g. iliac crest, chin, ramus); allogenic bone
(from other human donors); xenogenic bone (e.g., deproteinized bovine bone mineral [DBBM]);
and alloplastic materials (e.g., hydroxyapatite [HA] and beta tricalcium phosphate [β-TCP]).
Recently, the successful use of cultured mesenchymal stem cells (MSCs) or uncultured tissues
containing MSCs (e.g. bone marrow) for sinus augmentation has also been reported [697].
Autogenous bone was the first grafting material utilized to augment the maxillary sinus.
The list of bone grafting materials (BGMs) utilized to augment or replace sinus autogenous bone
is continuously expanding. While results with all of these BGMs have been published in the
literature, xenografts have by far been the most widely studied. Preoperative knowledge of the
sinus augmentation size may minimize potential intraoperative complications at donor sites and
can also be used to estimate the costs of additional materials used [698,699,700]. Several histologic
long-term studies have shown that inorganic particles may be present even more than 10 years
after the grafting procedure [701]. This confirms the view that a complete substitution of the graft
material by newly formed bone is not necessary for a successful augmentation procedure. If graft
particles become well-integrated and do not cause any damage or adverse reaction, they can remain
in place and maintain their support function. The question is whether graft particles function as
native bone in term of osseointegration i.e. BIC. Point counting as a method of estimating the
fraction of total surface area in contact with implant surface was established by Bellhouse and has

~ 256 ~
been used by numerous authors in the literature who have analyzed similar histological samples to
determine the functions of BGMs in term of osseointegration [702,703].

Autogenous bone (AB)

Autogenous bone (AB) is considered ‘the gold standard’ for augmentation of the sinus
floor. The original protocol as described by Boyne [351], and subsequently used by many other
clinicians for this procedure, utilized 100% autogenous bone harvested from the ilium as the
grafting material [309,588-591, 704, 705]. This was a logical choice as autogenous bone contains
all the elements necessary to promote vital bone formation, namely minerals, collagen matrix,
viable cells, growth factors and BMP. Autogenous grafts, therefore, can be both osteoinductive
and osteoconductive. Furthermore, iliac grafts have had a history of successful utilization for ridge
augmentation procedures and were preferred for their highly cellular composition. Iliac autografts
are utilized both in block form with simultaneous implant placement and in particulate form with
simultaneous or delayed placement, depending upon the ability to achieve primary implant
stability in the residual crestal bone.
Other sources for autogenous bone include, extraorally, the tibia and cranium, and
intraorally, the ramus, symphysis, and maxillary tuberosity. Of these, the tibial grafts have a high
cancellous content, whereas the ramus and symphysis contain mostly cortical bone. Autologous
cortical bone from the anterior maxillary wall, the zygomaticomaxillary buttress and the maxillary
tuberosity can be harvested with a bone scraper to reduce lateral bone thickness, allowing an easy
access to the sinus membrane. Vital bone formation in sinuses grafted with 100% autogenous bone
occurs more rapidly [706-708] and to a greater extent than it does when BGMs are utilized [709].
While the percentage of vital bone found in sinuses grafted with autogenous bone is greater than
that seen with BGMs at an early time period, studies show that bone formation with BGMs is equal
to that of bone formation with autogenous bone over time [709].
The utilization of autogenous bone as a graft material has certain disadvantages. Using a
100% autogenous bone graft requires a second surgical site (intraoral) or possible hospitalization
(extraoral), thereby increasing the length of time of the surgical intervention, the surgical risk, and
the postsurgical morbidity. Furthermore, clinicians have reported a greater than average degree of
graft resorption when using iliac grafts [489, 710, 711]. The Sinus Consensus Conference of 1996
reported a difference of 84.6% and 92.6% between implant survival rates in block grafts and in
particulate autogenous grafts respectively, at three years [489]. In one review, the survival rate for
implants placed in sinuses grafted with the block grafting technique was found to be 83.3% [597].
This must be compared with the 92.3% survival rate for implants placed in all types of particulate
grafts (both autogenous grafts and BGMs) and the overall lateral window implant survival rate of
91.8%. Another review reports an 87.7% survival rate for implants placed in 100% autogenous
grafts of all categories [613]. Explanations for the lower survival rate for implants placed in block
grafts may include a demanding surgical procedure that requires stabilization of the block as well
as the implants, the tendency of block grafts to resorb, low mineralized tissue in the matured graft
and the implant surface characteristics.
Two consensus statements from the 1996 Sinus Consensus Conference maintained that
autogenous bone was appropriate for sinus grafting and that allografts, alloplasts, and xenografts
alone, or in combination, may be effective in selected clinical situations [489]. The rationale for
this statement was not the poor performance of BGMs, except for demineralized freeze-dried bone
allograft (DFDBA), but the limited data that was available at that time.

~ 257 ~
 Over the past 19 years, that evidence has been forthcoming. It has been suggested that
autogenous bone grafts be used for extensive osseous reconstruction and that, in the case of sinus
grafting, non-resorbable or slowly resorped material be added to prevent sinus pneumatization
[712]. Particulate bone from either the iliac crest or the chin when used in sinus augmentation
procedures seems to remodel around the apical portion of implants and cause bulging of implants
within the sinus cavity. The use of autogenous bone blocks in sinus lifts may be a better option in
terms of implant success and graft stability [713]. A previous histomorphometric meta-analysis
considered block AB superior to particulate grafts in terms of new bone formation after sinus
augmentation [714]. Long-term volumetric stability and rapid new bone formation are both
desirable properties of bone grafting materials. Although AB is considered the gold standard
biomaterial for bone augmentation, it has previously been reported that resorption of AB in grafted
sinuses is unpredictable and could potentially complicate two-stage implant placement [317].
Therefore, the use of some bone substitute (BS) materials has been recommended, either alone or
in combination with AB, to provide volumetric stability [680,715]. According to Sbordone et al.,
the behavior of autologous bone from the chin is similar to that of xenogeneic material, probably
because of the dense cortical composition of such grafts [716]. Society would gain a lot from
alternative treatment modalities that do not require hip surgery, provided that the end result is
comparable or adequate [717].
Harvesting AB from intraoral sites can be associated with a number of problems like
devitalization of anterior mandibular teeth by involvement of tooth apices, changes in facial
esthetics, possible damage to the mental and lower dental nerve, and increased risk of mandibular
ramus fracture when an intraoral donor site is chosen [718]. Bone harvested from extraoral sites
may cause hemorrhage, instability of the sacro-iliac joint, hernia through the donor site, adynamic
ileum, or gait disturbances [700]. As a consequence, the use of AB for sinus floor augmentation
has been questioned [707]. Using AB will not protect patients from developing sinusitis or graft
loss. Resorption rates are not of concern and shouldn’t prompt the clinician to prefer or abandon
AB. The healing period length of the graft material could not be identified as a reason to prefer
AB over bone substitute. The aspect of AB harvesting costs cannot be ignored in sinus floor
augmentation procedures compared with BGM’s.

Allograft
DFDBA has a long and successful history of use as a grafting material in periodontal
defects. However, the utilization of DFDBA as a sinus grafting material, has not demonstrated this
level of success. Results from the Sinus Consensus Conference show poor results, as evidenced by
lower implant survival rates when used alone (85%) or in combination with autografts and
xenografts (82% and 80%, respectively) [490]. A histological report from Jensen et al. and a
clinical report demonstrate both poor-quality bone formation and a relatively low implant survival
rate (80%) [634,718]. If the expected result of sinus grafting is to create a mineralized, stable
implant receptor site, a non-mineralized graft material that is susceptible to re-pneumatization has
been shown to be a less than ideal choice. Turnover of this graft material to vital bone proceeds
slowly, as non-vital remineralization precedes vital bone formation.
Studies with mineralized allografts are more limited in nature. One would expect that
results with an allograft that retained its mineral content and human bone microstructure would be
far superior to that of a demineralized allograft. A randomized controlled trial [719] compared the
mineralized cancellous bone allograft (MCBA), Puros, to a known xenograft standard, DBBM, in
13 bilateral cases. Results showed a higher average percentage of vital bone with the allograft

~ 258 ~
(28.25% vs. 12.44%) accompanied by a lower percentage of residual graft material (7.65% vs.
33%). Allogeneic bone material has an osteoinductive potential because of the bone
morphogenetic protein (BMPs) released from the bone during the demineralization process [720].

Xenografts
The bone substitute (BS) material most frequently reported across studies is DBBM, used
either alone or in combination with other materials such as AB, allograft, bone marrow, or cultured
MSCs. Of all the investigated bone grafting materials, the results for xenografts are the most
complete and best documented. For some BS, such as DBBM and biphasic calcium phosphate
(BCP), the addition of other materials does not influence their volume stability when used for sinus
augmentation. Composites of DBBM with allogeneic bone (1:1) or cultured MSCs results in
comparatively greater average volume reduction (~40%) after one year. In the Wallace review,
which include 34 lateral window studies, 11 used xenografts [597]. The xenografts in this review
consist of deproteinized (anorganic) bovine bone. They were utilized alone, as part of a composite
graft with autogenous bone, hydrated with venous blood, or mixed with PRP. The survival rate for
implants utilizing xenografts is statistically the same as for implants placed in particulate
autogenous bone grafts [597]. The Del Fabbro review is more specific in his study of bone grafting
materials [613]. The most recent review reported implant survival rates in 100% autograft,
composite grafts with autogenous bone, 100% alloplast, 100% allograft, and 100% xenograft to
be 88%, 92%, 81%, 93.3% and 95.6% respectively [717].
Comparative studies show higher implant survival rates for 100% xenografts than for 100%
autogenous bone or composite grafts of xenograft and autogenous bone [598, 704, 721].
Additional studies not included in the reviews have presented histologic and histomorphometric
data demonstrating the extent of vital bone production with xenografts, alone or in combination,
at varying time intervals. The data are quite positive when compared with results achieved with
the ‘gold standard’ of autogenous bone. In light of the evidence, the efficacy of xenografts as a
BGM for sinus augmentation surgery cannot be ignored. As this bone substitute now enjoys
widespread use, an understanding of its efficacy and safety is essential.
The efficacy of xenografts as a sinus bone replacement graft may be due to a combination
of factors. Foremost would be the osteoconductive capacity of xenografts. In addition, they supply
minerals that are necessary for bone formation, their density provides stability to the graft and the
implants placed in them, and this density persists long term due to the fact that these grafts do not
completely resorb. In fact, remodeling around retained DBBM particles continue at 6 and 12
months [708, 709], 20 months and 7 years [722] and 9 years [723]. The osteoconductive properties
of xenografts in human sinus grafting have been well documented and are well demonstrated
histologically [708, 709, 722, 723]. They are due to both their chemical composition and their
macro- and micro-morphology. Histologic sections of sinus graft cores from the Froum studies
reveal bone apposition directly on the surface of xenograft particles [709]. Vital bone ‘bridging’
of the gaps between xenograft particles has also been seen. Transmission electron microscopy from
the Orsini [722] and Traini [723] studies demonstrate that the electron-dense layer present at the
bone-DBBM interface at an early time interval of 20 months was replaced with a direct contact,
appearing as an in-growth of bone into the DBBM structure at 7 years. Similar transmission
electron microscopy and histology at 9 years show this continued direct contact and biologic
incorporation of the DBBM with the host vital bone. This indicates that the peri-implant support
resulting from these grafts of 100% DBBM is both biologically acceptable and provides long-term
stability.

~ 259 ~
 Minimal re-pneumatization (slumping) is evidenced with xenografts when compared with
autografts and allografts in 3-year panoramic radiograph follow-ups according to the Consensus
Conference [9]. The fact that xenografts do not completely resorb, coupled with the fact that
histology of sinus explants indicates that the xenograft never contacts the implant surface and
therefore does not interfere with osseointegration, results in an implant bed that is significantly
denser than is found after the use of either autogenous bone or resorbable graft materials [724,
725]. Histomorphometric studies all show percentages of vital bone, connective tissue and residual
xenograft to be in the order of 25%, 50% and 25% respectively at a time interval of 6 to 12 months
after grafting [708, 709, 726, 727]. Due to the presence of this residual 25% xenograft volume, a
matured graft that is classified as type 3 or 4 by nature of its vital bone content functions like type
2 density bone.
However, bone substitute materials with a low substitution rate, are helpful in maintaining
the volume of augmentation. Hallman et al. stated that after 24 months, <10% volume change was
observed if bovine bone mineral was used [598]. The resistance against resorption can have a
variety of advantages. In sinus floor elevation, additional bone in the sinus cavity can enable a
later additional implant placement or in case of an implant failure a new implant with a larger
diameter can be performed without additional sinus grafting. Samples show that bovine bone
mineral is still present throughout the augmentation area, and that the augmented volume is still
maintained over a span of over 10 years, slowing the natural resorption of the alveolar process.
However, the total volume occupied by bovine bone mineral particles decreases significantly over
time, meaning that bovine bone mineral is incorporated into the natural remodeling process.
The advantages of xenografts are the following: no additional surgical site for bone
harvesting, reducing surgical time, lower resorption rates and lower costs [728]. Chackarchi et al.
concluded that there is no clinical or histological difference between using large (1-2 mm) or small
(0.25-1 mm) bovine bone mineral particles (BBM) for sinus floor augmentation procedures [729].
Both sizes of BBM granules reform equally well and achieve the aim of the sinus floor
augmentation procedure, insertion of implants of 10mm or longer with high primary fixation. The
selection of small or large BBM particles should be dependent on the personal preference of the
surgeon, sinus anatomy or the presence of membrane rupture. Bone substitutes can be used as a
replacement for autogenous bone grafts [730]. Grafting of the maxillary sinus with 100% DBBM
allows successful implant placement in the posterior maxilla [613,689,708,727]. The bone at the
time of implant insertion is of high density and adequate vascularity. This suggests that DBBM
can be used without additional autogenous bone or other grafting materials in maxillary sinus sites
with minimal bone height, provided that sufficient time is allowed for graft maturation and
regeneration of new bone [731]. The slumping of the graft material and the resulting loss of vertical
bone height as seen in autogenous bone-grafted sinuses does not occur with DBBM [732,733,734].
DBBM resorbs considerably slower that other materials [731,725,736]. The main concern with
using 100% DBBM in maxillary sinus floor elevation is the efficacy of its osteoconductive
properties. The relatively large volume may inhibit the osteoconductive properties of DBBM as
angiogenesis needs to traverse a much larger area [737]. Shorter bucco-palatal distances of the
maxillary sinus showed higher degrees of bone formation after six months of healing in sinuses
augmented with 100% allografts [738]. The amount of new regenerated tissue is not only time
dependent but also dependent on the augmentation location and depth [615, 630].
There is a controversy in the literature as to whether DBBM is resorbable or not. Several
authors have observed signs of resorption, i.e. the presence of osteoclasts on the particle surface
[616,707.725,732,733]. Other authors have claimed that DBBM particles are probably non-

~ 260 ~
resorbable [739-742]. Mordenfeld confirmed the presence of non-resorbed intact DBBM particles
11 years after maxillary sinus augmentation [743]. A case report demonstrated slow replacement
of the DBBM particles by newly formed bone, even with the addition of plasma-rich growth factors
[744].

Alloplasts
Beta tricalcium phosphate (β-TCP) and hydroxyapatite (HA) are widely used alloplastic
grafting materials. β-TCP is one of the most popular bone substitutes for bone augmentation [745].
In a previous report, Zerbo et al. reported molecular mechanisms of bone formation associated
with β-TCP and revealed the biological traits of β-TCP [746]. The augmentations performed with
β-TCP follows a certain philosophy in that β-TCP only occupies the space in which bone should
be regenerated. This material acts as an osteoconductive material, allowing osteoprogenitor cells
to grow over bone surface or into its pores, differentiate into osteoblasts, and induced bone
deposition [184]. Histological analysis has shown that the material is continually resorbed within
several years [614]. Clinical studies have shown that β-TCP is a suitable bone substitute material,
showing no significant difference from autogenous bone after six months [747]. Also, a recent
Cochrane review has stated that the data support both the use of bovine bone mineral and Cerasorb,
a pure-phase β-TCP [748]. Looking at implant survival rates, no statistically significant difference
could be observed between the two materials. However Artzi et al. have shown that in terms of
new bone formation, bovine bone mineral is superior to β-TCP in sinus grafting procedures using
the lateral approach [749].
Rapid revascularization and complete resorption of grafting material may not ultimately
serve their long-term goals, especially in certain augmentation cases, such as maxillary sinus
grafting [749]. In more demanding defect morphologies, such as lateral and vertical alveolar ridge
deficiencies, where the bone healing only takes place from the floor of the defect, β-TCP degrades
too fast to retain sufficient support for ideal bone formation [750]. Zerbo et al. reported that in
sinus floor elevation, the first few β-TCP particles, laying directly over the residual or original
bone of the maxilla, were often partially or even completely replaced by bone after 6 months [751].
A synthetic, resorbable, osteoconductive, alloplastic bioglass (BG), composed by two
different bioactive calcium phosphosilicate-like crystals (BG) has been developed as a bone
grafting material. The major component of this material is a melt-derived calcium phosphorus
sodium silicate, designed specifically for its absorbability and osteoconductive nature. The second
component of this material is a calcium-phosphorus silicate bioactive glass, chemically similar to
the major component, but derived via a solution-gelation (sol-gel) process. The sol-gel component
allows a more quickly absorption than the standard melt-derived component [752], thus opening
additional space between graft particles for tissue infiltration and eventually host bone [753]. This
material has been shown to accelerate osteogenic activity and early alkaline phosphatase
expression in vitro [754]. In addition, because it is naturally resorbed, a subsequent release of
calcium and phosphate ions occurs, which could stimulate osteoblast differentiation [755].

Composite graft materials

The composite graft combines the advantages of each material alone and reduces the
disadvantages of each when used separately. A biphasic hydroxyapatite/β-tricalcium phosphate
(HA/TCP) biphasic calcium phosphate (BCP) is a new bone graft substitute produced by a single
process to prevent clustering and to establish a new homogeneous molecule. Its 60:40 ratio of

~ 261 ~
HA/TCP gives it two phases of activity. HA/TCP is recognized as an osteoconductive and
bioactive material. The main advantage is that it is an excellent cell carrier of mesenchymal stem
cells to promote bone formation [756,757,758]. It has been claimed that an optimum balance of
the stable phase of HA and the soluble phase of TCP could increase new bone formation, as it
releases calcium and phosphate ions into the biological medium [759]. According to Artzi et al.,
particle area fraction is similar to that of other materials, i.e., alloplasts and xenografts, which have
been evaluated [637,760]. The rapid resorption of β-TCP [761,762] allows bone cell colonization
and the creation of space for the newly formed bone, while HA, which resorbs more slowly [763]
forms the scaffold required to maintain the obtained volume throughout the period of new bone
formation and remodeling [764]. The remaining particles of BCP are fully integrated into the
newly formed bone network [762]. Therefore, the partially resorbed BCP is replaced by lamellar
bone [765], which distinguished the mature bone from the less mature areas. Composite grafts of
β-TCP and autogenous bone demonstrate better bone formation. The small fraction of particular
autogenous bone could play an important role in the temporal course of regeneration through its
osteoinductive properties, meaning that it leads to a better initial bone formation. Any autogenous
bone included in the grafting protocol will accelerate bone formation compared to protocols using
bone substitute materials alone.

Plasma rich growth factors (PRGF)

PRGF is an autologous plasma product rich in platelets which, after activation with
calcium, enables the local release of multiple growth factors and bioactive proteins that modulate
the processes of wound healing and tissue engineering [766,767]. The preparation of rich in growth
factors (PRGF) is an optimized platelet-rich product [766,767]. PRGF is a 100% autologous
product that it is easily and rapidly obtained from patient’s blood, and because the donor and
receptor are the same, the immunological concerns are circumvented. The rationale for using
PRGF is that it provides a natural source of proteins such as fibrinogen, fibronectin and vitronectin,
and growth factors including platelet-derived growth factor, transforming growth factor-β,
vascular endothelial growth factor, insulin-like growth factor, hepatocyte growth factor,
angiopoietin, platelet factor-4, and thrombospondin among others to the local milieu, facilitating
the tissue regeneration mechanism [637]. Liquid PRGF can be used as a culture medium to
maintain the viability and functional properties of autologous bone [768], i.e., the original bone
window of the sinus. The use of platelet-derived growth factors could allow significant reduction
of the total treatment time.
Anitua el al. reported that significantly higher values of bone density were obtained when
PRGF and ABBM were used when compared with sinuses grafted with ABBM alone [769].
The use of particulate xenograft combined with an autogenous blood derivative rich in
growth factors presents a graft combination for sinus augmentation procedures that can provide
accelerated vascularization, improved soft tissue healing, less postoperative morbidity, and
enhanced bone regeneration [770].

Guidelines for choosing the proper grafting material

Histomorphometric analysis has shown that increasing amounts of DBBM results in
decreasing percentages of bone-to-implant contact [771], suggesting that the addition of AB may
be important for procedure optimization in terms of histological outcomes. In a recent meta-
analysis of histomorphometric new bone over total area (NBF) after sinus augmentation in

~ 262 ~
humans, AB yielded the highest NBF (63%) after 4.5 to 9 months of healing compared to all other
BS (allograft, xenograft, alloplast) and composite graft materials [772]. In addition, AB particulate
was reported to negatively influence NBF compared to the block form [714].
Jensen et al. concluded that bone-to-implant contact is significantly increased with
autogenous bone or DBBM mixed with autogenous bone in different ratios as compared to DBBM
alone [771]. Furthermore, early bone-to-implant contact formation adjacent to the implant surface
is more advanced with autogenous bone. Mixture of autogenous bone and DBBM should be used
as graft material for the maxillary sinus floor augmentation to diminish the graft resorption and to
increase bone-implant contact formation [687,771]. A major drawback of alloplastic and
xenogenic bone graft materials is the lack of osteoinductivity and the subsequent long healing time
before implant placement [773]. Furthermore, they are not very suitable as exclusive material for
large reconstructions [774,775]. Two important factors that may assist in clinical decision making
regarding the choice of biomaterial are (1) time-dependent “new” bone formation achieved at the
augmented site and (2) time-dependent volumetric stability of the graft.

~ 263 ~
 5. COMPLICATIONS IN LATERAL WINDOW SINUS FLOOR AUGMENTATION
SURGERY

Sinus augmentation is generally considered to be a safe surgical procedure with a low

prevalence of complications [35]. However, all surgical procedures have the potential to develop
complications, leading to additional surgery, prolonged hospital recovery, fatigue, and nutritional
disorders, which markedly compromise quality of life [37,776,777]. Complications may occur as
a consequence of inadequate surgical planning or aggressive surgical maneuvers [778].
Complications of maxillary sinus augmentation procedures may jeopardize the final
outcomes of bone grafting and implant placement. By making the appropriate evidence-based
decisions regarding grafting materials, implant surfaces surgical techniques, and the use of barrier
membranes over the lateral window, implant survival rates should exceed 95%. Complications
associated with these procedures are infrequent and those that occur during and after sinus grafting
procedures are for the most part localized and readily remedied [35, 19,779,780]. This chapter will
discuss the major intraoperative and postoperative complications and present recommended
prevention and treatment options. The most important method to avoid complications is to be
familiar with maxillary sinus anatomy and possible anatomical variations [46]. In addition to
internal sinus structures and adjacent vessels, the morphology of the maxillary sinus itself has been
shown to link strongly to the surgical complications [27, 781].
To minimize complications, training, medical status, risk factor analysis, piezo
instruments, composite grafts, cooperation and referral team work are recommended. It is critical
for a clinician to diagnose and treat any complications associated with sinus augmentation, since
improper management may bring patient discomfort, compromise bone healing, and prolong the
treatment time [782].

Intraoperative complications
Intraoperative complications are primarily the result of surgical difficulties encountered
during the course of the procedure. These may be the result of the presence of complex anatomic
situations (thin membranes, septa, arteries, thick or convex lateral walls), the choice of less
predictable treatment options, inadequate systemic or local diagnosis, or operator error. The most
common intraoperative complication is Schneiderian membrane perforation. Other complications
include possible excessive intraoperative bleeding, perforations in the buccal flap, and, much less
frequently, injury to the infraorbital nerve.

Schneiderian membrane perforation

Irrespective of the technique used, sinus augmentation is a technique-sensitive procedure
in which there is always the risk of sinus membrane perforation, which can be observed in 7% to
56% of the interventions, but does not seem to influence implant survival [744,783,784].
According to the literature, membrane perforation are associated with greater postoperative
complications, such as acute or chronic sinus infection, bacterial invasion, swelling, bleeding,
wound dehiscence, loss of graft material, and disruption of normal sinus physiologic function.
Most experienced clinicians estimate their perforation rate to be approximately 25%. A higher
perforation rate was observed in the following cases: when the membrane thickness was less than
1.5mm, an abnormal morphology of the maxillary sinus and septa or sharp angles, small residual
bone height, a ridge line, septa, spines, the anterior part of the sinus was narrow and the angle

~ 264 ~
between the medial wall and the lateral wall was less than 30° and smokers. The use of
piezosurgery in those cases has resulted in decreased membrane perforation rates [638]. Membrane
perforation may also disrupt physiologic sinus function, and subsequently lead to postsurgical
sinusitis including sinus congestion, and may threaten the graft as well as implant survival
[115,785,786].
However, data from clinical studies are in conflict with regards to the impact of membrane
perforation on implant survival or success rates. No significant difference was reported by number
of clinicians [644,781,783,786-788], whereas others reported lower implant success/survival rates
in the case of sinus floor elevation with a perforated membrane [589,789]. One study also reported
an inverse correlation between the extent of membrane perforation and the survival rate of
simultaneously placed dental implants [785] (Fig 5.1). Another survey reported no statistically
significant difference in peri-implant bone and soft tissue conditions for implants placed in sites
with or without membrane perforation during sinus floor elevation [790]. Some studies have
identified additional possible risk factors for membrane perforation: residual ridge height
[783,788], membrane thickness [783,788], gingival phenotype [788], hand instrumentation [791],
rotary instruments [792, 793], the presence of sinus septa [790] and overfilling with the graft
material. However, none of these studies has evaluated multiple risk factors for sinus membrane
perforation (Fig 5.1).

Fig 5.1: Assorted perforations of the maxillary sinus membrane. Perforations were covered with either a non-stabilized soft
repair membrane or a resorbable collagen membrane.

~ 265 ~
 Anatomical and technical factors implicating SMP
Possible potential risk factors for perforation of the sinus membrane were grouped into
patient-related, surgery-related, and maxillary sinus-related factors [772].

Patient-related factors
Patient-related factors include smoking, gender, and age. In smokers, the sinus membrane
may appear atrophic and extremely thin, fragile to touch, and prone to tearing [510]. Other patient
related factors, such as general medical condition and alcohol consumption, were not investigated.
Regarding gender, perforation rate of 26.5% in women and 11.9% in men was reported [775].
Recent CBCT studies assessing the thickness of the sinus membrane report significantly thinner
membranes in women thus explaining a possible gender effect [795, 796]. Becker et al. reported a
mean age of 55 years in cases with membrane perforation, versus a mean age of 56 years in cases
without perforation [787].

Surgery-related factors
Surgery-related factors consist of the type of surgical approach (simultaneous or staged
implant placement), side (left or right), number of tooth units (single or multiple), sites of treatment
(premolar, molar, or mixed) and technique of osteotomy (diamond bur, piezosurgery, or
combined). Regarding the surgical approach, simultaneous sinus floor elevation has a perforation
rate of 32%, compared to 18.5% for the staged approach [794]. Conflicting results were reported
by Becker et al. who observed more frequent membrane perforation with the staged approach
(25.7%) than with the simultaneous approach (13%) [787].
Differences in membrane perforation rates regarding right and left side, single versus
multiple unites, or location (premolar, molar, or mixed of sinus floor elevation) has not been
evaluated in clinical studies [792]. Regarding the osteotomy technique, Barone et al. assessed the
bone preparation technique on a 13 patient sample. In sites treated with piezosurgery, four
perforations (30.7%) were noted, and in sites treated with diamond burs, three perforations
occurred (23%) [792]. The difference was not statistically significant. In similar randomized
clinical trial, no difference was demonstrated between piezoelectric and rotary instruments for
lateral window preparation [639].
Wallace et al. reported a rate of 7% for membrane perforation. However, all perforation occurred
while using hand instrumentation [638]. A very low rate (3.8%) of membrane perforation when
piezosurgery was used was also reported by Blus et al. [797]. Thomas von Arx concluded that the
use of a piezoelectric device for sinus floor elevation reduced the frequency of membrane
perforation among surgeons with limited experience.

Maxillary sinus-related factors

Maxillary sinus-related factors include the presence and height of septa, spines, exostosis
residual ridge height, thickness of lateral sinus wall, width of antrum, and thickness and status
(healthy versus mucosal thickening) of the sinus membrane. Implant survival rates are not
distinctly different between the perforated and non-perforated. The frequencies of anatomical
abnormalities of the Schneiderian membrane disposed for perforation are listed in (Fig 5.2).

~ 266 ~
 Scars adhesion septum
previous operation Cyst Thin membrane
18%
5%
24%
29% 24%

18% 11%
Fig 5.2: Frequencies of anatomical abnormalities of the Schneiderian membrane.

a b
Fig 5.3a: Clinical view of a thin sinus membrane. Fig 5.3b: Perforation of the membrane during elevation.

More variation of the maxillary sinus septa are described in the literature, such as the partial
perpendicular septa, the partial horizontal septa, and the complete septation of the maxillary sinus
by a complete vertical septum.
The presence of septa can complicate the creation of the bony window in the lateral wall
and increase the risk of tearing the sinus membrane during its elevation. Thus, it is important to
analyze these septa on CT scans prior to surgery. Regular radiographs (panoramic or periapical)
might not show septa or might falsely suggest that these formations are a pathologic condition.
Sinuses with septa have a nearly 20% higher rate of membrane perforation (42.9%)
compared to sinus without septa (23.8%). Apparently, not only the presence of septa but also the
height of septa may influence the risk of membrane perforation. Schwartz-Arad el al. found that a
sinus with septa had a 52% chance of membrane perforation, whereas the perforation rate was
lower (42%) in sinuses without septa [640]. Malkinson and Irinkis reported membrane perforation
rates of 13.3% in subjects with septa in the area of surgery and 10.8% in cases without septa [793].

A minimum height of the residual ridge may tend to increase the risk of membrane
perforation. Ardekian et al. [783] concluded that in sites with three mm of residual ridge height,
perforation of the sinus membrane occurred 85% of the time, whereas in sites with six mm, the
perforation rate was only 25%. In another study with a 17% rate of membrane perforation, 10 of
11 perforations occurred in cases in which the residual ridge height was < 3.5 mm [788]. Yilmaz
and Tozum found a significant correlation between sinus membrane perforation and sinus
membrane <1 mm [788]. A thin sinus membrane may not withstand the force of elevation,
particularly when hand instruments are used. A recent CBCT study found that sinus membrane

~ 267 ~
thickness was correlated with presence of septa [796]. However, further data are needed to draw
any conclusions regarding perforation risk and the thickness as well as the shape of sinus
membrane. No correlation was found between the rate of sinus membrane perforation and a history
of clinical and/or radiographic signs associated with sinus pathosis [794]. The lateral wall
thickness does not influence the rate of membrane perforation [794]. Neiva et al. [25] evaluated
lateral wall thickness in cadavers and found that younger individuals present with thicker lateral
wall because of less pneumatization of the maxillary sinus. The angulation between the medial and
lateral walls of the maxillary sinus appears to influence the incidence of membrane perforation
during sinus floor elevation. Cho et al. reported perforation rates of 37.5% in subjects with an
angle <30 degrees, 28.6% for an angle of 30 to 60 degrees, and 0% in subjects with angle >60
degrees [781]. The perforation rate increases as the angle decreases, i.e., the narrower the sinus,
the greater the risk of membrane perforation [781]. However, no such correlation was observed by
van Arx when the width of the antrum was measured 5 mm above the lowest point of the maxillary
sinus [794]. Sharper angels that are often observed at second premolar sites are at a higher risk of
membrane perforation [27]. Similarly, the width of the sinus mediolaterally may determine the
easiness of performing a sinus lifting procedure, which might be associated with the incidence of
intra-operative complications. The mediolateral dimension of the maxillary sinus can be difficult
for sinus lifting procedures if it is too big or small. The angle of the buccolingual maxillary sinus
wall has been proposed as a factor to determine the likelihood of sinus perforation [27]. Another
study found that sharp angels were most commonly found in second premolar sites, with an
average 36.3˚, while in first and second molars, the mean angels were 58.2˚ and 47.7˚, respectively
[27]. It was concluded that sinus membrane elevation might be more challenging in second
premolar area.
Van Arx et al. failed to demonstrate statistically significant differences in the rate of
membrane perforation for any of the patient-related, surgery-related, and maxillary sinus-related
factors [794]. During sinus graft surgery, septa can be left intact by making two windows separated
by the septum, or they can be removed with a thin curved hemostat or Kerrison forceps. Septa can
impede the view of the sinus floor and may limit placement of autogenous bone grafts or bone
substitutes, thus preventing adequate filling of the sinus floor. According to Cakur et al., it was
suggested that because Underwood’s septa might be the reason for the thinness of the Schneiderian
membrane, the membrane perforation risk might be higher when Underwood’s septa existed [796].
Postoperative complications (infection, bleeding, persistent pain) can occur in any of the
sinus graft procedures with membrane perforation. Radiograph evaluation of non-perforated
membrane demonstrated sharp definition between the grafted and non-grafted area of the maxillary
sinus. Perforated membrane sinus appear to have graft particles beyond the borders of the
Schneiderian membrane and lack definition between the grafted and non-grafted sinus areas. In
areas where the graft material has been displaced beyond the boundaries of the sinus membrane,
resorption of the graft material is expected. In some cases, the grafted area of the perforated sinus
appears to be more radiolucent in comparison with a non-perforated sinus (Fig 5.4a-c).

~ 268 ~
 a b
Fig 5.4a: A panoramic radiograph demonstrates a lack of Fig 5.4b: A panoramic radiograph showing a sharp definition
definition between the grafted and not-grafted area if the between the grafted and non-grafted area of the sinus.
maxillary sinus.

Fig 5.4c: A panoramic radiograph showing displaced grafting

material into the sinus cavity due to sinus membrane perforation
c during surgery.

In some cases the procedure is discontinued intraoperatively due to the extent of the
perforation, or the graft material has to be changed (Fig 5.5a,b).

a b
Fig 5.5a: Rectangular lateral window preparation to access the Fig 5.5b: During membrane elevation, the membrane was torn
maxillary sinus. extensively and there were insufficient membrane fragments
remaining to enable the desired repair. At this point, a decision
has made to abort the procedure - note the Schneiderian
membrane is not visible at all.

The perforation should be treated to avoid displacement of the graft material into the sinus
cavity and subsequent sinusitis. It has been proposed that the regenerative result of the bone-
grafting procedure is inferior following sinus membrane perforation and that simultaneous implant
placement should not be conducted following repair of severe perforations [798]. A perforated
sinus has the risk of infection because of the communication with all other sinuses in the respiratory

~ 269 ~
system [799]. This risk may also be of concern for an implant that is apically exposed to the
environment of a maxillary sinus. The proper healing and remodeling of the graft material in the
sinus area depends on the vascularization of the sinus membrane, the surrounding bone walls, and
the elevated sinus wall [510]. From this point of view, the size of membrane perforations might
play a role on the long-term success of dental implants placed into the augmented sinus area.

Treatment
Punctual lesions do not require any special treatment, small perforations of the sinus
membrane are not treated, as these defects are closed off by the folding of the lifted membrane or
self-repaired with a small blood clot. Larger lesions are treated either by increasing elevation of
the sinus mucosa, to allow folding and easier closure of the tear, and/or the aid of resorbable
collagen membrane or oxidized regenerated cellulose sheets (Fig 5.6- Fig 5.8). In cases where the
sinus membrane is torn or perforated, the fragility of the remaining membrane increases and care
and delicacy are required to complete the elevation. The perforated membrane should be elevated
around the perforation carefully from the floor, medial, and anterior to the bony walls to allow the
blood supply from the bony walls to vascularize the graft and a resorbable collagen membrane,
double the tear’s size, should be cut and placed over the area to facilitate sinus membrane
dissection and elevation. It is necessary to stabilize the repair through grafting materials to keep it
securely in place, because without stabilization the repair membrane can become displaced or even
be drawn up through the perforation into the sinus lumen during or after graft material placement.
The amount of stability that can be achieved is directly proportional to the amount of coverage
over the intact portion of the sinus membrane. Care should be taken to not allow the repair
membrane to drift medially while the graft material is being placed. This is due to the convex shape
of the lateral wall in the molar eminence (first molar) area, the insufficiently wide repair
membrane, and the upward tenting of the membrane when packing. To avoid this shifting
tendency, it is recommended to use a large membrane (20x30 mm size) with a portion of it outside
folded on the lateral wall in superior direction. This is a secure procedure to prevent any membrane
shifting. In some cases, when a membrane perforation is discovered, the membrane surrounding
the perforation should be delicately dissected with a blunt instrument. Before insertion of the graft
material and in an attempt to relieve the pressure at the perforated area, a resorbable collagen
membrane should be used, and the lamellar bone from the sinus window is placed under it to
reinforce the reconstruction and.

Fig
a 5.6a: Large membrane perforation due to the thin membrane Fig
b 5.6b: Repair with the removed rectangular window. No
with simultaneous implant placement. stabilization is necessary.

~ 270 ~
 At this stage, the graft is placed. The posterior part of the cavity is grafted first, followed
by the anterior portion and finally the crestal area. When an extreme sinus membrane perforation
occurs, at this point a decision has to be made to perform a more extensive repair, not to abort the
procedure. A large 30x40 mm collagen membrane should be pushed into the window to create an
internal sinus repair membrane to hold the graft material, leaving a portion of it outside the window
for holding it in position.

a b

c d

e f

~ 271 ~
 g h
Fig 5.7a-h: Repair collagen membrane to repair small
perforations.

a b
Fig 5.8a: Membrane perforation in the distal compartment due Fig 5.8b:Membrane elevation performed on both sides of the
to the presence of a septum. septa – note the perforations in the separated compartments.

c d
Fig 5.8c: Nonstabilized double repair collagen membrane Fig 5.8d: Grafting the sinus.
forming a new roof.

The use of a bioabsorbable repair membrane against the elevated Schneiderian membrane
does not impede the blood supply. For large perforations, when the repair membrane completely
surrounds the graft, there can be a delay in graft vascularization from the sinus walls. In no cases
it is necessary to abort the grafting procedure and allow the sinus membrane to heal. The grafted
material is placed against the medial wall, and implants are placed using the surgical procedure
according to conventional surgical protocol. It is critical that primary stability is accomplished
with residual bone and that the remainder of the graft material fills the compartment to the contours
of the lateral wall.

~ 272 ~
 Perforations are classified according to simplified classification of membrane perforation
made by Fugazzotto and Vlassis: Class I, Class II A, Class II B, Class III [799].
 Class I perforations occur at any point along the most apical wall of the prepared sinus
window.
 Class II perforations occur along the lateral or crestal aspects of the prepared sinus window,
and are further subdivided according to their relative position to the most mesial, distal, or
crestal extension of the underlying sinus.
o A Class IIA sinus membrane perforation may occur anywhere along the expanse
of the lateral or coronal walls of the prepared sinus window, when the sinus cavity
to be augmented extends a minimum of 4 to 5 mm beyond the position of the
membrane perforation.
o Class IIB Sinus Membrane Perforations occur when the prepared aspect of the
sinus window approximates the extension of the sinus cavity in this area, no
additional space exists for performance of a further osteotomy to uncover intact
sinus membrane beyond the perforated area.
 Class III perforations occur at any location within the body of the prepared sinus window.
These perforations are often preexisting, and may be due to trauma during prior tooth
removal, resulting in membrane tear and/or oral antral fistula formation. A Class III sinus
membrane perforation may occur during preparation of the sinus window; however, such an
occurrence is rare in the hands of an experienced clinician.

Recommendations for treatment

 A very small perforation: self repair with a small blood clot.
 Small perforations: repair using bioabsorbable collagen barrier membrane, sutures and
sheets.
 Large perforation > 5mm: membrane, new roof
 Larger perforations > 10mm:
a) lamellar bone
b) pedicled buccal fat pad
c) bone block graft
d) Use large membrane 20x30mm size with a portion left outside
 Extreme perforations: abort the procedure or extensive repair using the Loma Linda pouch
technique with tacks [784]

Prevention of perforation
To avoid perforations, the rectangular osteotomy should be rounded and softened, so as to
minimize the risk of pinching the membrane when rotating the lateral wall of the osteotomy
medially and superiorly [510, 800, 801]. CT analysis is indispensable to assess bone thickness,
membrane thickness, septa sinus health, lateral wall defects and, discontinuities. The location of
lateral window will affects the membrane elevation safety. Keep hand instruments directly on the
bone surface and, choose the ideal location of the lateral window. The window should be located
both anterior and posterior to the septum and a piezoelectric surgical tool should be used to
minimize SMP.

~ 273 ~
 Intraoperative Bleeding
Intraoperative bleeding results from severing or damaging branches of the vascular supply
of the lateral wall of the sinus and the surrounding soft tissue, when performing an osteotomy in
the lateral wall of the sinus. This type of surgery can be complicated because of intrasinusal
anatomic structures. There are several vascular vessels that supply the maxillary sinus. These
vessels have to be taken into consideration during sinus augmentation because of the potential risk
of bleeding during the procedure (Fig 5.9).
This bleeding is usually minor and of relatively short duration, but in some instances it can
be profuse and difficult to control in a timely manner. Bleeding may occur either from the soft
tissue (extraosseous branch) during flap elevation or directly from the lateral bony wall
(intraosseous branch) during the osteotomy of the lateral window especially with rotary
instrumentation. There is also the possibility of bleeding from the medial wall of the sinus if the
posterior lateral nasal artery is damaged. A bleeding incident does not occur on every occasion
that the artery is damaged. Lateral window osteotomies bear the risk of arterial pedicle injury,
either when the practitioner burs the bone or elevates the membrane. For this reason, it is necessary
to insist on the following points related to arteries before operating:
 Position (superficial, intraosseous or intrasinus). In the intraosseous and intrasinus
location, the artery can be masked by the thickness of the osseous wall. In these cases,
removing the bone and detaching the membrane can cause the bleeding.
 Termination (free or anastomosed). Its precise course, and if possible, knowing where it
originates.
 Diameter. Because sometime these arteries have very large diameters (up to 2.5mm) with
intracanal or intraosseous location.
The practitioner must know that in more than 10% of cases, there is a risk of bleeding because
of an artery with a diameter of more than 0.5mm (1 to 2mm diameter). There is a high probability
of hemorrhage in about 57% of the cases. In a patient with an artery with diameter of more than
0.5mm, the probability of there being bilateral distribution of the vessels is more than 70%. Small
vessels may be broken and if these areas are located in the exposed Schneiderian membrane, it is
better to allow the hemostasis to occur naturally. Applying slight pressure with a gauze could help.

a a
Fig 5.9a,b: Artery (PSAA) dissected from the lateral wall.

It is recommended not to use electrocoagulation which may in fact cause membrane

necrosis. These vessels supply both the sinus membrane and the periosteal tissues as the PSAA
often has an extraosseous course.

~ 274 ~
 Fig 5.10: CT slices demonstrate the course of the PSAA.

In some cases the artery can be visualized within the lateral wall after elevation of the flap
and in some cases a window has to be made cranial and caudal to the location of the artery when
the artery was in an internal position (Fig 5.11).

a b
Fig 5.11a: Clinical view of dissected PSAA. The window was Fig 5.11b: Clinical view of elevated sinus membrane.
made cranially and caudally to the location of the artery.

c d
Fig 5.11c: Elevation of the membrane and grafting the sinus with Fig 5.11d: Clinical view of the intact artery after grafting the
an intact artery. sinus.

If the artery’s location according to the CT-scans increases the possibility of bleeding
complications, a window should be made that safeguards the integrity of artery and other soft
tissues and still is ideally located for the lateral window (Fig 5.12).

~ 275 ~
 a b
Fig 5.12a: Clinical view of the intrabony course of the PSAA. Fig 5.12b: Clinical view of the intrabony course of the PSAA.
The course of the PSAA is clearly visible. Window preparation Window preservation was made not to interfer with the PSAA.
was made that respected the integrity of the artery but still had
the ideal location of the lateral window.

Considerations related to intraoperative bleeding complication of sinus augmentation:

a) While performing antrostomy with a rotary cutting instrument, it is possible to damage
the vessel by intersecting with the vessel in the anterior area.
b) Even if there is no intraosseous vessel in the CT images, the risk of bleeding should be
considered when the sinus lateral wall is thick.
c) Women had a thinner mean lateral wall thickness 3 mm from the sinus floor, so the risk
of membrane perforation should be considered. On the other hand, men have a greater
vessel diameter than women. Men therefore, have greater tendency for bleeding than
women.
d) Many times older patients have wider diameter vessels. Therefore, there is a higher risk
of bleeding in older patients.
In these clinical cases, many techniques to control vascular bleeding are used. electro-
cautery and the use of a vasoconstrictor (1:50.000 epinephrine) are administered in controlling the
soft tissue bleeding that occurs in some cases when releasing incisions before elevation of the
mucoperiosteal flap are made (Fig 5.13a-c). Electrocautery is recommended to stop bleeding
caused by intersecting with the vessel.

a b
Fig 5.13a: Bleeding of the PSAA. Fig 5.13b: Use of electrocautery to control the bleeding. Care
has to be taken not to damage the membrane.

~ 276 ~
 c
Fig 5.13c: Controlled bleeding.

Care has to be taken not to damage the Schneiderian membrane when using electro-cautery.
If the bleeding occurs from intraosseous vessels, crushing the bleeding channel by compressing
the bone and vessel can be done to stop the bleeding. Care should be taken to avoid membrane
perforation through direct pressure. Because of the small size of the artery, the bleeding is usually
controlled by pressure with a gauze pad for several minutes resulting in a clot formation within the
bone channel surrounding the artery. In young patients (30-35 years) we have to be concerned
about possible compromise to the vessel because we know that the maxilla is very densely
vascularized in young and dentate individuals with large size intraosseous arteries. Conversely, in
older edentulous populations, the number of vessels and vessel diameter decreases, while
tortuosity of the vessels increases. In young patients, the incidence of bleeding can be reduced by
performing the osteotomy lateral window not to the full height and the membrane is then elevated
internally. The transection of a PSAA with a diameter over 2 mm is likely to produce bleeding and
impairment of vision. This may lead to a potential membrane perforation, thus prolonging the
overall operation time, interfere with the placement of the bone graft and constitute a true surgical
complication. In addition, the hemorrhage from this artery may displace the grafting material due
to a “washing” effect caused by the blood pressure, and may produce relevant hematomas of the
cheek area causing discomfort and creating an ideal “pabulum” for bacterial growth and
subsequent infection (Fig 5.14).

Fig 5.14: Hematoma one week after sinus augmentation.

The excision of a large diameter alveolar antral artery (AAA) in conjunction with the
inadvert tearing of the sinus membrane can potentially induce sinus mucosa swelling, extrusion of
blood into the sinus cavity as well as a postoperative sinusitis. If the maxillary sinus is even partly
filled up by mucosal edema, hematoma or seroma, a delay of maxillary sinus clearance may occur

~ 277 ~
because of the reduction of maxillary ostium patency, and maxillary sinusitis may develop as well,
compromising the success of the grafting procedure [110].

Intraoperative Bleeding
 Usually minor and of short duration
 Can be profuse and difficult to control
 Extraosseous branches by flap elevation
 Intraosseous branches-lateral wall
 From the medial wall-posterior lateral nasal artery

Bleeding consequences
 Impairment of vision
 Tearing of the SM
 Washing out of the GM
 Malnutrition of the graft

Techniques to control bleeding

 Direct pressure, bone wax
 Crushing the bone channel
 Use localized vasoconstrictor
 Electrocautery care of membranes
 Suturing the vessel proximal to the bleeding point

Recommendations
 Obtain preoperative CT images to locate the vessel.
 Visualize the vessel clinically
 Avoid the vessel when designing the window
 Use piezoelectric surgery to avoid trauma to the vessel
 Have materials on hand to control bleeding (electrocautery, local anesthesia with 1:50
000 epinephrine, bone wax)

Perforations in the buccal flap

Perforations in the buccal flap may result from attempting to release the flap to achieve
primary closure particularly when simultaneous ridge augmentation is performed. This is
especially true when the flap is thin in the area of release. In a typical sinus floor augmentation,
this procedure is unnecessary, since there is no change in the external dimensions. Therefore, the
flap can be closed tension free. Whereas releasing the flap is necessary as the changed external
dimensions are required. Care has to be taken by flap reflection.

Injury to the infraorbital nerve (ION)

During flap reflection, injury to the ION may result through blunt or pressure. It is also
possible to injure the ION when sharply dissecting to release the flap for tension free primary
closure. The ION exits the infraorbital foramen just below the infraorbital notch (Fig 5.15). If the
flap extension reaches to this position, the ION should be exposed and the retraction should be
placed distal to it. Location of this anatomic feature is crucial before performing flap retraction.

~ 278 ~
 Fig 5.15: Location of infraorbital foramen of a dry skull
specimen (red arrow).

Postoperative complications
Postoperative edema, ecchymosis, mild to moderate discomfort, minor nose bleed, minor
bleeding at the incision line, and mild congestion are within the scope of expected patient responses
to this procedure. Some are due to manipulation of the buccal flap and others to the manipulation
of the sinus membrane.
Major postoperative complications after sinus elevation surgery are relatively uncommon.
They include graft infections, postoperative sinusitis, profuse postoperative bleeding, flap
dehiscence, oroantral fistula formation, formation of inadequate graft volume for implant
placement, loss of graft material containment as a result of either sinus membrane perforation or
exfoliation of graft material through the sinus window, maxillary cyst formation [640,782],
migration of dental implants into the sinus graft or into the sinus cavity, atypical facial pain, peri-
implantitis and the failure of dental implants.
In a prospective study of 1000 consecutive sinus elevations Zijderveld et al. reported an
11% incidence of membrane perforations and a 2% incidence of bleeding as intraoperative
complications [780]. The postoperative complications listed in order of most frequent occurrence
were loss of implants (4%), wound dehiscence (3%), graft infections (2%), postoperative maxillary
sinusitis (1%), and loss of or inadequate graft volume (1%) [780]. While postoperative
complications are relatively infrequent, understanding how to deal with them may be vital for the
ultimate success of the procedure.
Complications of sinus grafting surgery can be classified into material related, technique related,
anatomical related, patient related and others.

Sinus graft infection

Infection of the graft after sinus augmentation is a major but infrequent complication. An
infected graft is particularly difficult to treat, as the graft itself lies within the sinus cavity,
underneath the elevated sinus membrane. Sinus graft infection is considered a major complication
requiring urgent treatment because there is risk that the infection could spread throughout the graft
and the sinus cavity or to adjacent anatomical structures [802]. A meta-analysis revealed that
infections occur in up to 4.7% of sinus graft procedures [803]. Treatment strategies reported in the

~ 279 ~
literature for sinus graft infections include administration of systemic antibiotics, endoscopic
exploration of the sinus, surgical exploration, and rinsing [782,803].
Graft infection can occur despite the absence of clinically detectable dehiscence. Moderate
graft infection, after the first surgery, can be recovered using antibiotic therapy, with no need for
additional surgery, Patients could experience one or more of the following clinical symptoms of
sinus graft infection between the first and fourth week after sinus elevation: abscesses, severe pain,
recurrent facial swelling, fistulous tract extending into the oral cavity, high body temperature, loss
of graft particles through the fistula or through the incision lines ("popcorn sign").
A postoperative CT scan must be performed to evaluate the involvement of the sinus lumen
(Fig 5.16). Some cases show sinus involvement others show thickening of the sinus membrane or
a complete opacification of the sinus cavity. The latter patients could experience severe pain 1 to
2 weeks post-surgery which can be resolved after few days. When patients have an elevated
temperature and recurrent facial swelling without an intraoral fistula, surgical intervention should
be considered at this time. A combined treatment regime for sinus graft infection is performed,
both surgical intervention to treat the infected graft material and systematic antibiotic treatment
for the infection. The full-thickness flap from the performed sinus floor elevation procedure is re-
elevated to expose the bone graft. Any loose grayish-looking graft particles, purulent exudates and
any loose membrane pieces should be removed and irrigated with sterile saline, until a more
confined, intact, stable, immature, healthy looking graft material is visible. The involved implants
should be also removed (Fig 5.17a-p , Fig 5.18a,b).

Fig 5.16: CT scan demonstrate the infected area. Solid grafting material separates the infected area from the maxillary sinus
cavity.

a b
Fig 5.17a: Fistulous tract extending into the oral cavity. Fig 5.17b: Full thickness flap elevation – the incision line is
designed to avoid the infected area. A slight palatal incision and
a sulcus incision are combined to facilitate access along with
mesial and distal releasing incisions.

~ 280 ~
 c d
Fig 5.17c: After flap elevation the infected bone graft is exposed. Fig 5.17d: Any loose grayish-looking graft particles, purulent
exudates and any loose membrane pieces are removed and
irrigated with sterile saline.

e f
Fig 5.17e: Debridement of infected bone graft is performed until Fig 5.17f: Collagen repair membrane is used after confined,
confined, intact, stable, immature, healthy looking graft material intact, stable, immature, healthy looking graft material is visible.
is visible. No additional grafting material is needed.

g h
Fig 5.17g: Primary closure and closure of fistulus tract. Fig 5.17h: Flap elevation for implant placement six months after
removal of infected graft. Note that two implants were inserted
at site 14,17 four months after graft removal.

~ 281 ~
 i j
Fig 5.17i: Residual infected graft was debrided. Fig 5.17j: Infected graft material was removed until healthy
looking solid bone was present.

k
Fig 5.17k: Implant site preparation. Fig
l 5.17l: Implant placement in site 15,16.

m n
Fig 5.17m: Implants in situ. Fig 5.17n: Repair membrane was used to seal the sinus
membrane perforation.

o p
Fig 5.17o: Additional bone grafting was performed. Fig 5.17p: Collagen membrane coverage.

~ 282 ~
 a b
Fig 5.18a: After flap elevation, the infected graft with the Fig 5.18b: The loose grayish graft particles, purulent exudate
involved implants was exposed. and infected membrane pieces are clearly demonstrated. The
involved implants and graft material were totally removed.

It is a subjective decision to determine which graft zone is not involved in the infection. A
locally applied antibiotic is empirically used to treat the remainder of the sinus graft and reduce
the risk of the persistent infection. One hundred to 200 mg of doxycycline powder with saline can
be placed in the bone graft for two minutes followed by washing out with sterile saline. To ensure
the formation of a blood clot, the defect is gently debrided to establish bleeding of the area resulting
in a five-wall defect within the sinus graft and preserving the elevated sinus. The flap is closed and
sutured for primary closure where there is no detectable communication between the defect and
the sinus cavity.
Systemic antibiotics should be given to prevent the infection to spread throughout the
remaining graft and the sinus or other adjacent vital anatomic structures. In addition to systemic
antibiotics (augmentin 875 mg, twice a day), anti-inflammatory medication (50mg diclofenac
potassium three times a day) should be prescribed for one week following surgery. For patients
with concomitant sinusitis, a nasal decongestant spray should be prescribed three times a day for
four days. The total healing time prior to implant placement is logically extended to allow new
bone formation in the defect. Any remaining bone deficiencies have to be grafted after the time of
implant placement (Fig 5.19a-f).

a b
Fig 5.19a: Clinical view of the infected sinus graft two months Fig 5.19b: The infected area is well demonstrated after flap
following sinus augmentation due to the use of improper elevation.
grafting material.

~ 283 ~
 c d
Fig 5.19c: Infecteed soft tissue is totally removed. Fig 5.19d: The infected grafting material was removed and the
area was debrided until a confined healthy looking solid bone
was visible.

e f
Fig 5.19e: After removal of infected material, the sinus Fig 5.19f: No communication to the sinus cavity is visible.
membrame is clearly visible.

It must be emphasized that there should be no detectable communication between the

infected graft and the sinus cavity, as observed during the re-entry procedure. Some of the patients
with a communication between the infected graft and the sinus cavity, or patients who develop
infections, may need to be treated more aggressively with complete graft removal and/or
endoscopic sinus surgery by an ENT specialist to prevent more serious complications.
Early recognition of signs and symptoms is critical to prevent the spread or an increase in
the severity of the infection. The goal of the treatment to eliminate the infection and to prevent its
progression to the sinus cavity and additional vital structures. The surgical treatment seems logical,
but it must be considered empirical, since there are no objective tools to confirm that any infection
remains in the sinus graft after the cleansing procedure. It is recommended that an individual
treatment plan for each patient who develops a sinus graft infection should be based on evaluations
by both the treating and the consulting clinician. In the event that a complication occurs, treatment
is easier and more successful if an implant is not involved, as bacteria may adhere to the implant
surface. The through elimination of the infected graft material can enable bone regeneration in
areas to which the infection has not yet spread and even permit regeneration of the majority of the
resulting five-walled bone defect, showing new bone formation in a previously “empty” space.
The decision to add no new augmentation material during the treatment of sinus infection is a
safety measure to prevent repeated infection.

~ 284 ~
 Dome phenomenon
The “Dome phenomenon” is observed in infected augmented sinuses, that in spite of an
inflammatory complication that warranted further surgical intervention, a dense, solid, hard tissue
is maintained in the apical aspect of the grafted area. This tissue represents a calcification of the
grafting material that was previously grafted in the sinus together with initial bone formation
originating in the Schneiderian membrane. This dome provides a 3- to 4-wall defect inside the
maxillary sinus, which is completely filled with bone and enables dental implant insertion without
the need of additional sinus augmentation (Fig 5.20a-d, Fig 5.21a-h).

a b
Fig 5.20a: Infected graft core after SFA with implant Fig 5.20b: One implant remained and the infected core was
placement. debrided and cleaned without bone augmentation.

c d
Fig 5.20c: Despite the surgical intervention, a dense, solid, hard Fig 5.20d: No detectable communication between the empty
tissue is maintained. space and the sinus cavity is evident.

a b
Fig 5.21a: CT scan demonstrating infected graft with loose graft Fig 5.21: No communication was detected between the sinus
particles. cavity and the infected area.

~ 285 ~
 c d
Fig 5.21c: Slightly palatal incision line and full thickness flap Fig 5.21d: After flap elevation, the infected graft particles are
elevation. well demonstrated.

e f
Fig 5.21e: Infected soft tissue was0 removed. Fig 5.21f: the exposed infected graft material was removed.

g h
Fig 5.21g: Additional removal of infected grafts. Fig 5.21h: After flap elevation the exposed infected grafting
material was removed and the created cavity was debrided until
healthy solid bone was visible. No additional grafting material
was placed.

In human histomorphometric analysis, the area in proximity to the Schneiderian membrane

exhibits higher new bone formation than area adjacent to the residual crest. Thus, the potential
source for the above described dome is likely to be the Schneiderian membrane.

Clinical case presentations

Case 1: A 56 year old man underwent sinus augmentation with simultaneous one implant
placement. The sinus was grafted with DBBM and covered with a collagen membrane. The
Schneiderian membrane was intact. The patient received antibiotics (augmentin 875mg,
Smithkline) for 10 days and was instructed to mouth rinse with 0.2 chlorhexidine. The patient had

~ 286 ~
reentry for second stage implant placement surgery after six months and surgical debridement.
During the surgery, loose grayish-looking graft particles and loose membrane pieces were visible.
Infected graft particles in addition to membrane pieces and infected soft tissue were totally
removed including the inserted implant. After surgical debridement a dome of solid graft material
could be palpated using a blunt instrument, this solid material was also evident radiographically.
After healing and resolution of the inflammation, implants were placed without additional
augmentation because of complete bone fill.

a b
Fig 5.22a: Panoramic radiograph demonstrate infected graft in Fig 5.22b: After flap elevation, the infected loose membrane
the right posterior maxilla and the “black hole” in the left pieces were exposed.
posterior maxilla.

c d
Fig 5.22c,d: The infected graft material and membrane pieces Fig 5.22d: The involved implants were removed in addition to
were exposed. the granulation tissue and inflammatory tissue.

e
f
Fig 5.22e: The black hole is well demonstrated after flap Fig 5.22f: Implants were placed and the defect was grafted with
elevation and was debrided. The apical border of the augmented additional DBBM.
sinus was intact.

~ 287 ~
Case 2: In a 62 years old patient, four weeks postoperatively, suppuration was evident with
fistulous tract existence into the oral cavity, facial swelling and severe pain, abscess, and loss of
graft particles through the fistula. Antibiotics were prescribed 1.5g/d amoxicillin clavulanate and
1g metronidazole. After 10 days, the clinical symptoms improved and the pain had subsided. The
obtained panoramic scan showed loss of integration of one implant. The infected area was treated
locally with the surgical approach described earlier by sinus infection, and the implant was
removed along with the granulation and inflammatory tissue. It appeared that the infection had not
yet involved the entire graft. The apical border of the augmented sinus was intact with dense, solid
tissue separating the remaining defect from the sinus cavity. The remaining bone deficiencies were
grafted simultaneously and were covered with a collagen membrane. A post operation panoramic
radiograph showed a radiopaque dome at the most superior border of the augmented sinus. After
the infection was treated, the acute symptoms disappeared within few days, and the patient healed
uneventfully afterward. The total healing time prior to implant placement was seven months for
this patient. After the healing period, the defect demonstrated bone formation and the defected area
was greatly reduced in size. A CT scan showed a radiolucent area in the center of the grafted area
with a cloud shaped radiopacity at the most apical border to sinus cavity. New implants were
inserted and the gap was filled with additional DBBM. No further complication was evident.
Implants were loaded four months after placement and are still functioning five years post
operation. Whether preoperative antibiotics would have reduced the sinus graft infection rate
remains to be investigated. A single dose of preoperative antibiotics therapy may slightly decrease
the failure rate of dental implants [805].

a b
Fig 5.23a: After flap elevation, the infected area beside the Fig 5.23b: No communication to the sinus cavity was detected.
granulation and inflammatory tissue were removed.

c d
Fig 5.23c: The remaining bone deficiencies were grafted with Fig 5.23d: The grafted area was covered with a collagen
DBBM. membrane.

~ 288 ~
 Sinusitis following sinus augmentation
Maxillary sinusitis can occur when the sinus mucosa is damaged after a sinus elevation
procedure, thus causing disorder in the ciliary movement of the sinus mucosa, or when the natural
excretion system inside the sinus is obstructed as the ostium narrows because of the inflow of
foreign substances or severe sinus mucosal edema [76,510]. Sinusitis is a frequently occurring
complication after the sinus elevation procedure [806], with an incidence rate of 3 to 20% [807].
In previously healthy sinuses, regardless of other factors, opinions differ on whether the occurrence
of sinusitis directly affects the prognosis of dental implants. Kahnberg et al. [591] reported
successful outcomes after carrying out the sinus elevation procedure and implant placement in
patients in whom there was a preoperative suspicion of sinusitis (mucosal thickening, etc). Kaptein
et al. [808] rejected any relationship between sinus membrane perforation and the incidence of
sinusitis or the failure of implants. Raghoebar et al. [809] concluded that perforation itself does
not predispose the patient to develop sinusitis and has no relationships to the prognosis of dental
implants.
Sinusitis is reported in up to 27% of cases related to intraoperative events such as SM
perforations, dislocation of grafting material and implants, history of sinusitis or sinus clearance
dysfunction due to: a) mucosa hyperplasia b) partial or complete ostium obstruction c) nasal
anatomic alterations d) pseudocysts, mucous retention cyst.

a b
Fig 5.27a: Panoramic view of CT scan showing implant Fig 5.27b: Removed implant
placed in grafted sinus – note the gap between the grafted attached to the grafting
material and the native bone material

Patients can experience in the postoperative period sinus graft infections with varying
degrees of sinusitis symptoms, from thickening of the sinus mucosa to a purulent infection. The
prevalence of acute infection following sinus augmentation is significantly greater in smokers
(75%), compared to non-smokers (25%).
The literature concerning infectious complications following sinus floor elevation and
grafting is based solely on case reports and case series with a very limited patient sample
[619,641,806,810-812]. This seems to be determined by the fact that post-operative complications,
in particular infection, after sinus augmentation procedures is relatively uncommon, or rarely
published. It is worth noting that one of the first studies that underlined the role of pre-existing
naso-sinusal pathologies in elevating the risk of complications following sinus lifting has been
published by Tammenga et al. in 1997 [807]. This aspect has not been adequately developed after
this publication. The only aspects supported by significant data reported in the literature are the
following:

~ 289 ~
 (i) post-operative complications after sinus grafting procedures are more frequent in
patients with a history of sinusitis prior to the surgical intervention [807];
(ii) some risk factors related to anomalies/alterations of the maxillary sinus-ostium-
middle meatus complex exist, such as the concha bullosa, turbinate hypertrophy,
significant septum deviation, and these alterations can interfere with the normal
ventilation and clearance of the maxillary sinus [639, 807].
Infections may be limited to the maxillary sinus treated with floor elevation and grafting,
but they may also diffuse to other paranasal cavities and, in the most severe cases, involve the
orbital cavity and the anterior and middle cranial fossae [809]. Moreover, sinus infections may
determine the formation of oro-antral fistula with chronic suppuration often associated with the
expulsion of grafting material particles from the fistula also known as a ‘popcorn sign’ (Fig 5.24a).
It is therefore mandatory to treat these complications as soon as possible and following
safe and reliable treatment protocols (Fig 5.24b).

a b
Fig 5.24a: Oral antral fistula six weeks after sinus Fig 5.24b: Oral antral fistula four weeks after sinus
augmentation. augmentation.

Treatment
Sinusitis occurring after sinus elevation procedure can be treated with antibiotics and
decongestants in some cases, but effective therapy for sinusitis requires proper surgical treatment.
Clearly, when sinusitis occurs, it is likely that the survival rates of implants drop remarkably.
It’s noteworthy to mention that there are no well-designed proposed protocols for the
treatment of infectious complications.
After treatment of antibiotics, the site had to be incised and drained.

Fig 5.28: Penrose drain in situ

~ 290 ~
 In some patients it is still possible to complete the prosthetic rehabilitation by modifying
the dimension, position, and/or number of the originally placed implants. Although part of the
bone graft can be lost, 2 to 4 implants can be inserted after 6 months of graft consolidation.
While in some patients, due to loss of grafted bone, implant placement is impossible. It is
evident in those patients that the major part of the graft material for SFE had been lost. Reentry
for re-augmentation can be considered only after 6 months of healing following the failure of
previous surgery.
In sinus infection cases in conjunction with and oro-antral communication following a
sinus floor elevation procedure, the traditional approach has been represented for many years by
the sinusal toilette with an intra-oral approach in association with an inferior meatal antrostomy
(Caldwell-Luc approach) and with the closure of oro-antral communications with local flaps
[641,813,814]. The aim of this approach is removing the infected grafting material from the sinus
cavity,
Other infectious complications following maxillary sinus floor elevation and grafting can
occur, These include: (i) infections of other paranasal cavities (ethmoid, frontal sinus, sphenoid
sinus) that cannot be treated via and intra-oral approach; (ii) a primary or secondary ostium
obstruction determined by hyperplasia of the reactive mucosa can be often present, sometimes
associated with secondary medialization of the uncinate process that further hinders the sinus
ventilation and drainage; and (iii) predisposing conditions (septum deviation, concha bullosa,
hypertrophic turbinates, etc.) may be present. In these cases, the sinusal toilette with an intra-oral
approach in association with an inferior meatal antrostomy may prove to be insufficient to obtain
a complete recovery of the sinusal functions.
It was indeed demonstrated that in case of maxillary sinusitis, the treatment of choice is
nowadays represented by a transnasal endoscopic approach, internationally known as FESS
(functional endoscopic sinus surgery) [815-817]. Sinus endoscopy was first performed in 1901
using a modified cystoscope [818]. Modern sinus endoscopy was described in the 1960s by
Messerklinger and it was introduced in the United states in 1985 [819]. It enables the evaluation
of the maxillary sinus by direct observation [820]. The endoscopic surgical technique focus on
minimizing the removal of normal mucous membrane and critical paranasal sinus structures,
thereby minimizing trauma and preserving mucociliary function [820-822].
In many surgical specialties, traditional surgical procedures have been replaced by
minimally invasive ones and have become the appropriate state-of-the-art care [823, 824].
Minimally invasive procedures such as endoscopically assisted techniques shorten the duration of
a surgery and lower the complication rates [825].
FESS is a relevant improvement as compared with the traditional Caldwell-Luc approach
for several reasons: (i) it is less invasive; (ii) it allows for the recovery of the normal sinusal
function, characterized by the spontaneous drainage from the natural ostium; (iii) it eliminates the
need for total sinus mucosa removal, as suggested by Caldwell and Luc; (iv) it is possible to
manage the other paranasal cavities possibly involved in the infection, which would not be
reachable via an intra-oral approach; (v) it can correct/eliminate the anatomic risk factors that as
co-factors, contribute to infection relapse. As far as this latter aspect is concerned, even in healthy
sinuses, the osteomeatal complex generally has a small diameter.
The presence of anatomic anomalies such as the concha bullosa, a relevant septum
deviation, and turbinate hypertrophy may further reduce the sinusal clearance. In healthy
conditions, these anomalies may be silent. However, in case of sinusal infection, the concomitant

~ 291 ~
reactive hypertrophy of the mucosa of the ostium-meatus complex may contribute to render the
sinus drainage very difficult or impossible, with scarce possibilities of compensation and healing.
With the FESS approach, it is possible in one single surgery to treat all these aspects and
factors and promote the functional recovery of the sinus , once the primary cause of infection is
eliminated ( the septic material, implant or foreign body dislocated into the sinusal cavity).
However, the FESS approach alone may not be sufficient for the complete removal of the infected
grafting material from the maxillary sinus (due to the impossibility of reaching every portion of
the sinus with the available surgical instrument and does not allow the closure of oro-antral
communications, if present. Therefore, the most appropriate approach for the treatment of
maxillary sinusitis following sinus floor elevation and grafting might be a combination of FESS
and intra-oral surgery. The endoscopic phase (FESS) always represents the first part of the surgical
intervention, carried out in all cases under general anesthesia with oro-tracheal intubation. First,
an inferior uncinectomy is performed to expose the ostium, followed by a wide middle antrostomy
that allows for the removal of pus and infected grafting material dislocated inside the maxillary
sinus. No attempt to entirely remove the sinus mucosa, differently from the traditional Caldwell-
Luc technique, is indicated. Only hypertrophic or polypoid tissue should be removed, with the
objective being to reduce as much as possible bone exposure inside the sinus. Once the FESS phase
is completed, the intra-oral phase begins without the placement of nasal packing, to permit a final
control at the end of the surgical intervention. A full thickness mucoperiosteal flap is elevated in
the lateral-posterior maxilla to expose the antero-lateral wall of the maxillary sinus. The flap is
designed according to the position and dimension of the oroantral communications to allow a safe
removal of the fistulae and an appropriate suture. The window used for the initial sinus grafting
attempt is used to gain access to the maxillary sinus and to remove the remnants of the infected
grafting material. These are generally localized on the floor of the maxillary sinus and in its
anterior recess, as these areas are not easily reachable via the transnasal approach.
Additional endoscopic control is performed to verify the completion of the toilette of the
maxillary sinuses. Sutures are then applied, after careful flap mobilization by means of periosteal
incisions, to allow a tension-free, water tight closure of the surgical wound. In patients presented
with a large oro-antral communications, a double layer closure of the communications is
performed. The first layer is represented by a buccal fat pad flap sutured to the palatal side of the
communication, while the second layer is represented then by a buccal mucosal flap, suture to the
palate over the buccal fat pad flap. Finally, after nasal and sinusal hemostasis is checked by direct
inspection, a nasal package is applied.
As far as the intra-oral approach is concerned it allows the surgeon to complete the FESS
treatment with procedures that are not possible to perform from the nasal access, such as:
(i) the removal of infected implants with apical portions penetrating into the maxillary
sinus;
(ii) the removal of infected grafting material not retrievable via the endoscopic
approach;
(iii) closure of oroantral communications (Fig 5.25).
A new antibiotic therapy with Levofloxacin (750 mg/day for 15 days) is administered to
patients for whom the presence of Staphylococcus aureus is confirmed.

~ 292 ~
 a b
Fig 5.25a: Oro-antral fistula Fig 5.25b: Oro-antral fistula closure.

c d
Fig 5.25c: Panoramic radiograph showing a bone defect in the Fig 5.25d: Swelling of the maxillary sinus membrane with an
right side. open ostium.

e f
Fig 5.25e: Swelling of the maxillary membrane has disappeared Fig 5.25f: Closed oro-antra fistula.
– note the extended alveolar bone defect [815].

~ 293 ~
a b c
Fig 5.26a: Marked sinus membrane swelling with bone particulates within the sinus membrane. b: Extended bone
defect. c: closure after removal of the lesion and sequestrum [826].

Displacement and Migration of Implants into the Maxillary Sinus

Dental implant migration to the paranasal sinuses have been reported over the last 18 years.
[620,822,825]. Migration in the ethmoid, sphenoid sinus, nose and anterior cranial fossa, orbital
floor is much more sporadic.
Since the first case was described in 1995 [618], other authors have depicted the occurrence
of this adverse event into the maxillary and other paranasal sinuses. Most reports have included a
limited number of implants [630,822,825,827], with only a couple that include a slightly larger
series of cases [828, 829].
Implant migration to the maxillary sinus cavity is an increasingly serious complication
influenced by multiple factors that involves three main factors: implant, patient, and surgeon
related factors. Although it is a rare complication it has serious consequences. Complications can
include: sensory disturbance, maxillary sinusitis, oroantral fistula, foreign-body reaction with
serious complications, acute or chronic sinusitis in paranasal sinuses, intracranial cavity,
meningitis or brain abscesses are also reported. Encapsulated migrated implants without sinus
symptomatology but thickening may be present.
Implants can be displaced in the maxillary sinus cavity at the time of surgery or can migrate
several years after placement due to spontaneous bone loss. It is crucial to realize that this emerging
complication could be primarily derived from the lack of adequate information or knowledge to
make a proper clinical judgment and surgical performance.
Displacement of implants into the sinus determines the following events: a) the
spontaneous expulsion through the antrum, b) migration of the implant to other paranasal sinuses,
c) persistence in the maxillary sinus.
Primary stability could be enhanced by bicortical anchoring of implants, but conversely,
this could be a major risk factor for accidental displacement of dental implants into the maxillary
sinus [829] (Fig 5.29).

~ 294 ~
 a b
Fig 5.29a: Panoramic radiograph showing migrated and Fig 5.29b: Panoramic radiograph showing migrated and
displaced implants into the left maxillary sinus. displaced implants into the right maxillary sinus.

c d
Fig 5.29c: Panoramic radiograph showing migrated and Fig 5.29d: Panoramic radiograph showing migrated and
displaced implants into the left maxillary sinus. displaced implants into the right maxillary sinus.

e f
Fig 5.29a-f: Panoramic radiograph showing migrated and Fig 5.29a-f: Panoramic radiograph showing migrated and
displaced implants into the right maxillary sinus. displaced implants into the left maxillary sinus.

a b
Fig 5.30a: Sagittal CT scan demonstrating a displaced implant Fig 5.30b: Transverse CT scan demonstrating a displaced
in the orbital cavity. implant in the orbital cavity.

~ 295 ~
 a b
Fig 5.31a,b: Distortion of panoramic imaging can lead to Fig 5.31b: A repeated panoramic radiograph clearly
misinterpreting the right diagnosis. A projected implant may demonstrates that there is no implant migration in the sinus
cause the observer to think that an implant has migrated into thee cavity.
sinus cavities.

It’s well known that both cellular activity and vital bone content are higher in areas grafted
with a mixture of anorganic bovine bone plus cortical autogenous bone as compared to maxillary
pristine bone [830]. In light of this information, it is reasonable to assume that a successful
maxillary sinus augmentation may prevent implant migration. In the majority of the reported cases,
implant placement was performed by a general dentist who did not follow proper protocol as the
majority of these doctors do not have the advanced training that is required to conduct these
sophisticated procedures. This can be a problem because articles and course promotional brochures
emphasize the simplicity of placing implants by using novel systems, protocols or devices. One
clear example is a recent article titled “Technology helps an "amateur" place implants” [831]. This
type of advertisement encourages an increasing number of dentists, with limited or no surgical
training, to perform implant surgical procedure in their practice. Another imported factor to
consider is that many of the courses on surgical implant placement are sponsored by implants
companies and are limited short time courses.

Various mechanisms explain the migration

Inadequate treatment may lead to implant migration in term of excessive force used for
implant placement. In addition, changes in intrasinusal and nasal air pressures can produce a
suction effect due to the negative pressure exerted by these cavities [620]. This could be explained
by the centrifugal expansion of the sinus, which may have had bone removed apically around the
implant and thus produce the aforementioned suction effect.
A second possible explanation for implant migration into maxillary sinus would be bone
destruction secondary to the infections at the implant site either before or after implantation. An
example would be the previous presence of apical foci involving the teeth, producing osteitis and
bone weakening with resorption of certain parts of the maxilla. Another explanation is that peri-
implantitis produced by progressive resorption of bone around the implant, permits the implant’s
mobility.
Incorrect distribution of occlusal forces may lead to implant migration to the sinus
produced by prosthetic restorations. This mechanism may explain the loss of anchorage by
implants subjected to early loading and their movement into the maxillary sinus.
Previously suffered bone i.e. infection, GBR, destruction of the surrounding bone surgical
trauma and the lack of primary stability is a major cause of implant displacement. Osteoporosis,

~ 296 ~
osteopenia and sinus membrane perforation may indirectly lead to implant displacement due to
inadequate primary stability.

Treatment
Various treatment modalities have been employed to deal with this complication. The
treatment of choice is the immediate removal to prevent irritation of the sinus mucosa, which may
lead to ciliary dysfunction and consequently sinusitis. Where implant removal is contraindicated
because of systemic pathology, or is rejected by the patient, there should be regular clinical and
radiographic observation. Displacement of the oral implant into the maxillary sinus may be
followed by no relevant complications (besides the presence of a foreign body in a paranasal
cavity) [828], but also by an infectious reaction of the maxillary sinus which may involve other
paranasal cavities or even the orbital cavity and the intracranial cavity, with potential major
complications [832-834]. It is therefore recommended to remove foreign bodies from the maxillary
sinus as soon as possible.
Different techniques have been proposed over the years to remove implants such as:
a) functional endoscopic sinus surgery through the nasal cavity FESS [835];
b) an endoscopic removal via an intraoral approach through the anterior wall of the
maxillary sinus [822];
c) an intraoral approach “ad modum Caldwell-Luc”, with removal of part of the anterior-
lateral wall of the maxillary sinus [836, 837];
d) an intraoral approach with creation of a bone lid pedicle to the periosteum overlying
the anterior wall of maxillary sinus [838, 839]; and finally,
e) an intraoral approach with the creation of a bony window pedicle to the Schneiderian
membrane, as proposed the first time by Bigioli & Goisis [840].
An endoscopic approach via a trasnasal access (FESS) has been successfully performed for
the removal of foreign bodies from the paranasal sinuses [828, 835] (Fig 5.32).

Fig 5.32: Endoscopic view of a migrated dental

implant in the left maxillary sinus.

However, it must be underlined that this technique, presents some limits, in particular
regarding the removal of foreign bodies located in the anterior and inferior part of the maxillary
sinus. This area is difficult to be reached by the present endoscopic instruments. Finally, it must
be underlined that FESS normally requires general anesthesia and, to be effective, needs an
enlargement of the natural ostium. FESS is therefore the procedure of first choice in cases of

~ 297 ~
foreign bodies displaced into the maxillary sinus associated with relevant sinus infection and/or
inflammatory reaction of the sinus mucosa and, in particular, when an ostium obstruction is present
and/or other paranasal sinuses are involved by local infection [828]. In such clinical conditions,
only FESS can solve all the aforementioned problems in the most proper and least aggressive way.
If the sinus does not present relevant infections, the ostium is not obstructed by an
inflammatory reaction of the sinus mucosa, and the other paranasal sinuses do not present
inflammatory/infections reactions, an intraoral approach seems to be an excellent choice. It must
be underlined that also in cases of moderate sinus mucosa reaction, once the foreign body is
removed both sinus anatomy and function recover and return to their healthy state the majority of
the time. This was demonstrated by the results reported by Federico et al. However, an endoscopic
approach via an intraoral access in the area corresponding to the canine fossa may represent
another alternative [835]. Briefly, a little defect is made into the anterior wall of the sinus, and
endoscopic instrument are inserted including optic fibers, a suctioning system, and pliers or
urological retrieval baskets to retrieve the foreign body (Fig 5.33).

Fig 5.33: Urological retrieval baskets

Advantages are represented by: (a) the possibility to perform the procedure under local
anesthesia; (b) the surgical access is limited; (c) the postoperative recovery is favorable (limited
pain and swelling). However, the control of the surgical field might be limited, and foreign bodies
displaced in the posterior and/or upper part of the maxillary sinus are not easily reachable.
An intraoral approach “ad modum Caldwell-Luc” with removal of part of the anterior-
lateral wall of the maxillary sinus and part of the sinus mucosa [836, 837], allows an excellent
access and visibility of the maxillary sinus, thus rendering the removal of foreign bodies displaced
into the sinus very easy, but leaves a wide bone defect which can be followed by the formation of
a scar tissue which may lead to the retraction of the soft tissue of the cheek and to paresthesia and
pain in case of infra-orbital nerve branch involvement [625, 841].
Consequently, several alternatives techniques have been developed to avoid these
complications. Such a procedure consists of an epi-periosteal plane of dissection followed by the
creation of a “U-shaped” window. The upper margin of the bony window is created by a
spontaneous fracture during the upward rotation of the window to access the sinus. However, some
drawbacks have been found such as: (a) higher bleeding due to the epi-periosteal dissection; (b)
reduced visibility because of the limited possibility to rotate the window upwards; (c) the fracture
of the upper border is uncontrolled and may lead to an unexpected shape of the bony window; (d)
the infraorbital nerve foramen might be involved into the upper margin of the window, with
subsequent paresthesia and/or pain.

~ 298 ~
 To reduce these side effects and complications, Biglioli and Goisis described the intraoral
approach with the creation of a bony window pedicle to the Schneiderian membrane [840]. The
bony window design was very similar to that adopted for the classical sinus grafting procedure via
a lateral approach [354, 830]. However, instead of maintaining the whole, three sides were cut
(inferior, medial, distal) and only the superior one remained intact, this procedure allows to obtain
a bony window pedicled and vascularized by the thin blood vessels of the sinus mucosa.
Advantages of this procedure: (a) the subperiosteal dissection limits bleeding and optimize access
to the anterior-lateral wall of the maxillary sinus; (b) the infraorbital nerve foramen is easily
visualized and the upper horizontal osteotomy can be performed without exposing the nerve to
potential damage; (c) the vascularization provided by the sinus mucosa ensures the survival of the
bony window(with no significant resorption) and it allows ossification of the margins of the bony
window; (d) the procedure can be performed under local anesthesia in a relatively short operating
time with reduction in postoperative morbidity and rapid healing of the sinus mucosa; (e) the
frequently complete reossification of the bone lid margins may allow, if indicated, a re-entry
procedure via a lateral approach.

Clinical case presentations

Case 1: A 53-year old woman was referred to our private practice to undergo sinus
augmentation with simultaneous implantation. During the surgery, a dental implant was
displaced into the sinus lumen while inserting it. A panoramic radiograph revealed the presence
of the implant within the superior region of the maxillary sinus. The maxillary sinus was
carefully inspected until the migrated implant was visible and removed with the help of washing
effect of the sinus with normal saline. This event did not compromise the completion of the
surgical procedure as planned.
Case 2: A 56 year old woman underwent sinus grafting with simultaneous three implants
placement in the right posterior maxilla. No complications had occurred during the surgery. The
implants were considered to be stable at the surgical time of placement. Prior to second-stage
surgery, the obtained panoramic radiograph detected displacement of one implant into the right
maxillary sinus. The patient was in good medical health and had no sinus complains. A thorough
medical history and clinical and radiographic examinations including CT scan revealed neither
history nor actual sign of sinus related pathology. The implant was located in the region of the
tuber. The patient was treated for implant removal. To remove the implant, the lateral wall of the
sinus was fenestrated with a round bur; care was taken to preserve as much grafting material as
possible. A small part of the placed grafting material was removed to reach the raised sinus
membrane. A 1cm incision was made through the membrane, and inspection of the maxillary
sinus was performed. Thereafter, the implant was visible and could be removed with a forceps.
The perforation in the sinus membrane was covered with an absorbable collagen membrane.
After grafting the space underneath the membrane and the mucoperiosteal flap was repositioned
and sutured. The patient received a broad spectrum antibiotic for one week and a nasal
decongestant. The patient was instructed to use a 0.2 % chlorhexidine mouth rinse for 2 weeks.
No complication was observed postoperatively.
Six months after implant removal and second bone grafting, bone consolidation seemed to
be sufficient for the placement of one implant. After 3 months, the prosthesis was delivered. During
a follow up period of 5 years, no maxillary sinus complains were noted, and no implants were lost.
The postoperative period was uneventful.

~ 299 ~
 Case 3: A 45-years old man was referred to our private practice with a mobile cemented
multi-unit bridge in the upper right side. After clinical examination, a panoramic radiograph was
taken. The radiograph showed well integrated implants in the maxillary left side and an implant
with its abutment that migrated into the maxillary sinus adjacent to the nasal cavity.
The patient presented no sinus symptomalogy or discomfort on palpation. Patient refused
to undergo surgery to remove the migrated implant and remained asymptomatic for two years after
the migration of the implant.

Prevention
Education of general dentists.
Recommend advanced training, cooperation, and encourage referral and team work.
Professional interexchange and understanding.
Proper patient selection.
Assessment of quality and quantity of bone via CT-scans.
Key factor is primary stability assessed by insertion torque (periotest, or osstell), removal torque
test (RTT).
Prevent continuous micromotion > 150 µm.
The longer the implant, the stronger the association with migration although illogical result.

Postoperative Maxillary cyst

Misch, 1991, described a case of postoperative maxillary cyst as a round, well-defined 1cm
cystic cavity in the central part of grafted sinus, lined with membrane similar to normal sinus
membrane (SM) with clear aseptic fluid (Fig 5.34).
Histology: membrane consists of sclerosus sinus mucosa lined with respiratory ciliated epithelium.
Complete enucleation is necessary to prevent recurrence of the cyst.
Etiology: we can assume that a fragment of mucosa, entrapped in the grafted bone, caused the
occurrence of a cyst.

a b
Fig 5.34a: CT scan demonstrating a rounded, well-defined Fig 5.34b: Panoramic view of CT-scan demonstrating a well
cystic lesion in the central part of the grafted sinus. defined cystic lesion in the lefft augmented sinus.

~ 300 ~
 c d
Fig 5.34c: CT scan obtained six months after the Fig 5.34d: Panoramic view of CT-scan obtained six months after
inoculation of cystic lesion and regrafting. regrafting of enuculated cystic lesion.

Accidental grafting of the nasal passage

In cases with no residual bone, it is possible to find the nasal passage in a location where
the maxillary sinus would be expected. Caution must be taken not to graft the nasal passage
accidentally. If this happens, the treatment of choice is the immediate removal of any accidentally
grafted materials (Fig 5.35).

a b
Fig 5.35a: Preoperative CT-scan showing the location of the Fig 5.35b: Postoperative CT shows additionally to sinus
nasal passage in proximity to the sinus cavity grafting, the nasal passage has been grafted

Exfoliation of Grafting Material

A reported postoperative complication is the loss of graft material through the access
window as a result of displacement of the nonstabilized collagen barrier membrane. the loss of
graft material can be related to the increased intrasinus pressure caused by postoperative
inflammation, bleeding from within the sinus, and patient sneezing or nose blowing [843, 844]
(Fig 5.36). To reduce graft displacement after sinus surgery, a novel technique for placing a
collagen barrier membrane (cross-linked or non-cross-linked) over the antrostomy is suggested by
Testori et al [845]. After the graft is placed into the sinus, the access window is measured and
outlined mesiodistally and apicocoronally. The planned barrier collagen membrane should be at
least 2 mm larger than the size of the antrostomy. The membrane is then placed over the window
and its borders gently tucked between the inner side of the bony wall and the particulate graft
material. A second barrier membrane may be placed over the antrostomy if the clinician desires
greater barrier function. This procedure prevents graft exfoliation caused by postoperative
inflammation, bleeding from within the sinus, and sneezing or nose blowing without the need to
stabilize the barrier membrane with tacks or sutures.

~ 301 ~
 Fig 5.36: CT view demonstrating exfoliation of grafting material one week after surgery and three months
postoperative [815]

Wound dehiscence
The spontaneous early exposure of a grafted sinus is a complication that could affect
uneventful healing and compromise the augmentation procedure’s outcome.
Dehiscence of the surgical wound occurs more often in patients treated with sinus grafting
in association with horizontal GBR. Tal reported a prevalence of 4.6% to 13.7% wound dehiscence
in submerged implant surgery [846]. An increased prevalence of soft tissue dehiscence was noted
when barriers were placed as part of a guide bone regeneration procedure. While the treatment
time or number of surgical procedures may be reduced by doing maxillary sinus elevation with
simultaneous ridge augmentation, this approach may also increase the risk of wound dehiscence
and compromise the final treatment. Other factors contributing to wound opening may include
poor flap design, faulty suturing technique, strained flap closure, infection, and trauma from
inadequate free provisional prostheses or antagonistic teeth [847]. In some patients, the exposed
bone graft should only be treated with cautious curettage, antibiotic therapy, chlorhexidine gel,
with spontaneous healing by secondary intention. In some cases, infection may occur despite this
treatment and the graft has to be partially removed until spontaneous healing is completed.

Peri-implantitis
At the level of knowledge we have today, 50 years after the advent of osseointegration,
“peri-implantitis” is a minor problem in the range of 1 to 2% of modern implants at 10 years. Koka
and Zarb [848] recently questioned whether peri-implantitis is a disease entity at all. These authors
suggested terms such as osseoinsufficiency or osseoseparation to describe problematic implants.
In contrast, in a recent systematic review, Mombelli et al. [849] reported on peri-implantitis
epidemiology including 23 mainly cross-sectional, retrospective studies. The authors concluded
that “the prevalence of peri-implantitis seems to be in the order of 10% implants and 20% patients
during 5-10 years after implant placement. A number of studies have documented that plaque
formation at implant sites results in mucositis [850-852]. This means that peri-implant mucositis
commonly occurs. The term “peri-implantitis” was coined to illustrate that this condition had
several features in common with periodontitis, including, soft tissue inflammation and marginal
bone loss. The validity of this comparison between periodontitis and peri-implantitis, is questioned
by several authors who suggest that numerous factors differentiate peri-implantitis from
periodontitis, including patient-, clinician-, and foreign body-related factors as well as trauma from
occlusion may be related to the “biologic failure of osseointegration”. “Peri-implantitis” was used
to describe implant sites at which crestal or marginal bone loss was associated with mucosal
inflammation. Koldslant et al. [853] demonstrated that the prevalence of peri-implantitis is
dependent on the definitions applied as to the amount of crestal bone loss and the depth of the soft

~ 302 ~
tissue pocket. Patients suffering for revisable peri-implant mucositis can be managed by an oral
hygiene program to maintain peri-implant tissue health. Patients with developed peri-implantitis,
with angular bony destruction of more than 3mm, necessitate a flap surgery for maintenance of
peri-implant tissue health. The principles of the cumulative interceptive supportive therapy
protocol are employed in the treatment. Patients who develop local peri-implant infections should
be treated with local irrigation of the peri-implant sulcus with chlorhexidine-digluconate 0.2%,
twice a day for two weeks.

Persistent idiopathic facial pain (PIFP)

Atypical facial pain(AFP)
Persistent idiopathic facial pain (PIFP) is considered one of the most frustrating facial pain
conditions that challenges medical and dental clinicians [854]. Although this facial pain condition
was first described in 1947 by McElin and Horton by the term atypical facial pain (AFP) [855], so
far there is still a lack of consensus in the medical and scientific community regarding terminology,
classification, and diagnostic criteria. PIFP is diagnosed by excluding all other pathologies that
may provoke facial pain in the affected area. PIFP is best described as a chronic form of facial pain
that is normally continuous, deep, and poorly localized, of low to moderate intensity, with sporadic
episodes of intense pain. Some patients, however, may describe their pain as throbbing, burning,
or even stabbing. The pain is not associated with sensory loss or other physical signs. Certain
individuals may report that their pain started without any recognizable lesion to the facial
structures and therefore, the term idiopathic is used. Indeed, several studies have shown a strong
correlation between PIFP and several psychological conditions, such as depression, anxiety, and
sleep disorders [856-858]. Most authors, nonetheless, identify PIFP as a neuropathic pathology.
Certain medications used for the treatment of neuropathic pain, among these tricyclic
antidepressants (TCAs), appear to be the most effective in treating PIFP [854, 859]. Amitriptyline
is effective at doses ranging from 25 to 100 mg a day [860]. Other studies also demonstrate that
phenothiazine [861], β-blockers [862], and certain anticonvulsants [862,863] are effective
treatments. When pain is extreme and cannot be controlled with these medications, opiate
analgesics such as morphine sulphate, methadone, or fentanyl may be used in selected individuals
[858,863]. The prevalence of PIFP following dental implant placement is unknown. PIFP is a
possible complication of dental implant surgery [864]. A combination of nortriptyline,
clonazepam, and relaxation training procedures may be helpful in the management of PIFP [864].

Case 1: A 39 year old female experienced an unexplained facial pain in the right maxilla
after maxillary sinus augmentation and delayed three implants insertion. The pain started a few
weeks after implant placement and continued for an additional eight months. No clear cause for
the pain could be defined even after consultation of an ENT specialist and a neurologist. The
diagnosis was atypical facial pain. The implants were later removed and the patient reported an
improvement in the pain for a limited period of time.
Case 2: One patient who had received a total of four implants bilaterally of sinus
augmentation, two implants in the right maxillary were surgically removed after 12 months
because of increasing persistent pain in the peri-implant region. After removal of the implants, the
patients stated a slight improvement of the pain.

~ 303 ~
 Cholesterol Granuloma
Cholesterol granuloma (CG) is a histological term describing a granulomatous tissue
reaction to cholesterol crystals precipitation. It is extremely rare in the paranasal sinuses, and,
when they are involved, the maxillary sinus tends to be the most commonly affected [865]. The
occurrence of CG in the maxillary sinus (CGMS) was first reported in 1978 by Graham and
Micheals [866]. Since that time, only 42 documented cases of maxillary sinus involvement were
reported in the literature. The clinical and radiographic features of CGMS are nonspecific, and,
therefore, the preoperative diagnosis of CGMS is rarely suspected. Clinically, patients affected by
CGMS generally report vague and nonspecific symptoms. Nasal discharge, nasal obstruction and
congestion, postnasal drip, facial pain and headache, and otalgia are the most common reported
symptoms. Other less common reported symptoms include foul smelling, cheek swelling, and
epistaxis. Radiographic findings of CGMS are also generally nonspecific and cannot be
differentiated from allergic or inflammatory sinus diseases [867]. Most common changes are
antrum opacification and cystic appearance. CT scanning usually reveals nonspecific findings.
However, MRI was reported to be more accurate in the diagnosis of CGMS. Histological
examination remains the “gold standard” for the definitive diagnosis of CGMS. The characteristic
findings include abundant cholesterol clefts surrounded by granulation tissue, foreign-body type
giant cells and mixed chronic inflammatory cell infiltrate in addition to localized old and recent
microhemorrhages (Fig 5.37). Many authors highlight the importance of disturbed ventilation,
inadequate drainage, and hemorrhage into bony cavity as factors responsible for CF development
[865].

Fig 5.37: Histopathologic features of cholesterol granuloma;

multiple cholesterol clefts surrounded by granulation tissue
and foreign-body giant cells.

Benign paroxysmal positional vertigo

Benign paroxysmal positional vertigo (BPPV) is defined as a disorder of the inner ear
characterized by repeated sudden short episodes of spinning sensation produced by changes in
head position relative to gravity [868,869].
It comes in two types, primary or idiopathic BPPV and secondary BPPV. The most
common cause of secondary BPPV is thought to be due to canalithiasis. The otoliths from the

~ 304 ~
membrane of the utricle macula are displaced into the posterior semicircular canal (90% of the
cases) [870,871] or into the lateral semicircular canal of the vestibular apparatus. They alter the
gravity-dependend endolymph system and cause abnormal neural firing from the hairy cell of the
ampullae that result in abnormal nystagmus and vertigo with head motion in the plane of the canal.
This occurs most often as a result of aging, head trauma, vestibular neuritis, and Meniere’s disease.
Another common cause includes prolonged positioning on the back (supine) [872] during surgical
procedure.
BPPV can occur as an unexpected complication during implant surgical or allied surgical
procedure. This can be caused by using specific instrumentation and also by prolonged
hyperextended head position.
Despite many articles in the literature confirming the role of trauma in causing BPPM
during osteotomy type sinus augmentation procedures, no clear reason was found pointing to the
cause of positional vertigo during lateral osteotomy sinus floor elevation [873]. Among the
possible causes is the prolonged supine position with hyperextention of the neck during the
procedure or the traumatic force spread during lateral window opening with a rotating tool that
might dislodge the otoliths [874].

~ 305 ~
 CONCLUSIONS
Sinus augmentation surgery with simultaneous implant placement is a predictable and very
versatile procedure that enables implant-prosthetic rehabilitation of the edentulous atrophic
posterior maxilla with a very high implant survival rate. Based on these promising results, this
procedure is considered a standard of care, provided that the patient is not medically compromised.
Two-stage sinus augmentation procedure with biomaterials, either alone or combined with
autogenous bone graft material has a predictable outcome. The method is reliable and useful for
patients with severe resorption of the posterior maxilla. The low failure rate and the low rate of
post-operative complications show that sinus grafting is an established technique that can be used
with good prognosis. Local sinus lift with sinus bone augmentation and single tooth replacement
in the posterior maxilla is a predictable method as well. The studies show that none of the following
variables: grafting materials used, associated procedures, associated materials, simultaneous or
delayed implant placement, presence of comorbidities, and smoking habits are detrimental to
implant survival.
A thorough understanding of the anatomic and physiologic features of the maxilla is a
prerequisite for successful placement of implants capable of securing oral implant-supported
reconstructions coupled with satisfactory aesthetics. These features include: the maxillary sinus,
the morphofunctional changes of the maxilla following tooth loss, the anatomical manifestation of
different bone resorption pattern and alterations in bony and mucosal contours post-extraction in
the posterior maxilla, character of the overlying soft tissues and the course of neurovascular
structures.
The posterior maxilla has the greatest surgical difficulty as well as the greatest occlusal
need. Treatment planning and precise improved surgical protocols are crucial to success. There is
no doubt that factors like the small quantity of subsinuosal bone, pneumatization of the maxillary
sinus, and low bone density in the maxillary tuberosity may pose difficulty in the rehabilitation of
the posterior maxilla. For patients with severely resorbed posterior maxilla, two therapeutic
approaches are mainly carried out for implant-supported fixed rehabilitation: either sinus
augmentation or the placement of implants in the pre-existing anatomic features. The sinus floor
elevation by lateral access has proved to be highly predictable and can be the solution for
inadequate height.
Sinus grafting is a demanding surgical procedure and it is quite invasive. The one step sinus
elevation with simultaneously implant insertion is similar to the two step technique. The most
important difference is that less time elapses before initiation of the prosthetic therapy. The two
protocols have yielded different cumulative success rates: from 83% to 100%. The clinician must
make the appropriate selection of graft material and technique based on the size, shape and
dimensions of the defect. Confounding reports have appeared in the literature as to implant success
and survival rates for implants placed into bone-grafted sites. This procedure is more time
consuming, involves higher costs to the patients, utilizes grafting materials, increases morbidity,
and requires a highly skilled clinicians.
Despite the trend toward sinus grafting commonly used in patients with severely resorbed
posterior segments of the maxilla, more attention should be given to the possibilities of implant
placement using the anatomic features of the arches without the use of bone grafting procedures.
This increases the possibility for a simpler rehabilitation. Placing implants in pre-existing bone
must be considered to avoid more complex surgical procedures such as maxillary sinus floor
augmentation, using alternative anatomic features to place the implants, such as in the anterior and
the posterior maxillary sinus wall, the palatal curvature, and the pterygoid process. Tilted implants,

~ 306 ~
short implants, pterygomaxillary implants, palatal positioned implants, zygomatic implants
facilitate rehabilitation with fixed prosthesis in the severely atrophic maxillae. This surgical
method reduces the duration of surgery and treatment by eliminating the graft healing period, thus
reducing the cost of treatment, patient and practitioner discomfort, and risks of morbidity.
The concept of a shortened dental arch must also be considered. The work of Kayser [874]
shows that patients maintain adequate chewing capacity of 50-80% with a premolar occlusion
[875].
All surgical procedures have the potential to develop complications leading to additional
surgery, prolonged hospital recovery, fatigue and nutritional disorders, which markedly
compromise quality of life. The most frequently reported complication is membrane perforation.
Membrane perforation is not an absolute contraindication to continuing surgery, provided that the
perforation does not allow the passage of graft material inside the maxillary cavity. Membrane
perforation affects implant survival negatively and correlates inversely with the size of the
perforations. Treating the complications, particularly of sinus graft infection, using surgical and
pharmacological regimens leads to successful outcomes.

The following can improve the implant success rate:

 Choosing the right implant length and considering volume changes of grafted materials.
For a 13mm long implant, a residual height of 15mm is needed which includes 2mm safety
margin.
 Placement of a longer implant with sinus augmentation does not decrease the stress in
native bone. However, it does reduce the stress in grafted bone due to the increased area of
contact within the grafted sinus.
 The use of high stiffness grafted bone decreases the stress in native bone, which might
reduce the risk of bone loss due to overloading.
 The use of a wide implant decreases the stress in the native bone and in grafted bone due
to the enlarged contact surface area.

More studies are required to determine the conditions and the techniques needed to improve
the success rate and to gain a better understanding for success and failure of dental implants.

~ 307 ~
 TERMINOLOGY AND DEFINITIONS OF USED TERMS

Definitions and some comments on the terms used, are presented, which will help in
better understanding and communication of the insights gained. The following definitions were
adopted from the Glossary of Oral and Maxillofacial Implants [876].

Autograft
Tissue transferred from one location to another within the same individual. (synonymous with
autologous/autogenous graft)

Allogeneic bone graft

Graft between genetically dissimilar members of the same specites. Iliac cancellous bone and
marrow, freeze-dried bone allograft (FDBA), and demineralized freeze-dried bone allograft
(DFDBA) are available commercially from tissue banks. Called also allograft.

Allograft
Graft between genetically dissimilar members of the same species [877, 878].

Alloplast
Inorganic, synthetic, or inert foreign material implanted into tissue [877, 878].

Alloplastic graft
Graft material such as hydroxyapatite (HA), tricalcium phosphate (TCP), poly-
methylmethacrylate (PMMA) and hydroxyethylmethacrylate (HEMA) polymer, or bioactive
glass that is derived either synthetically of from a foreign, inert source.

Alveolar ridge augmentation a. r. a.

Surgical augmentation of the alveolar ridge in a horizontal and/or vertical direction using one of
several approaches based on the size and/or location of the defect.

Bone grafting for a. r. a.

Surgical procedure by which the residual alveolar ridge is enhanced in height and/or width with
an autogenous graft, allograft, synthetic graft, or any combination of these materials.

Guided bone regeneration for a. r. a.

Principle of guided bone regeneration (GBR) using barrier membranes, either resorbable or
nonresorbable, to exclude certain cell types such as rapidly proliferating epithelium and
connective tissue, thus promoting the growth of slower-growing cells capable of forming bone.
GBR is often combined with bone grafting procedures.

Augmentation
Grafting procedure designed to increase the volume of existing tissues, usually referring to bone
for the purpose of adequate bony support around implants and/or improving tissue contours for
esthetic purposes.

~ 308 ~
Autogenous bone graft
Bone graft taken from an intraoral or extraoral site and placed in the same individual. Origin of
the graft will determine whether it is cortical, corticocancellous, or cancellous in nature.
Particulate grafts may be harvested with hand instruments or prepared by introducing chips into a
bone mill. Block grafts can be harvested when a cortical component exists (ie, symphysis, ramus
buccal shelf, calvarium, or iliac crest), when volume is not sufficient, and/or if the need to retard
resorption is required. Autogenous bone grafts are often mixed with allografts, alloplasts, or
xenografts. Called also autograft.

Autogenous graft
Tissue transferred from one location to another within the same individual.

Biodegradable material
Solid polymeric material that breaks down because of macromolecular degradation with
dispersion in vivo; no proof for elimination from the body.

Bioresorbable material
Solid polymeric material that shows bulk degradation and further resorbs in vivo, resulting in
total elimination of the initial foreign material. Compare: Resorbable.

Bone graft
Bone taken from a donor site of the patient (autogenous) or from an outside source (allograft,
alloplastic graft, or xenograft). A bone graft is used to augment a bone deficiency in neous or
subsequent implant placement.

Bone healing
Cellular events, recapitulating embryogenesis. After initiation of woven bone formation,
deposition of parallel-fibered bone ensues. These two primary types of bone repair the defect
within weeks; thereafter, the formation of perivascularly arranged lamellar bone takes place with
simultaneous resorption of the two primary bone types. This substitution, which gives strength to
the bone, may take months to years, depending upon the size of defect. Finally, a structural
rearrangement of trabeculae in response to function (Wolff law) takes place. Healing of fractures
of long bones may often be characterized by a callus formation in the initial stages, where woven
bone is mixed with cartilage, resulting in c clinically as well as radiologically visible thickening
of the fracture site. This callus will disappear along with the osseous maturation.

Bone modeling
Processes producing functionally purposeful skeletal organs aimed at characteristic adult shape
and form; includes longtidinal, transversal, and appositional growth.

Bone regeneration
Renewal or repair of lost bone tissue. Also: cellular events during wound healing; recapitulation
of cellular events of embrygenesis. The quantitative extent is defect dependent and influenced by
cellular race.

~ 309 ~
Bone remodeling
Basic physiologic remodeling of bone takes place in a biologically coupled system of activation,
resorption, formation (ARF). Histomorphologically, the process starts in cortical bone as a
cutting cone, consisting of a group of osteoclasts, digs a tunnel with a breakdown of 20 um per
day with a simultaneous increase in diameter of the tunnel in magnitude of 5 um per day until a
width of approximately 100um in radius is reached. When the resorption ceases, the osteoclasts
are replaced by osteoblasts after a short resting period. The osteoblasts form new lamellar bone
at a speed of 1 um per day, and thereby the tunnel is closed again. The length of the entire cone
is typically around 1,500 to 1,600 um. The entire course is also named creeping substitution.
Similar remodeling takes place in trabecular bone as surface resorption, creating a 60- to 70-um
– deep crateriform cavity that is filled in with lamellar osteoid over a 4-month period.

Bone substitute
Nonviable biomaterial for reconstruction of bone, producing only a scaffold for formation of new
bone. Supports the inherent potential for bone regeneration.it may be resorbable or remain in an
unchanged version at the site of implantation. It also may assist in preservation of contour of an
osseous reconstruction.

Collagen
Insoluble fibrous protein of vertebrates that is the principal constituent of the fibrils of
connective tissue and the organic substance of bones.Composed of tropocollagen molecules.
Collagen membrane
Resorbable barrier membrane made of heterogenic collagen, developed for guided tissue
regeneration (GTR) or guided bone regeneration (GBR) techniques. The resorption time of
collagen membranes can be controlled using methods of collagen cross-linking.
Composite graft
Graft composed of multiple graft types (eg, autogenous-synthetic graft or autogenous-xenograft),
which may be mixed or layered within the defect.
Demineralized bone matrix (DBM)
Bone matrix, usually allogeneic in origin, that may induce bone formation via release of growth
factors and bone morphogenetic proteins (BMPs) from the matrix, occasionally after osteoclastic
breakdown. Osteoinductive potential may vary, dependent on method of prepation and degree of
demineralization.
Extracellular matrix (ECM)
Material produced by cells and excreted to the extracellular space within the tissues. It takes the
form of both ground substance and fibers and is composed chiefly of fibrous elements, proteins
involved in cell adhesion, glycosaminoglycans, and other space-filling molecules. It serves as a
scaffolding for holding tissues together, and its form and composition help determine tissue
characteristics. The matrix may be mineralized to resist compression (as in bone) or dominated
by tension-resisting fibers (as in tendon).

~ 310 ~
Graft
Originally, a graft was a transplant, but subsequently it was considered to be bone taken from a
donor and transferred to a recipient. Synthetic bone substitutes, such as hydroxyapatite and
tricalcium phosphate, are thus not grafts in the original sense. However, for the sake of clarity,
we use the term "graft" for all kinds of bone augmentation materials. Living tissue placed in
contact with injured tissue to repair a defect or supply a deficiency. To induce union between
normally separate tissues. Graft options may include both vital and nonvital materials.
Graft healing
The restoration of implanted living tissue to its original intergrity. Bone graft healing has two
different routes: either it fails to incorporate and gradually disappears, or it becomes incorporated
as a mechanically functioning part of the host bone. Osteoblasts or osteoprogenitor cells may be
transferred to recipient site. Via resorption of bone graft, various growth factors are released
from the noncollagenour part of bone matrix.
Graft consolidation
We use this term for the process at the end of which the graft is surrounded by newly formed
bone. The graft consolidation process is similar to the process of bone regeneration and leaves a
conglomerate of bone and grafting material. This conglomerate may be, but is not necessarily,
replaced by bone. However, catabolic processes may occur that lead to the complete resorption
of the graft together with the newly formed bone. Based on our definition, graft consolidation is
restricted to the anabolic phase of bone formation.
Guided bone regeneration (GBR)
Follows the principle of maintaining a surgically created space at a bony defect via a barrier
membrane, thus excluding rapidly proliferating epithelial cells and fibroblasts and permitting the
growth of slower-growing bone cells and blood vessels. Graft material may also be used in
combination with barrier membranes in GBR procedures to support the membrane and prevent
its collapse. In addition, bone grafts provide a scaffold upon which new bone can for. Protection
of a blood clot in the defect and exclusion of gingival connective tissue and provision of a
secluded space into which osteogenic cell from the bone can migrate are essential for a
successful outcome [879].
Guided tissue regeneration (GTR)
Surgical procedure aimed at regenerating lost periodontal attachment. Creation of a secluded
space favoring angiogenic and osteogenic cells, protecting the vascular and cellular elements
while probably supporting accumulation of growth factors. True periodontal regeneration must
include new cementum formation, periodontal ligament, and alveolar bone on a previously
diseased root surface. GTR follows the principle of maintaining a surgically created space
around teeth via a barrier membrane, thus allowing the slower – proliferating periodontal
ligament cells, bone cells, and possibly cementoblasts to populate the root surface. This term is
not to be confused with guided bone regeneration (GBR), which describes a similar principle for
isolated bone defects following tooth loss and concerns the regeneration or augmentation of bone
only.

~ 311 ~
Lateral window technique
Surgical technique using a window onto the lateral wall of the maxillary sinus to gain access to
the maxillary sinus membrane. Following mobilization and elevation of the sinus membrane,
bone augmentation materials (ie, autografts, allografts, alloplasts, xenografts, or combination
mixtures) are used to elevate the sinus floor and allow the placement of dental implants. If the
original bone height permts sufficient primary implant stability, then a simultaneous procedure
can be used. Otherwise, a staged approach is recommended [880, 881]. Compare: Osteotome
technique.
Maxillary sinus floor elevation
Augmentation procedure for the placemenet of implants in the posterior maxilla where
pneumatization of the maxillary sinus and/or vertical loss of alveolar bone have occurered.
Autografts are often mixed with bone substitutes to increase the volume of the augmentation
material or prevent graft resorption during remodeling. Two surgical techniques are well known
and routinely used in daily practice: the lateral window technique, first described by Boyne and
James in 1980 [880]; and the transalveolar osteotome technique, first described by Summers in
1994 [881, 882].
Maxillary sinus floor graft
Graft used to augment the vertical height in the maxillar sinus for implant placement. A
particulate mixture of autogenous bone and a bone substitute is often used.
Maxillary sinus membrane
Thin mucous membrane lining the sinus cavity and characterized by respiratory epithelium.
"Sinus mucosa" and "Schneiderian membrane" and "sinus membrane" are also frequently used
synonymously.
Nonresorbable membrane
Membrane made of nonabsorbable biomaterial, most often of expanded poltetrafluoroethylene
(e-PTFE). Use of a nonresorbable membrane requires a second surgery to remove it.
Osseointegration
Direct structural and functional connection between ordered, living bone and the surface of a
load-carrying titanium implant. (Original definition attributed to –P-I Branemark published in
1985 based on microscopic findings.) The implication is that an interface between an inert
metallic surface and living bone is created without an interpositional tissue. Commercially pur
titanium (CPTi) and titanium alloy (Ti-6AI-4V) have been proven clinically and microscopically
to be biocompatible materials for achieving osseointegration. Osseointegration is considered to
be the phenomenon of direct apposition of bone on an implant surface, which subsequently
undergoes structural adaptation in response to a mechanical load [883, 884].
Osseous repair
Restoration of form and function of deficient osseous tissue.

~ 312 ~
Ossification
Formation and development of bone, of which two types are distinguished endochondral and
intramembranous ossification.
Osteoconduction
Physical aid to osteoid formation via species-specific or alloplastic scaffold with nonending
porosity. Which is the property of the graft that ensures an intimate contact with newly formed
bone. This is basic requirement of all grafting materials. Without it grafts cannot guide new bone
into the augmented area.
Osteocunductive graft
autografts, treated allografts, and bone substitutes that provide a scaffold for osteoid formation.
Osteogenesis
Generation, regeneration, and remodeling of bone via concerted action of bone cells.
Osteogenetic
Quality of any substance, biologic or nonbiologic, that is able to initiate or stimulate normal
osteogenesis.
Osteogenic
Refers to the stimulation of bone formation produced by modulations of batural biochemical
processes such as growth factors and bone. Autografts, that initiate and maintain and/or support
bone formation during a healing response. Grafts are considered osteogenic when they contain
cells with the potential to form bone, but thisdoes not necessarily mean the these cells also
contribute to bone formation.
Osteoinduction
Transformation of osteoprogenitor cells to active osteoblasts via paracrine signals to appropriate
receptors. Therefore, bone formation is induced by osteoprogenitor cells in heterotopic sites,
mostly via endochondral ossification. Traditionally: the initiation of heterotopic bone formation.
Biologically: the initiation of osteogenesis via growth factiors. means that a graft is capable of
initiating de novo bone formation. Osteoinduction usually recapitulates the embryonic processes
underlying bone formation – basically by targeting mesenchymal stem cells and causing their
differentiation via osteogenic or chondrogenic cells is the basis for the definition of the term
"osteogenic".
Osteointegration
Ankylotic anchorage of a titanium implant in living bone to achieve a solid bond. Histologically
and radiographically described by Andre Schroeder and colleagues in 1991 [885].
Osteotome technique
Surgical technique using a translaveolar approach to elevate the sinus floor by using osteotome
instruments. Anatomic aspects, such as an oblique sinus floor or insufficient bone height, can
limit the use of this delicate surgical technique in daily practice [871, 886]. Compare: Lateral
window technique.

~ 313 ~
Periotest
Instrument used to measure the relative mobility of teeth and dental implants. Device utilizes a
tapping piston to percuss a tooth or an implant four times per second. Rate of deceleration
recorded at the point of contact is measured as the relative stiffness of the tooth or implant.
Periotest values range from -08 to +50, with the -08 to +09 range indicating no discernable
movement, +10 to +19 just discernable movement, +20 to +29 obvious movement, and +30 to
+50 mobile on pressure [887]. Photo P125.
Pterygoid implant
Implant placement through the maxillary tuberosity and into the pterygoid plate. Treatment
approach can be used in patients with severe maxillary atrophy of following tumor resection.
Implant is placed into pterygoid bone structure to serve as distal abutments for implant
restorations [888, 889]. Compared: Zygomatic implant.
Resorbable membrane
Membrane made of absorbable natural or synthetic materials used to avoid a second surgery for
its removal. After implantation in the body, membranes are degraded by enzymatic activity
(collagen membranes) or by hydrolyses (polylactic acid and copolymers of polylactic and
polyglycolic acids membranes).
Restitution ad integrim
Re-establishment of original form and function.
Sinus lift
Misnomer used to describe surgical techniques for maxillary sinus floor elevation. There are
several synonyms for sinus augmentation including sinus lift and sinus elevation. We will use the
term sinus augmentation.
Turned implant surface
The surface texture of an implant as generated by milling machines used in manufacturing of the
final implant shape. The surface is not altered subsequent to the machining process. Called also
machined implant surface. Compare: Polished implant surface.
Wolff Law
Principle of bone healing and/or remodeling based upon the understanding that bone remodeling
based upon the understanding that bone remodels in response to physical stress by depositing
bone in locations of increased stress and resorbing bone in areas of little or no stress [890, 891]
Xenograft
Graft taken from a donor of another species. Called also heterograft.

~ 314 ~
 LIST OF ABBREVIATINS

AAA Alveolar antral artery

AB Autogenous bone
ABL Apical bone loss
AFP Atypical facial pain
AIDS Acquired immune deficiency syndrome
ALARA As Low as Reasonably Achievable
ARF Activation, resorption, formation
ASAA Anterior superior alveolar artery
BCP Biphasic calcium phosphate
BG Bioglass
BGM’s Bone grafting materials
BI Bleeding index
BIC Bone-to-implant contact
BMD Bone mineral density
BMP Bone morphogenetic protein
Bisphosphonate-related osteonecrosis of the
BRONJ jaws
BS bone substitute
BV bone volume
CaP Calcium-phosphate
CBCT cone beam computed tomography
CC chief complaint
CG Cholesterol granuloma
CGMS Cholesterol granuloma in the maxillary sinus
CPTi Commercially pur titanium
CT conventional tomography
DBBM deproteinized bovine bone mineral
DFDBA demineralized freeze-dried bone allograft
Digital Imaging and Communications in
DICOM Medicine
EA extraosseous anastomosis
EAO European Association for Osseointegration
ECM extracellular matrix
EH external hexagons
ENT ear, nose and throat
e-PTFE Expanded polytetrafluoroethylene
FDBA freeze-dried bone allograft

~ 315 ~
FESS functional endoscopic sinus surgery
GA general anesthesia
GBR guided bone regeneration
GI gingival index
GTR guided tissue regeneration
HA hydroxyapatite
HEMA hydroxyethylmethacrylate
human maxillary sinus Schneiderian
hMSSM membrane
HU Hounsefield units
IA intraosseous anastomosis
IH internal hexagons
IL interleukin
IOA infraorbital artery
ION Infraorbital nerve
IS implant stability
ISQ Implant stability quotient
ISQ Implant Stability Quotient
IT insertion torque
IV intravenous
KM keratinized mucosa
LA Local anesthesia
MBL Marginal bone loss
MCBA mineralized cancellous bone allograft
MF magnification factor
MF magnification factor
micro-
CT Microcomputed tomography
MSCs mesenchymal stem cells
MSCT Multi-slice computer tomography
MSH maxillary sinus hypoplasia
N-BPs nitogen-continng bisphosphonates
NO nitric oxide
ONJ Osteonecrosis of the jow
PIFP Persistent idiopathic facial pain
PMH past medical history
PMMA poly-methylmethacrylate
PREC potentially reversible contraindication
PRGF Plasma rich growth factors
PSAA posterior-superior alveolar artery

~ 316 ~
PTV Periotest-Value
RBH Residual alveolar bone height
RFA Resonance Frequency Analysis
RPM rounds per minute
RTT reverse torque test
SFE sinus floor elevation
SFEPs sinus floor elevation procedures
SFFR sulcus fluid flow rate
SM Schneiderian membrane
SMP Schneiderian membrane Perforation
TCAs tricyclic antidepressants
TCP tricalcium phosphate
TNF-α tumor necrosis factor α
TSFE transcrestal sinus floor elevation
TV total volume
VV voxel value
β-TCP beta tricalcium phosphate

~ 317 ~
 REFERENCES

1. Marcus SE, Drury JF, Brown LS et al: Tooth retention and tooth loss in the permanent detition of adults:
United States, 1988-1991, J Dent Res 75:684-695, 1996.
2. Jung RE, Pjetursson BE, Glauser R, Zembic A, Zwahlen M & Lang NP. Asystematic review of the 5-
year survival and complication rates of implant-supported single crwons. Clinical Oral Implants
Research 2008; 19: 119-130
3. Ellis E: The nature of vertical maxillary deformities: Implications for surgical intervention. J Oral
Maxillofac Surg 43:756, 1985.
4. Wolff, J. (1986) The Law of Bone Remodeling (Maquet, P. & Furlong, R., trans.)/ Berlin, Heidelberg:
Springer-Verlag.
5. Ulm, C.W., Solar, P., Gsellmann, B., Matejka, M. & Watzek, G. (1995) The edentulous maxillary
alveolar process in the region of the maxillary sinus-a study of physical dimention. The International
Journal of Oral & Maxillofacial Surgery 24: 279-282.
6. Tulasne JF. Osseointegrated fixtures in the pterygoid region. In: Worthington P, Branemark P-I (eds).
Advanced Osseintegraticn Surgery: Applications in theMaxillofacial Region. Chicago: Quintessence,
1992: 182-188.
7. Reiser GM. Implant use in the tuberosity, pterygoid, and palatine region: Anatomic and surgicall
considirations. In: Nevins M, Mellonig JT(eds). Implant Therapy: Clinical Approaches and Evidance of
Success, vol 2> Chicago: quintessence, 1998:197.
8. Lee SP, Paik Ks, Kim MK. Anatomocal study of the pyramidal process of the palatine bone in relation to
implant placement in the posterior maxilla. J Oral Rehabil 2001;28:125-132.
9. Rodriguez X, Rampla F, Lopez LDM, Mendez V, Vela X, Garcia JJ. Anatomical stude of the
pterygomaxillary area for implant placement: cone beam computed tomographic scanning in 100 patient.
Int J Oral Maxillofac Implants 2014;29:1049-1051 .
10. Bidra AS, Huynh-Ba G. Implants in the pterygoid region: A systematic review of the literature. Int J Oral
Maxillofac Surg 2011;8:773-781
11. Rodrigues X, Mendez V, Vela X, Segala M. Modified surgical protocol for placing implamts in the
pterygomaxillary region: Clinical and radiological study of 454 implants. Int J Oral Maxillofac Implants
2012;27:1547-1553.
12. Berkovitz BKB, Holland GR, Moxhab BJ. A Colour Atlas and Textbook of Oral Anatomy, Histology
and Embryology, ed 2. London: Wold, 1997.
13. Al-faraji L. Surgicak and Radiographic Anatomy for Oral Impplants, 2013; Quintessence publishing CO.
Ltd.
14. Traxler, H., Windisch, A., Geyerhofer, U., Surd, R., Solar, p. & Firbas, W. (1999) Arterial blood supply
of the maxillary sinus. Clinica Anatomy 12: 417-421.
15. Blitzer A, Lawson W, Friedman WH, editors: surgery of the paranasal sinuses, Philadelphia, 1985, WB
Saunders.
16. Jun BC, Song SW, Park CS, Lee DH, Cho KJ, Cho JH. The analysis of maxillary sinus alteration
according to aging process; volume assessment by 3-dimensional reconstruction by high-resolutional CT
scanning. Otolaryngol Head Neck Surg 2005; 132:429-434.
17. Neivert H. Surgical anatomy of the maxillary sinus. Laryngoscope 1930; 40:1-4.
18. Watzek G, Ulm Ch, Haas R. Anatomic and physiologic fundamentals of sinus floor augmentation. In
Jensen O (ed). The Sinus bone graft. Chicago: Quintessence, 1999:31-47.
19. Khoury F. Bone Augmentation in oral implantology, 2007; Quintessence publishing CO. Ltd.
20. Misch C. Contemporary implant dentistry, Third edition 2008 by Mosby.
21. Pignataro L, Mantovani M, Torretta S, Felisati G, Sambataro G. ENT assessment in theintegrated
management of candidate for maxillary sinus lift. Act Otorhinolaryngol Ital 2008; 28:110-119.
22. Xie B, Yuan J, Zheng X, Wu Z, Wan J, Guo Y. Measurement of ostium area of maxillarysinus on three-
dimensional imaging. Zhonghua Er Bi Yan Hou Ke Za Zhi 2002; 37:38-40.

~ 318 ~
23. Kim SG, Kim YK, Use of a bone wax analogue to determine the amount of chin boneneeded for sinus
augmentation. J Oral Maxillofac Surg 2002; 60:600.
24. Graney D, Rice D. Anatomy. In: Cummings Ch, Fredrickson J, Harker L, Krause Ch,Schuller D,
Richardson M (eds). Otolaryngology & head and neck surgery. St. Louis: Mosby, 1998:1059-64.
25. Neiva RF1, Gapski R, Wang HL. Morphometric analysis of implant-related anatomy in Caucasian skulls.
J Periodontol. 2004 Aug;75(8):1061-7.
26. Yang HM1, Bae HE, Won SY, Hu KS, Song WC, Paik DJ, Kim HJ. The buccofacial wall of maxillary
sinus: an anatomical consideration for sinus augmentation. Clin Implant Dent Relat Res. 2009 Oct;11
Suppl 1:e2-6.
27. Velloso GR, Vidigal GM Jr, de Freitas MM, Garcia de Brito OF, Manso MC, Groisman
M.Tridimensional analysis of maxillary sinus anatomy related to sinus lift procedure. ImplantDent 2006;
15:192-196.
28. Shankar, L. & Evans, K. (2006) An atlas of imaging of the paranasal sinusitis, 2nd edition. Norwich, UK:
Informa Healthcare.
29. Chan HL1, Suarez F, Monje A, Benavides E, Wang HL. Evaluation of maxillary sinus width on cone-
beam computed tomography for sinus augmentation and new sinus classification based on sinus width.
Clin Oral Implants Res. 2014 Jun;25(6):647-52.
30. White, S.C. & Pharoah, M.J. (2004) Oral Radiology – Princibles and interpretation, 5th edition. St. Louis,
MO:Mosby.
31. White, S.C. & Pharoah, M.J. (2004) Oral Radiology – Princibles and interpretation, 5th edition. St. Louis,
MO:Mosby.
32. Bolger WE, Woodruff WW, Morehead , Parsons DS. Maxillary sinus hypoplasia: Classification and
description of associated uncinated hypoplasia. Otolaryngol Head Neck Surg 1990;103:759-765.
33. Lana JP, Carneiro PM, de Marchado VC, de Souza PE, Manzi FR, Horta MC. Anatomic variations and
lesions of the maxillary sinus detected in cone beam computed tomography for dental implants. Clin Oral
Implants Res 2012;23:1398-1403.
34. Allareddy V, Vincent SD, Hellstein JW, Qian F, Smoker WR, Ruprecht A. incidental findings on cone
beam computed tomography images. Int J Dent 2012;Article ID 871532,doi:10.1155/2012/871532.
35. Rege IC, Sousa TO, Leles CR, Mendonca EF. Occurance of maxillary sinus abnormalities detected by
cone beam CT in asymptomatic patients. BMC Oral Health 2012;12:30. doi:10.1189/1472-6831-12-20.
36. Mardinger O, Manor I, Mijiritsky E, Hirshberg A. Maxillary sinus augmentation in the presence of antral
pseudocyst: A clinical approach. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2007;103:180-184.
37. Ziccaedi VB, Betts NJ. Complications of maxillary sinus augmentation. In:Jensen OT9(ed). The Sinus
Bone Graft. Chicago: Quintessence, 1999:201-208.
38. Lin Y, Hu X, Metzmacher AR, Luo H, Heberer S, Nelson K. Maxillary sinus augmentation following
removal of a maxillary sinus pseudocyst after shortened healing period. J Oral Maxillofac Surg
2010;68:2856-2860.
39. Kara IM, Kucuk D, Polat S. Experience of maxillary sinus floor augmentation in the presence of antral
pseudocysts. J Oral Maxilofac Surg 2010;68:1646-1650.
40. Amedee RG, Miller AJ. Simus anatomy and function. In: Bailey, BJ, Johnson JT, Newlands SD (eds).
Heand and Neck Surgery-Otolaryngology, ed 4. Philadelphia: Lippincott, Williams & Wilkins,
2006:321-328.
41. Momeni, A.K, Roberts, C.C & Chew, F.S (2007) Imaging of chronic and exotic sinonasal disease:
review. American Journal of Roentgenology 189:235-45.
42. Zinreich, S.J., Abayram, S., Benson, M.L. & Oliverio, P.J. (2003) The ostiomeatal complex and
functional endoscopic surgery. In: Som, P.M. & Curtin, H.D., eds. Head and Neck Imaging, 4th edition,
149-174. St. louis, MO: Mosby.
43. Wald, E.R. (1993) Radiographics sinusitis: illusion or delusion? The Pediatric Infectious Disease Journal
12:792-793.
44. Lana JP, Rodrigous PM. Anatomic variations and lesions of the maxillary sinus detented in cone beam
computed tomography for dental implants. Clin. Oral Imp.Res.23, 2012, 1398-1403.

~ 319 ~
45. Kretzschmar, D.P. & Kretzschmar, J.L. (2003) Rhinosinusitis: review from dental perspective. Oral
Surgery, Oral Medicine, Oral Pathology, Oral Radiology & Endodontics 96: 128-135.
46. Engstorm H, Chamberlain D, Kiger R, Egelberg J. Radiographic evaluation of the effect of initial
periodontal therapy on thickness of the maxillary sinus mucosa. J Periodontol 1988;59:604-608.
47. Van Cauwenbrege P, Watelet JB. Epidemiology of chronic rhinosinusitis. Thorax 2000;55(Suppl.
2):S20-S21.
48. Chan, H.L. & Wanng, H.L. (20110 Sinus pathology and anatomy in relation to complications in lateral
window sinus augmentation. Implant Dentistry 20: 406-412.
49. Wang, J.H., Jang, Y.J. & Lee, B.J. (2007) Natural course of retention cysts of the maxillary sinus: Long-
term follow-up results. Laryngosope 117:341-344.
50. Yaman, H., Yilmaz, S., Karali, E., Guclu, E. & Ozturk, O. (2010) Evaluation and management of
antrochoanal polyps. Clinical & Experimental Otorhinolaryngology 3: 110-114.
51. Rodrigues, M.T.V., Munhoz, E.A., Cardoso, C.L., Freitas, C.A. & Damante, J.H. (2009) Chronic
maxillary sinusitis associated with dental impression material. Medicina Oral, Patologia Oral y Cirugia
Bucal 14:e163-166.
52. Laskin, D.M & Dierks, J.D. (1999) Diagnosis and treatment of diseases and disorders of the maxillary
sinus. Oral & Maxillifacial Surgery Clinics of North America 11:55-164
53. Beaumont C, Zafirpoulos GG, Rohmann K, Tatakis DN. Prevelance of Maxillary Sinus Disease and
Abnormalities in Patients Scheduled for Sinus Lift Procedures. J Periodontol 2005;76:461-467.
54. Melen I, Friberg B, Anderasson L, Ivarsson A, Jannert M, Lindahl L. Ostial and nasal patency in chronic
maxillary sinusitis. A long-term post-treatment study. Acta Otolaryngol 1986;102:500-508.
55. Gilbert JG. Antroscopy in maxillary sinus disease associated with nasal polyposis. J Laryngol Otol
1989;103:861-863.
56. Elian N, Wallace S, Cho SC, Jalbout ZN, Froum S. Distribution of the maxillary artery as it relates to
sinus floor augmentation. Int J Oral Maxillofac Implants 2005; 20:784-787.
57. Solar P, Geyerhofer U, Traxler H, Windisch A, Ulm C, Watzek G. Blood supply to the maxillary sinus
relevant to sinus floor elevation procedures. Clin Oral Implants Res 1999; 10:34-44.
58. Flanagan D.Arterial supply of maxillary sinus and potential for bleeding complication duringlateral
approach sinus elevation. Implant Dent 2005;14:336-339.
59. Watzek G, Bernhart T, Ulm C. Complications of sinus perforations and their management in
endodontics. Dent Clin North Am. 1997 Jul;41(3):563-83.
60. de Souza Nunes LS, Bornstein MM, Sendi P, Buser D. Anatomical characteristics and dimentions of
edentulous sites in posterior maxillae of patients referred for implant therapy. Int J Period Rest Dent
2013;33:337-345.
61. Solar P, Geyerhofer U, Traxler H, Windisch A, Ulm C, Watzek G. Blood supply to the maxillary sinus
relevant to sinus floor elevation procedures. Clin Oral Implants Res 1999; 10:34-44.
62. Hur, M.S., Kim, J.K., Hu, K.s., Bae, H.E., Park, H.S. & Kim, H.J. (2009) Clinicl implications of the
topograpgy and distribution of the posterior superior alveolar artery. Jornal of Craniofacial Surgery 20:
551-554.
63. Taschieri, S. & Rosano, G. (2010) Management of the alveolar antral artery during sinus floor
augmentation procedure. The International Journal of Oral and Maxillofacial Surgery 68: 230.
64. Gaudy J-F. (2003) Anatomie Clinique. Rueil-Malmaison Cedex: Groupe Liaisons, Editions CdP.
65. Rosano G, Taschieri S, Gaudy J-F, Del Fabbro M. (2009) Maxillary sinus vascularization: a cadaveric
study. Journal of Craniofacial Surgery 20: 940-943.
66. Ella B, Sedarat C, Da Costa Noble R Normand E, Lauverjat Y, Siberchicot F, Caix P, Zwetyenga N.
(2008) Vascular connections of the lateral wall of the sinus: surgical effect in sinus augmentation. The
International Journal of Oral & Maxillofac Implants 23: 1047-1052.
67. Mardinger O, Abba M, Hirshberg A, Schwartz-Arad D. (2007) Prevalence, diameter and course of the
maxillary intraosseous vascular cancal with relation to sinus augmentation procedure: a radiographic
study. The International Journal of Oral and Maxillofac Sugery 36: 735-738.

~ 320 ~
68. Apostolakis D, Bissoon AK. Radiographic evaluation of the superior alveolar canal: measurements of its
diameter and of its position in relation to the maxillary sinus floor: a cone beam computerized
tomography study.
69. Sato, I., Kawai, T., Yoshida, S., Miwa, Y., Imura, K., Asaumi, R., Sunohara, M. & Yosue, T. (2010)
Observing the bony canal structure of the human maxillary sinus in Japanese cadavers using cone beam
CT. Okajimas Folia Anatomica Japonica 87: 123-128.
70. Cawood JJ, Howell RA: A classification of the edentulous jaws classes I to VI, Int J Oral Maxillofac
Surg 1988; 17:232-279.
71. Güncü GN1, Yildirim YD, Wang HL, Tözüm TF. Location of posterior superior alveolar artery and
evaluation of maxillary sinus anatomy with computerized tomography: a clinical study. Clin Oral
Implants Res. 2011 Oct;22(10):1164-7.
72. Rosano G, Tachieri S, Gaudy JF, Weinstein T, Del Fabbro M. Maxillary sinus anatomy and its relation to
sinus lift surgery. Clin. Oral Impl. Res. 22, 2011;711-715.
73. Toppozada HH, Talaat MA. The normal human maxillary sinus mucosa. An electronmicroscopic study.
Acta Otolaryngol 1980; 89:204-213.
74. Kang S, Shin SI, Herr Y, Kwon YH, Kim GT, Chung JH. Anatomical structures in the maxillary sinus
related to lateral sinus elevation:. A cone beam computed tomographic analysis. Clin. Oral Impl. Res.
24(Suppl. A100), 2013, 75-81.
75. Temmerman A, Hertele S, Teughels W, Dekeyser C, Jacobs R, Quirynen M. Are panoramic images
reliable in planning sinus augmentation procetures?. Clin. Oral Impl. Res. 22, 2011; 189-194.
76. Graf W, Martensson G. Microscopical anatomy of the nerves in the lateral wall of the maxillary sinus.
Acta Otolaryngol 1957; 47:114-122.
77. Darguad J, Lamotte C, Dianotti JP, Morin A. Venous drainage and innervations of the maxillary sinus.
Clin Anat 1999;12: 417-421.
78. Chanavaz M. Maxillary sinus: anatomy, physiology, surgery, and bone grafting related to implantology –
eleven years of surgical experience (1979-1990). J Oral Implantol 1990;16: 199-209.
79. Underwood AS. An inquiry into the anatomy and pathology of the maxillary sinus. J Anat Physiol 1910;
44:354-369.
80. Ulm CW, Solar P, Krennmair G, Matejka M, Watzek G. Incidence and suggested surgical management
of septa in sinus-lift procedures. Int J Oral Maxillofac Imaplnts 1995; 10:462-465.
81. Krennmair G, Ulm GW, Lugmayr H, Solar P. The incidence, location, and height of maxillary sinus
septa in the edentulous and dentate maxilla. J Oral Maxillofac Surg 1999; 57:667-671.
82. Zijderveld SA, van den Bergh JP, Schulten EA, ten Bruggenkate CM. Anatomical and surgical findings
and complications in 100 consecutive maxillary sinus floor elevation procedures. J Oral Maxillofac Surg
2008; 66: 1426-1438.
83. Tang HM, Bae HE, Won SY, Hu KS, Song WC, Paik DJ, et al. The buccofacial wall of maxillary sinus:
an anatomical consideration for sinus augmentation, Clin Implant Dent Relat Res 2009; 11:e2-e6.
84. Ella B, Noble Rda C, Lauverjat Y, et al. Speta within the sinus: Effect on elevation of the sinus floor. Br
J Oral Maxillofac Surg 2008; 46:464-467.
85. Kasabah S, Slezak R, Simunek A, Krug J, Lecaro MC. Evaluation of the accuracy of panoramic
radiograph in the definition of maxillary sinus septa. Acta Medica (Hradec Kralove) 2002;45:173-175.
86. Lugmayr H, Krennmair G, Holzer H. Morphologie und Inzidenz von Kieferhohlensepten [The
morphology and incidence of maxillary sinus septa]. Rofo 1996;165:452-454.
87. Velasquez-Plata D, Hovey LR, Peach CC, Alder ME. Maxillary sinus septa: a 3-dimensional
computerized tomographic scan analysis. Int J Oral Maxillofac Implants 2002; 17:854-860.
88. Uemura J. Morphological studies on the maxilla of the edentulous skulls and the skulls with teeth. 1. On
the sinus if the maxilla. Shikagakuhou 1974;74:1860-1889.
89. Naitoh M, Suaenaga Y, Kondo S, Gotoh K, Ariji E. Assessment of maxillary sinus septa using cone-
beam computed tomography: etiological consideration. DOI 10.1111/j.1708-8208.2009.

~ 321 ~
90. van Zyl AW, van Heerden WFP. A retrospective analysis of maxillary sinus septa reformatted
computerized tomography scans. Clin. Oral Impl. Res 20, 2009; 1398-1401.
91. Gannon PJ, Doyle WJ, Ganjian E, Marquez S, Gnoy A, Gabrielle HS, et.al. Maxillary sinus mucosal
blood flow during nasal vs tracheal respiration. Arch Otolaryngol Head Neck Surg 1997;123: 1336-1340.
92. Blanton PL, Biggs NL. Eighteen hundred years of controversy: the paranasal sinuses. Am J Anat
1969;124: 135-147.
93. Tepper G, Haas R, Schneider B, Watzak G, Mailath G, Jovanovic SA, et.al. Effects of sinus lifting on
voice quality. A prospective study and risk assessment. Clin Oral Implants Res 2003;14: 767-774.
94. Leopold D, Zinreich SJ, Simon BA, Cullen MM, Marcucci C. Xenon-enhanced computed tomography
quantifies normal maxillary sinus ventilation. Otolaryngol Head Neck Surg 2000;122: 422-424.
95. Hood CM, Schroter RC, Doorly DJ, Blenke EJ, Tolley NS. Computational modeling of flow and gas
exchange in models of the human maxillary sinus. J Appl Physiol 2009;107: 1195-1203.
96. Musebeck K, Rosenberg H. Measurement of air flow in the maxillary sinus by hot-film technique.
Rhinology 1978;16: 11-18.
97. Wodak E. Comparative temperature measurements in the maxillary sinus mcosa. Monatsschr
Ohrenheilkd Laryngorhinol 1961;95: 278-282.
98. Kirihene RK, Rees G, Wormald PJ. The influence of the size of the maxillary ostium on the nasal and
sinus nitric oxide levels. Am J Rinhol 2002;16: 261-264.
99. Brook I. Aerobic and anaerobic bacterial flora of normal maxillary sinuses. Laryngoscope 1981;91: 372-
376.
100. Cook HE, Haber J. Bacteriology of the maxillary sinus. J Oral Maxillofac Surg 1987;45: 1011-1014.
101. Carothers DG, Graham SM, Jia HP, Ackermann MR, Tack BF, McCray PB Jr. Production of beta-
defensin antimicrobial peptides by maxillary sinus mucosa. Am J Rhinol 2001;15: 175-179.
102. Pang KP, Siow JK, Tan HM. Migration of a foreign body in the maxillary sinus illustrating natural
mucociliary action. Med J Malaysia 2005;60: 523-525.
103. Toskala E, Rautiainen M. Effects of surgery on the function of maxillary sinus mucosa. Eur Arch
Otorhinolaryngol 2005;262: 236-240.
104. Asai K, Haruna S, Otori N, Yanagi K, Fukami M, Moriyama H. Saccharin test of maxillary sinus
mucociliary function after endoscopic sinus surgery. Laryngoscope 2000;110: 117-122.
105. Kim YM, Lee CH, Won TB, Kim SW, Kim JW, Rhee CS, et.al. Functional recovery of rabbit maxillary
sinus mucosa in two different experimental injury models. Laryngoscope 2008;118:541-545.
106. Guo Y, Majima Y, Hattori M, Seki S, Sakakura Y. Effects of functional endoscopic sinussurgery on
maxillary sinus mucosa. Arch Otolaryngol Head Neck Surg 1997; 123:1097-1100.
107. Wiltfang J, Schultze-Mosgau S, Merten HA, Kessler P, Ludwig A, Engelke W. Endoscopic and
ultrasonographic evaluation of the maxillary sinus after combined sinus floor augmentation and implant
insertion. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000;89: 288-291.
108. Ludwig A, Merten HA, Wiltfang J, Engelke W, Wiese KG. Evaluation of B-scan ultrasound, 3-D
ultrasound, roentgen diagnosis and sinus endoscopy in follow-up assessment of the maxillary sinus after
sinus floor elevation. Mund Kiefer Gesichtschir 2002;6: 341-345.
109. Peleg M, Chaushu G, Mazor Z, Ardekian L, Bakoon M. Radiological findings of the post-sinus lift
maxillary sinus: a computerized tomography follow-up. J preiodontol 1999;70: 1564-1573.
110. Timmenga NM, Raghoebar GM, Liem RS, van Weissenbruch R, Manson WL, Vissink A. Effects of
maxillary sinus floor elevation surgery on maxillary sinus physiology. Eur J Oral Sci 2003;111: 189-197.
111. Brook, I. (2009) sinusitis. Periodontology 2000 49: 126-39.
112. Carmeli G, Artzi Z, Avital K, Yoram S, Landsberg R. Antral computerized tomography pre-operative
evaluation : relationship between mucosal thickening and maxillary sinus function. Clin. Oral Impl. Res.
22, 2011: 78-82.
113. Inanli S, Tutkun A, Batman C, Okar I, Uneri C, Sehitoglu MA. The effect of endoscopic sinus surgery on
mucociliary activity and healing of maxillary sinus mucosa. Rhinology 2000;38: 120-123.
114. Toppozada HH, Talaat MA. The normal human maxillary sinus mucosa. An electron microscopic study.
Acta Otolaryngol 1980;89: 204-213.

~ 322 ~
115. Pommer B, Unger E, Suto D, Hack N. & Watzek G. (2009) Mechanical properties of the Schneiderian
membrane in vitro. Clinical Oral Implants Research 20: 633-637.
116. Srouji S1, Kizhner T, Ben David D, Riminucci M, Bianco P, Livne E. The Schneiderian membrane
contains osteoprogenitor cells: in vivo and in vitro study. Calcif Tissue Int. 2009 Feb;84(2):138-45.
117. Gruber R1, Kandler B, Fuerst G, Fischer MB, Watzek G.Porcine sinus mucosa holds cells that respond to
bone morphogenetic protein (BMP)-6 and BMP-7 with increased osteogenic differentiation in vitro. Clin
Oral Implants Res. 2004 Oct;15(5):575-80.
118. Scala A, Botticelli D, Faeda RF, Rangel Jr IG, de Oliveira JA, Lang NP. Lack of influence of the
Schneiderian membrane in forming new bone apical to implants simultaneously installed with sinus floor
elevation: an experimental study in monkeys. Clin. Oral Impl. Res. 23, 2012; 175-181.
119. Aust R, Backlund L, Drettner B, Flack B, Jung B. Comparative measurements of the mucosal blood flow
in the human maxillary sinus by plethysmography and by xenon. Acta Otolaryngol 1978;85: 111-115.
120. Flack B, Aust R, Svanholm H, Backlund L. The effect of physical work on the mucosal blood flow and
gas exchange in the human maxillary sinus. Rhinology 1989;27: 241-250.
121. Li Y, Yang M, Fang Z, Du Z, Zhao W. Microcirculation evaluation of the maxillary sinus mucosa in
patients with chronic sinusitis. Lin Chuang Er Bi Yan Hou Ke Za Zhi 2002;16: 579-580.
122. Flack B, Svanholm H, Aust R. The effect of Xylometazoline on the mucosa of human maxillary sinus.
Rhinology 1990b;28: 239-247.
123. Aimetti M, Massei G, Morra M, Cardesi E. & Romano F. (2008) Correlation betweengingival phenotype
and Schneiderian membrane thickness. The International Journal of Oral & Maxillofac Implants 23:
1128-1132.
124. Janner S, Caversaccio M, Dubach P, Sendi P, Buser D, Bornstein M. Characteristics anddimensions of
the Schneiderian membrane: a radiographic analysis using cone beamcomputed tomography in patients
referred for dental implant surgery in the posterior maxilla.Clinical Oral Implants Research 2011; 22:
1446-1453.
125. Mathew AL, Pai KM, Sholapurkar AA. Maxillary sinus findings in the elderly: a panoramic radiographic
study. J Contemp Dent Pract 2009; 10:E041-E048.
126. Carmeli G, Artzi Z, Avital K, Yoram S, Landsberg R. Antral computerized tomography pre-operative
evaluation : relationship between mucosal thickening and maxillary sinus function. Clin. Oral Impl. Res.
22, 2011: 78-82.
127. Vallo J, Suominen-taipale L, Huumonen S, Soikkonen K, Norblad A. (2010) Prevalence ofmucosal
abnormalities of the maxillary sinus and their relationship to dental disease inpanoramic radiography:
results from the Health 2000 Health Examination Survey.
128. Janner SFM, Caversaccio MD, Dubach P, Sendi P, Buser D, Bornstein MM. Characteristics and
dimensions of the schneiderian membrane: a radiographic analysis using cone beam computed
tomography in patients referre for dental implant surgery in the posterior maxilla. Clin. Oral Impl. Res.
22, 2011; 1446-11453.
129. Min, Y., Lee, J. & Shin, J. (1994) Radiographic assessment of diseased mucosa of the maxillary sinus
after functional endoscopic sinus surgery. Acta Otolaryngologica 114: 657-662.
130. Patel, K., Chavda, S.V., Violaris, N. & Pahor, A.L. (1996) incidental paranasal sinus inflammatory
changes in a Brotosh population. The Journal of Laryngology and Otology 110: 649-651.
131. Cagici, C.A., Yilmazer, C., Hurcan, C., Ozer, C. & Ozer, F. (2009) Appropriate interslice gap for
screening coronal paranasal sinus tomography for mucosalthickening. European Archives of Oto- Rhino-
Laryngology 266: 519-525.
132. Quirynen M, Lefever D, Hellings P, Jacobs R. transient swelling of the Schneiderian membrane after
transversal sinus augmentation: a pilot study. Clin. Oral Impl. Res. 25, 2014, 36-41.
133. Manor, Y., Mardinger, O., Bietlitum, I., Nashef, A., Nissan, J. & Chaushu, G. (2010 Late signsand
symptoms of maxillary sinusitis after sinus augmentation. Oral Surgery, Oral Medicine, Oral Pathology,
Oral Radiology, and Endodontolgy 110: e1-e4.

~ 323 ~
134. Shanbhag S, Karnik P, Shirke P, Shanbhag V. Cone-beam computed tomographic analysis of sinus
membrane thickess, ostium patency, and residual ridge heights in the posterior maxilla: implications for
sinus floor elevation. Clin. Oral Impl. Res. 25, 2014, 755-760.
135. Amler MH. The time sequence of tissue regeneration in human extraction wounds. Oral Surg Oral Med
Oral Pathol 1969;273: 309-318.
136. Cardarpoli, G., Araujo, M. & Lindhe, J. (2003) Dynamics of bone tissue formation in tooth extraction
sites. An experimental study in dogs. Journal of Clinical Periodontology 30: 809-818.
137. Araujo, M.G., Sukekava, F., Wennstrom, J.L. & Lindhe, J. (2005) Ridge alternations following implant
placement in fresh extraction sockets: an experimental study in the dog. Journal of Clinical
Periodontology 32:646-652.
138. Araujo M.G., Lindhe J. (2005) Dimensional ridge alterations following tooth extraction. An experimental
study in the dog. Journal of Clinical Periodontology 32: 212-218.
139. Schropp L, Wenzel A, Kostopoulos L, Karring T. (2003) Bone healing and soft tissue contour changes
following single-tooth extraction: a clinical and radiographic 12-month prospective study. International
Journal of Periodontics and Restorative Dentistry 23: 313-323.
140. Johnson K. (1969) A study of the dimensional changes occurring in the maxilla following tooth
extraction. Australian Dental Journal 14: 241-244.
141. Pietrokovski, J. & Massler, M. (1967) Alveolar ridge resorption following tooth extraction. Journal of
Prosthetic Dentistry 17: 21-27.
142. Lekovic, V., Carnargo, P.M., Klokkevold, P.R., Weinlaender, M., Kenney, E.B., Dimitrijevic, B. &
Nedic, M. (1998) Preservation of the alveolar bone in extraction sockets using bioabsorbable membranes.
Journal of Periodontology 69: 1044-1049.
143. Carnargo, P.M., Lekovic, V. Weinlaender, M. Klokkevold, P.R., Kenney, E.B., Dimitrijevic, B., Nedic,
M. Jancovic, S. & Orisini, M. (2000) Influence of bioactive glass on changes in alveolar process
dimensions after exodontia. Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology and
Endodontics 90: 581-586.
144. Pietrokovski, J., Starinsky, R., Arensburg, B. & Kaffe, I. (2007) Morphologic characteristics of bony
edentulous jaws. Journal of Prosthodontics 16: 141-147.
145. Ohnishi H, Fujii N, Furami T, Taguchi H, Kusakari H & Maeda T. A histochemical investigation of the
bone formation process by guided bone regeneration in rat jaws. Effect or PTFE membrane application
periods on newly formed bone. Journal of Periodontology 2000;71: 341-52.
146. Wood D.L, Hoag P.M, Donnenfeld O.W, Rosenberg D.L. (1972) Alveolar crest reduction following full
and partial thickness flap. Journal of Periodontology 34: 487-503.
147. Ridge preservation
148. Van der Weijden F, Dell'Acqua F, Slot D.E. (2009) Alveolar bone dimensional changes of post-
extraction sockets in humans: a systematic review. Journal of Clinical Periodontology 36: 1048-1058.
149. Misch CE. Contemporary Implant Dentistry, ed 2. St Louis: Mosby, 1999.
150. Razavi R, Zena R.B, Khan Z, Gould A.R. (1995) Anatomic site evaluation of edentulous maxillae for
dental implant placement. The International Journal of Prosthodontics 4:90-94.
151. Trombelli L, Farina R, Pramstraller M, Franceschetti G, Pramstraller C. Alveolar ridge dimensions in
maxillary posterior sextants: a retrospective comparative study of dentate and edentulous sites using
computerized tomography data. Clinical Oral Implants Res 2011; 22:1138-1144.
152. Garg, A.K. (1999) Augmentation grafting of the maxillary sinus for placement of dental implants:
anatomy, physiology, and procedures. Implant Dentistry 8: 36-46
153. Smiler, D.G., Johnson, P.W., Lozada, J.L., Misch, C., Rosenlichy, L.L., Tanum, O.H. & Wagner, J.R.
(1992) Sinus lift grafts and endosseous implants. Dental Clinics of North America 36: 151-186.
154. Botticelli D, Berglundh T, Lindhe J. Hard-tissue alterations following immediate implant placement in
extraction sites. J Clin Periodontol. 2004 Oct;31(10):820-8.
155. Covani U1, Ricci M, Bozzolo G, Mangano F, Zini A, Barone A. Analysis of the pattern of the alveolar
ridge remodelling following single tooth extraction. Clin Oral Implants Res. 2011 Aug;22(8):820-5.

~ 324 ~
156. Iasella J.M, Greenwell H, Miller R.L, Hill M, Drisko C, Bohra A.A, Scheetz J.P. (2003) Ridge
preservation with freeze-dried bone allograft and a collagen membrane compared to extraction alone for
implant site development: a clinical and histologic study in human. Journal of Periodontology 74: 990-
999.
157. Thomas A, Raman R.A Comparative study of the pneumatization of the mastoid air cells and the frontal
and maxillary sinuses. Am J Neuror adiol 1989;10(5 suppl):S88.
158. Misch CE: Divisions of available bone in implant dentistry, Int J Oral Implantol 7:9-17,1990.
159. Wehrbein H, Diedrich P. Progressive pneumatization of the basal maxillary sinus after extraction and
space closure [in German]. Fortschr Kieferorthop 1992;53:77-83.
160. Ikeda A, Ikeda M, Komatsuzaki A. A CT study of the course of growth of the maxillary Sinus: Normal
subjects and subjects with chronic sinusitis. J O torhinolaryngol Relat Spec 1998;60:147-152.
161. Ohba T, Langlais RP, Morimoto Y, Tanaka T, Hashimoto K. Maxillary sinus floor in edentulous and
dentate patients. Indian J Den Res 2001;12:121-125.
162. Wehrbein H, Diedrich P. The initial morphological state in the basally pneumatized maxillary sinus-A
radiological-histological study in man [in German] Fortschr Kieferorthop 1992;53:254-262.
163. Lekholm U, Zarb G: Patient selection and Preparation in Branemark PI, editor: Tissue integrated
prostheses: osseointegration in clinical dentistry, Chicago, 1985, Quintessence.
164. Misch CE, Chiapasco M: Identification for and classification of sinus bone grafts. In Jensen O, editor:
The sinus bone graft, ed 2, Carol Stream, III, 2006, Quintessence.
165. Nimigean V, Nimigean VR, Maru N, Salavastru DI, Badita D, Tuculina MJ. The maxillary sinus floor in
the oral implantology. Rom J Morphol Embryol 2008; 49:485-489.
166. Chiapasco M1, Zaniboni M, Rimondini L. Dental implants placed in grafted maxillary sinuses: a
retrospective analysis of clinical outcome according to the initial clinical situation and a proposal of
defect classification. Clin Oral Implants Res. 2008 Apr;19(4):416-28.
167. Buchter A, Kleinheinz J, Joos U, Meyer U. Primary implant stability with different bone surgery
techniques. An in vitro study of the mandible of the minipig [in German]. Mund Kiefer Gesichtschir
2003;7:351-355.
168. Shalabi MM, Wolke JGC, Jansen JA. The effects of implant surface roughness and surgical technique on
implant fixation in a vitro model. Clin Oral Implants Res 2006; 17:172-178.
169. Shahlaie M, Gantes B, Schulz E et.al: Bone density assessments of dental implant sites: quantitative
computed tomography, Int J Oral Maxillofac Implants 2003; 18:224-231.
170. Misch CE: Density of bone: effect on treatment plans, surgical approach, healing, and progressive
loading, Int J Oral Implant 1990; 6:23-31.
171. Trisi P, Rao W. Bone classification: Clinical-histomorphometric comparison. Clin Oral Implants Res
1999; 10:1-7.
172. Norton MR, Gamble C. Bone classification: An objective scale of bone density using the computerized
tomography scan. Clin Oral Implants Res 2001; 12:79-84.
173. Rebaudi A, Trisi P, Cella R, Cecchini G. Preoperative evaluation of bone quality and bone density using
a novel CT/microCT-based Hard-Normal-Soft classification system. Int J Oral Maxillofac Implants
2010; 25:75-85.
174. Trisi P, Lazzara R, Rao W, Rebaudi A. Bone-implant contact and bone quality: Evaluation of expected
and actual bone contact on machined and Osseotite implant surfaces. Int J Periodontics Restorative Dent
2002; 22:535-545.
175. Shapurian T, Damoulis P, Reiser G, T, Rand W. Quantitative evaluation of bone density using the
Hounsfield index. Int J Oral Maxillofac Implants 2006; 21:290-297.
176. Becker W, Hujol PP, Becker BE, Willingham H. Osteoporosis and implant failure: An exploratory case-
control study. J Periodontol 2000; 71:625-631.
177. Soikkonen, K. & Ainamo, A. (1995) Radiographic maxillary sins findings in the elderly. Oral Surgery,
Oral Medicine, Oral Pathology,Oral Radiology, and Endodontics 80: 487-491.
178. Branemark P-I, Zarb GA, Albrektsson T (eds). Tissue-Integrated Prostheses: Osseointegration in Clinical
Dentistry. Chicago: Quintessence, 1985:11.

~ 325 ~
179. Adell R. Surgical principles of osseointegration. In: Worthington P, Branemark PI (eds). Advanced
Osseointegration Surgery: Applications in the Maxillofocial Region. Chicago: Quintessence, 1992:94-
119.
180. Wall I1, Donos N, Carlqvist K, Jones F, Brett P. Modified titanium surfaces promote accelerated
osteogenic differentiation of mesenchymal stromal cells in vitro. Bone. 2009 Jul;45(1):17-26.
181. Guo J, Padilla RJ, Ambrose W, De Kok IJ, Cooper LF. The effect of hydrofluoric acid treatment of TiO2
grit blasted titanium implants on adherent osteoblast gene expression in vitro and in
vivo.Biomaterials. 2007 Dec;28(36):5418-25
182. Mendonça G, Mendonça DB, Aragão FJ, Cooper LF. The combination of micron and nanotopography by
H(2)SO(4)/H(2)O(2) treatment and its effects on osteoblast-specific gene expression of hMSCs. J
Biomed Mater Res A. 2010 Jul;94(1):169-79.
183. Branemark P-I, Hansson BO, Adell R, et al. Osseointegrated implants in the treatment of the enedtulous
jaw. Experience from a 10-year period. Scand J Plast Reconstr Surg Suppl 1977;16:1-132.
184. Albrektsson T, Johansson C. Osteoinduction, osteoconduction and osseointegration. Eur Spine J
2001;10(suppl 2):S96-S101
185. Schroeder A, Prohler O, Sutter F. Gewebereaktion auf ein Titan-Hohlzylinder implantat mit Titan-
Spritzschicht oberflache. Schweiz Monatsschr Zahnheilkd 1976;86:713-727
186. Hobo S, Ichida E, Garcia LT. Introduction. In: Osseointegration and Occlusal Rehabilitation. Tokyo:
Quintessence, 1989:3- 18.
187. Albrektsson T, Branemark PI, Hansson HA, Lindstrom J. Osseointegrated titanium implants.
Requirements for ensuring a long-lasting, direct bone-to-implant anchorage in man. Acta Orthop Scand
1981; 52:155-170.
188. Miyamoto I, Tsuboi Y, Wada E, Suwa H, lizuka T. Influence of cortical bone thickness and implant
length on implant stability at the time of surgery: Clinical, prospective, biomechanical, and imaging
study. Bone 2005;37:776-780.
189. Guizzardi S, Galli C, Martini D, et al. Different titanium surface treatment influences human mandibular
osteoblast response. J Periodontol 2004;75:273-282.
190. Baier RE, Meyer AE, Natiella JR, Natiella RR, Carter JM. Surface properties determine bioadhesive
outcomes; Methods and results. J Biomed Mater Res 1984;18:337-355.
191. Albrektsson T, Jacobsson M. Bone-metal interface in osseointegration. J Prosthet Dent 1987; 57:597-
607.
192. Ratner BD Porter SC. Surfaces in biology and biomaterials; description and characterization. In:Brash
JLW (ed). Interfacial Phenomena and Bioproducts. New York: Marcel Dekker, 1996:57-83.
193. Schwartz Z, Boyan BD. Underlying mechanisms at the bone-biomaterial interface. J Cell Biochem
1994;56:340-347.
194. Boyan BD, Lossdorfer S, Wang L, et al. Osteoblasts generate an osteogenic microevironment when
grown on surfaces with rough microtopographies. Eur Cell Mater 2003.
195. Ivanoff CJ, Widmark G, Johansson C, Wennerberg A. Histologic evaluation of bone response to oxidized
and turned titanium micro-implants in human jawbone. Int J Oral Maxillofac Implants 2003;18:341-348.
196. Ronold HJ, Lyngstadaas SP, Ellingsen JE. A study on the effect of dual balsting with TiO2 on titanium
implant surfaces on functional attachment in bone. J Biomed Mater Res 2003;67A(2):524-530.
197. Albrektsson T1, Wennerberg A. Oral implant surfaces: Part 2--review focusing on clinical knowledge of
different surfaces. Int J Prosthodont. 2004 Sep-Oct;17(5):544-64.
198. Becker W1, Becker BE, Ricci A, Bahat O, Rosenberg E, Rose LF, Handelsman M, Israelson H. A
prospective multicenter clinical trial comparing one- and two-stage titanium screw-shaped fixtures with
one-stage plasma-sprayed solid-screw fixtures. Clin Implant Dent Relat Res. 2000;2(3):159-65.
199. Turkyilmaz I1, Aksoy U, McGlumphy EA. Two alternative surgical techniques for enhancing primary
implant stability in the posterior maxilla: a clinical study including bone density, insertion torque, and
resonance frequency analysis data. Clin Implant Dent Relat Res. 2008 Dec;10(4):231-7.

~ 326 ~
200. Buser D, Schenk RK, Steinemann S, Fiorellini JP, Fox CH, Stich H. Influence of surface characteristics
on bone integration of titanium implants. A histomorphometric study in miniature pigs. J Biomed Mater
Res 1991;25:889-902.
201. Albrektsson T, Wennerberg A. oral implant surfaces: Part 1-Review focusing on topographic and
chemical properties of different surfaces and in vivo responses to them. Int J Prosthodont 2004;17:536-
543.
202. Juodzbalys G, Sapragoniene M, Wennerberg A, Baltrukonis T. Titanium dental implant surface
micromorphology optimization. J Oral Implantol 2007;33:177-185.
203. Wennerberg A, Albrektsson T. Effects of titanium surface topography on bone integration: A systematic
review. Clin Oral Implants Res 2009;20(suppl 4):172-184.
204. Wennerberg A, Albrektsson T. On implant surfaces: A review of current knowledge and opinions. Int J
Oral Maxillofac Implants 2010;25:63-74.
205. Kasemo B, Lausmaa J: Metal selection and surface characteristics. In: Branemark P-I, Zarb GA,
Albrektsson T (eds). Tissue Integrated Prostheses : Osseointegration in Clinical Dentisitry. Chicago:
Quintessence, 1985:99-116.
206. Junker R, Dimakis A, Thoneick M, Jansen JA. Effects of implant surface coatings and composition on
bone integration: A systematic review. Clin Oral Implants Res 2009;20(suppl 4):185-206.
207. Sul YT. The significance of the surface properties of oxidized titanium to the bone response: Special
emphasis on potential biochemical bonding of oxidized titanium implant. Biomaterials 2003;24:3893-
3907.
208. Romanos G, Toh C, Siar C, et al. Peri-Implant bone reactions to immediately loaded implants. An
experimental study in monkeys. J Periodontol 2001;72:506-511.
209. Nkenke E, Lehner B, Weinzierl K, et al. Bone contact, growth and density around immediately loaded
implants in the mandible of mini pigs. Clin Oral Implants Res 2003;14:312-321.
210. Roccuzzo M, Bunino M, Prioglio F, Bianchi SD. Early loading of sandblasted and acid-etched (SLA)
implants: A prospective split mouth comparative study. Clin Oral implants Res 2001;12:572-578
211. Bornstein MM, Schmid B, Belser UC, Lussi A, Buser D. Early loading of non-submerged titanium
implants with a sandblasted and acid-etched (SLA) surface: 5-year results of a prospective study in
partially edentulous patients. Clin Oral Implants Res 2005; 16:631-638.
212. Bornstein MM, Lussi A, Schmid B, Belser UC, Buser D. Early loading of nonsubmerged titanium
implants with a sandblasted and acid-etched (SLA) surface: 3-year results of a propective study in
partially edentulous patients. Int J Oral Maxillofac Implants 2003;18:659-666.
213. Ferguson SJ, Broggini N, Wieland M, et al. Biomechanical evaluation of the inter facial strength of a
chemically modified sandblasted and acid-etched titanium surface. J Biomed Mater Res A 2006;78:291-
297.
214. Cooper LF, Zhou Y, Takebe J, et al. Fluoride modification effects on osteoblast behavior and bone
formation at TiO2 grit-blasted c.p. titanium endosseous implants. Biomaterials 2006;27:926-936.
215. Peter B, Gauthier O, Laib S, et al. Local delivery of bisphosphonate from coated or thopedic implants
increases implants mechanical stability in osteoporotic rats. J Biomed Mater Res A 2006;76:133-143.
216. Fiorellini JP, Buser D, Riley E, Howell TH. Effect on bone healing of bone morphogenetic protein
placed in combination with endosseous implants: A pilot study in beagle dogs. Int J Periodontics
Restorative Dent 2001;21:41-47.
217. Strnad Z1, Strnad J, Povýsil C, Urban K. Effect of plasma-sprayed hydroxyapatite coating on the
osteoconductivity of commercially pure titanium implants. Int J Oral Maxillofac Implants. 2000 Jul-
Aug;15(4):483-90.
218. Weinlaender M1. Bone growth around dental implants. Dent Clin North Am. 1991 Jul;35(3):585-601.
219. Schiegnitz E1, Palarie V, Nacu V, Al-Nawas B, Kämmerer PW. Vertical osteoconductive characteristics
of titanium implants with calcium-phosphate-coated surfaces - a pilot study in rabbits. Clin Implant Dent
Relat Res. 2014 Apr;16(2):194-201
220. Thalji G, Cooper LF. Molecular assessment of osseointegration in vivo: A review of the current
literature. Oral Craniofac Tissue Eng 2012;2:9-22.

~ 327 ~
221. Thalji G, Gretzer C, Cooper LF. Comparitive molecular assessment of early osseointegration in implant-
adherent cells. Bone 2012 Aug 3 [Epub ahead of print]. 6:22-27.
222. Boyan BD, Hummert TW, Dean DD, Schwartz Z. Role of material surfaces in regulating bone and
cartilage cell response. Bio-materials 1996;17:137-146.
223. Schwarz F, Wieland M, Schwartz Z, Zhao G, Rupp F, Geis-Gerstorfer J, Schedle A, Broggini
N, Bornstein MM, Buser D, Ferguson SJ, Becker J, Boyan BD,Cochran DL. Potential of chemically
modified hydrophilic surface characteristics to support tissue integration of titanium dental implants. J
Biomed Mater Res B Appl Biomater. 2009 Feb;88(2):544-57
224. Tugulu S, Löwe K, Scharnweber D, Schlottig F. Preparation of superhydrophilic microrough titanium
implant surfaces by alkali treatment. J Mater Sci Mater Med. 2010 Oct;21(10):2751-63.
225. Buser D, Broggini N, Wieland M, Schenk RK, Denzer AJ, Cochran DL, Hoffmann B, Lussi
A, Steinemann SG. Enhanced bone apposition to a chemically modified SLA titanium surface. J Dent
Res. 2004 Jul;83(7):529-33
226. Milleret V, Tugulu S, Schlottig F, Hall H. Alkali treatment of microrough titanium surfaces affects
macrophage/monocyte adhesion, platelet activation and architecture of blood clot formation. Eur Cell
Mater. 2011 May 15;21:430-44
227. Hong J1, Kurt S, Thor A. A hydrophilic dental implant surface exhibits thrombogenic properties in vitro.
Clin Implant Dent Relat Res. 2013 Feb;15(1):105-12.
228. Hamlet S1, Alfarsi M, George R, Ivanovski S. The effect of hydrophilic titanium surface modification on
macrophage inflammatory cytokine gene expression. Clin Oral Implants Res. 2012 May;23(5):584-90.
229. O’Sullivan D, Sennerby L, Meredith N. Measurements comparing the initial stability of five designs of
dental implants: A human cadaver study. Clin Implant Dent Relat Res 2000;2:85-92.
230. Glauser R, Portmann M, Ruhstaller P, Gottlow J, Scharer P. Initial implant stability using different
implant designs and surgical techniques. A comperative clinical study using insertion torque and
resonance frequency analysis. Appl Osseointegration Res 2001;2:6-8.
231. Misch CE. Bone density: A key determinant for clinical success. In: Misch CE (ed). Contemporary
Implant Dentistry. St Louis: Mosby Year Book, 1999:109-118
232. Chun HJ, Cheong SY, Han JH, et al. Evaluation of design parameters of osseointegrated dental implants
using finite element analysis. J Oral Rehabil 2002;29:565-574.
233. Shi L, Li H, Fok AS, Ucer C, Devlin H, Horner K. Shape optimization of dental implants. Int J Oral
Maxillofac Implants 2007;22:911-920.
234. Duyck J, Corpas L, Vermeiren S, et al. Histological, histomorphometrical, and radiological evaluation of
an experimental implant design with a high insertion torque. Clin Oral Implants Res 2010;21:877-884.
235. O'Sullivan D1, Sennerby L, Meredith N. Influence of implant taper on the primary and secondary
stability of osseointegrated titanium implants. Clin Oral Implants Res. 2004 Aug;15(4):474-80.
236. Urist MR. Bone: Formation by autoinduction. 1965. Clin Orthop 2002;395:4-10.
237. Davies JE. Bone Engineering. Toronto: Em Squared, 2000:1-11, 295, 582, 583.
238. Zoldos J, Kent JN. Healing of endosseous implants. In: Block MS, Kent JN (eds). Endosseous Implants
for Maxillofacial Reconstruction. Philadelphia: Saunders, 1995; 40-70.
239. Marx RE, Ehler WJ, Peleg M. Mandibular and facial reconstruction: Rehabilitation of the head and neck
cancer patient. Bone 1996;19(1 suppl):59S-82S
240. Cooper LF. Biologic determinants of bone formation for osseointegration: Clues for future clinical
improvements. J Prosthet Dent 1998;80:439-449.
241. Davies JE. Mechanisms of endosseous integration. Int J Prosthodont 1998;11:391-401
242. Kieswetter K, Schwartz Z, Dean DD, Boyan BD. The role of implant surface characteristics in the
healing of bone. Crit Rev Oral Biol Med 1996;7:329-345.
243. Jayaraman M, Meyer U, Buhner M, Joos U, Wiesmann HP. Influence of titanium surfaces on attachment
of osteoblast-like cells in vitro. Biomaterials 2004;25:625-631
244. Osborn JF, Newesley H. Dynamics aspects of the implant-bone interface. In: Heimke G (ed). Dental
Implants-Materials and Systems. Munich: Carl Hanser, 1980:111-123.

~ 328 ~
245. Barglundh T, Abrahamsson I, Lang NP, Lindhe J. De novo alveolar bone formation adjacent to
endosseous implants. Clin Oral Implants Res 2003;14:251-262.
246. Cooper LF, Masuda T, Yilheikkila PK, Felton DA. Generalizations regarding the process and
phenomenon of osseointegration. Part II. In vitro studies. Int J Oral Maxillofac Implants 1998;13:163-
174.
247. Davies JE. In vitro modeling of the bone/implant interface. Anat Ree 1996;245:426-445.
248. Bosshardt DD1, Salvi GE, Huynh-Ba G, Ivanovski S, Donos N, Lang NP. The role of bone debris in
early healing adjacent to hydrophilic and hydrophobic implant surfaces in man. Clin Oral Implants
Res. 2011 Apr;22(4):357-64.
249. Lang NP1, Salvi GE, Huynh-Ba G, Ivanovski S, Donos N, Bosshardt DD. Early osseointegration to
hydrophilic and hydrophobic implant surfaces in humans. Clin Oral Implants Res. 2011 Apr;22(4):349-
56.
250. Duyck J1, Rønold HJ, Van Oosterwyck H, Naert I, Vander Sloten J, Ellingsen JE. The influence of static
and dynamic loading on marginal bone reactions around osseointegrated implants: an animal
experimental study. Clin Oral Implants Res. 2001 Jun;12(3):207-18.
251. Kao RT1, Curtis DA, Richards DW, Preble J. Increased interleukin-1 beta in the crevicular fluid of
diseased implants. Int J Oral Maxillofac Implants. 1995 Nov-Dec;10(6):696-701.
252. Lam, R.V. (1960) Contour changes of the alveolar processes following extractions. The Journal of
Prosthitic Dentistry 10: 25-32.
253. Huebsch RF, Hansen LS. A histopathologic study of extraction wounds in dogs. Oral Surg Oral Med
Oral Pathol 1969;282: 187-196.
254. Otha Y. Comparative changes in microvasculature and bone during healing of implant and extraction
sites. J Oral Implantol 1993;193: 184-198.
255. Bodner L, Dayan D, Rothchild D, Hammel I. Extraction wound healing in desalivated rats. J Oral Pathol
Med 1991;20: 176-178.
256. Amler MH, Johnson PL, Salman I. Histological and histochemical investigation of human alveolar
socket healing in undisturbed extraction wounds. J Am Dent Assoc 1960;61: 32-44.
257. Evian CI, Rosenberg ES, Cosslet JG, Corn H. The osteogenic activity of bone removed from healing
extraction sockets in human. J Periodontol 1982;53: 81-85.
258. Ferrus J1, Cecchinato D, Pjetursson EB, Lang NP, Sanz M, Lindhe J.
Factors influencing ridge alterations following immediate implant placement into extraction sockets. Clin
Oral Implants Res. 2010 Jan;21(1):22-9.
259. Matarasso S1, Salvi GE, Iorio Siciliano V, Cafiero C, Blasi A, Lang NP.
Dimensional ridge alterations following immediate implant placement in molar extraction sites: a six-
month prospective cohort study with surgical re-entry. Clin Oral Implants Res. 2009 Oct;20(10):1092-8.
260. Lai HC1, Zhang ZY, Wang F, Zhuang LF, Liu X. Resonance frequency analysis of stability on ITI
implants with osteotome sinus floor elevation technique without grafting: a 5-month prospective study.
Clin Oral Implants Res. 2008 May;19(5):469-75.
261. Zhou W1, Han C, Yunming L, Li D, Song Y, Zhao Y. Is the osseointegration of immediately and delayed
loaded implants the same? comparison of the implantstability during a 3-month healing period in a
prospective study. Clin Oral Implants Res. 2009 Dec;20(12):1360-6.
262. Roccuzzo M1, Wilson T. A prospective study evaluating a protocol for 6 weeks' loading of SLA implants
in the posterior maxilla: one year results. Clin Oral Implants Res. 2002 Oct;13(5):502-7.
263. Chao E.Y & Inoue N. Biophysical stimulation of bone fracture repair, regeneration and remodelling.
European Cells and Materials Journal 2003;31: 84-85.
264. Ignatius A, Ehrnthaller C, Brenner R.E, Kreia L, Schoengraf P, Lisson P, Blakytny R, Recknagel S,
Claes L, Gebhard F, Lambris J.D & Huber-Lang M. The anaphylatoxin receptor C5aR is present during
fracture healing in rats and mediates osteoblast migration in vitro. The Journal of Trauma 2011;71: 952-
960.
265. Yasui N, Sato M, Ochi T, Kimura T, Kawahata H, Kitamura Y & Nomura S. Three modes of ossification
during distraction osteogenesis in the rat. Journal of Bone Joint Surgery (br) 1997;97-8: 824-830.

~ 329 ~
266. Grimes R, Jepsen K.J, Fitch J.L, Einhorn T.A & Gerstenfeld L.C. The transcriptome of fracture healing
defines mechanisms of coordination of skeletal and vascular development during enchondral bone
formation. Journal of Bone Mineral Research 2011;26: 2597-2609.
267. Scammell B.E & Roach H.I. A new role for the chondrocytes. Journal of Bone Mineral Research
1996;11: 737-745.
268. Amir L.R, Becking A.G, Jovanovic A, Perdijk F.B.T, Everts B & Bronckers A.L.J.J. Formation of new
bone during vertical distraction osteogenesis of the human mandible is related o the presence of blood
vessels. Clinical Oral Implants Research 2006;17: 410-416.
269. Takahashi N, Udagawa N, Takami M, Suda T. Cells of bone: osteoclast generation. In: Bilezikian JP,
Riasz LG, Rodan GA (eds). Principles of bone biology, vol 1, 2nd ed. Bilezikian JP, Riasz LG, Rodan GA
(Eds). San Diego: Academic Press, 2002:109-126.
270. Brandi M.L & Collin-Osdoby. Vascular biology and the skeleton. Journal of Bone Mineral Research
2006;21: 183-192.
271. Linau J, Schmidt-Bleek K, Peters A, Haschke F, Duda G.N, Perka C, Bail H.J, Schutze N, Jakob F &
Schell H. Differential regulation of blood vessel formation between standard and delayed bone healing.
Journal of Orthopaedic Research 2009;27: 1133-1140.
272. Alt V, Kogelmaier D.V, Lips K.S, Witt V, Pacholke S, Heiss C, Kampschulte M, Heinemann S, Hanke
T, Schnettler R & Langheinrich A.C. Assessment of angiogenesis in osseointegration of a silica-collagen
biomaterial using 3D-nano-CT. Acta Biomaterials 2011;7: 3773-3779.
273. Qu D, Li J, Li Y, Gao Y, Zuo Y, Hsu Y & Hu J. Angiogenesis and osteogenesis enhanced by bFGF ex
vivo gene therapy for bone tissue engineering in reconstruction of calvarial defects. Journal of
Biomedical Material Research 2011;A 96: 543-551.
274. Hankenson K.D, Dishowitz M, Gray C & Schenker M. Angiogenesis in bone regeneration. Injury.
International Journal Care Injured 2011;42: 556-561.
275. Hermey D.C, Popoff S.N & Marks S.C. Jr. Reduced bone resorption in toothless (osteopetrotic) rats-an
abnormality of osteoblasts related to their inability to activate osteoclast activity in vitro. Connective
Tissue Research 1996;35: 273-278.
276. Peters K, Unger R.E, Brunner J & Kirkpatrick C.J. Molecular basis of endothelial dysfunction in sepsis.
Cardiovascular Research 2003;60: 49-57.
277. Nakata E, Nakanishi T, Kawai A, Asaumi K, Yamaai T, Asano M, Nishida T, Mitani S, Inoue H &
Takigawa M. Expression of connective tissue growth factor/hypertrophic chondrocyte-specific gene
product 24 (CTGF/Hcs24) during fracture healing. Bone 2002;31: 441-447.
278. Kanyama M, Kuboki T, Akiyama K, Nawachi K, Miyauchi F.M, Yatani H, Kubota S, Nakanishi T &
Takigawa M. Connective tissue growth factor expressed in rat alveolar bone regeneration sites after tooth
extraction. Archives of Oral Biology 2003;48: 723-730.
279. Guyton AC, Hall JE. Bone and its relations to extracellular calcium and phosphates. In: Guyton AC, Hall
JE (eds). Textbook of Medical Physiology, ed 9. Philadelphia: Saunders, 1996; 989-992.
280. Mosby's Dental Dictionary, ed 2. St Louis: Mosby, 2008.
281. Canay S, Akca K. Biomechanical aspects of bone-level diameter shifting at implant-abutment interface.
Implant Dent 2009;18: 239-248.
282. Hansson S. Implant-abutment interface: Biomechanical study of flat top versus conical. Clin Implant
Dent Relat Res 2000;2: 33-41.
283. Tsuge T, Hagiwara Y, Matsumura H. Marginal fit and microgaps of implant-abutment interface with
internal anti-rotation configuration. Dent Mater J 2008;27: 29-34.
284. van Kesteren, C.J., Schoolfield, J., West, J. & OATES, T. (2010) Aprospective randomized clinical study
of changes on soft tissue position following immediate and delayed implant placement. The International
Journal of Oral Maxillofacial Implants 25: 562-570
285. Devlin, H. & Sloan, P. (2002) Early bone healing events in the human extraction socket. The
international Journal of Oral and Maxillofacial Surgery 31: 641-645.
286. Trombelli, L. Farina, R. Marzola, A., Bozzi, L. Liljenberg, B. & Lindhe, J. (2008) Modeling and
remodeling of human extraction sockets. Journal of Clinical Periodontology 35: 630-639.

~ 330 ~
287. Lang N.P., Pun B.L., Lau I.K.Y, Li K.Y. & Wong M.C.M. A systematic review on survival and success
rates of implants placed immediately into fresh extraction sockets after at least one year. 2012;23(Suppl.
5): 39-66.
288. Fickl, S. Zuhr, O., Wachtel, H., Bolz, W. & Huerzeler, M. (2008a) Tissue alternations after tooth
extraction with and without surgical traumaL a columetric study in the beagle dog. Journal of Clinical
Periodontology 35: 356-363
289. Fickl, S. Zuhr, O., Wachtel, H., Stappert, C.F., Stein, J.M. & Hurzeler, M.b. (2008b) Dimensional
changes of the alveolar ridge contour after different socket perservation techniques. Journal of Clinical
Periodontology 35: 906-913.
290. Araujo, M.G. & Lindhe, J. (2009) Ridge alternation following tooth extraction with and without flap
elevation: an experimental study in the dog. Clinical oral implants research 20: 545-549.
291. Vignoletti F, Matesanz P, Rodrigo D, Figuero E, Martin C & Sanz M. Surgical protocols for ridge
preservation after tooth extraction. A systematic review. Clinical Oral Implants Research 2012;23(Suppl.
5): 22-38.
292. Ten Heggeler, J.M., Slot, D.E. & Van der Weijden, G.A. (2010) Effect of socket preservation therapies
following tooth extraction in non-molar regions in humans: a systematic review. Clinical oral Implants
Research 22:779-778.
293. Artzi, Z., Tal, H. & Dayan, D. (2000) Porous bovine bone mineral in healing of human extraction
sockets. Part 1: Histomorphometric evaluations at 9 months. Journal of Periodontology 71: 1015-1023.
294. Carnagnola, D., Adraens, P. & Berglundh, T. (2003) Healing of human extraction sockets filled with bio-
oss. Clinical Oral Implants Research 14: 137-143.
295. Brugnami F, Then P.R, Moroi H & Leone C.W. Histologic evaluation of human extraction sockets
treated with demineralized freeze-dried bone allograft (DFDBA) and cell occlusive membrane. Journal
of Periodontology 1996;67: 821-825.
296. Smukler H, Landi L & Setayesh R. Histomorphometric evaluation of extraction sockets and deficient
alveolar ridges treated with allograft and barrier membrane: a pilot study. The International Journal of
Oral & Maxillofacial Implants 1999;14: 407-416.
297. Molly L, Vandromme H, Quirynen M, Schepers E, Adams J.L & van Steenberghe D. Bone formation
following implantation of bone biomaterials into extraction sites. Journal of Periodontology 2008;79:
1108-1115.
298. Becker W, Clokie C, Sennerby L, Urist M.R & Becker B.E. Histologic findings after implantation and
evaluation of different grafting materials and titanium micro screws into extraction sockets: case reports.
Journal of Periodontolgy 1998;69: 414-421.
299. Nyman S, Lang N.P, Buser D & Bragger U. Bone regeneration adjacent to titanium dental implants using
guided tissue regeneration: a report of two cases. The International Journal of Oral & Maxillofacial
Implants 1990;5: 9-14.
300. Buser D, Dula K, Belser U.C, Hirt H.P & Berthold H. Localized ridge augmentation using guided bone
regeneration. II. Surgical procedure in the mandible. Internantion Journal of Periodontics and Restorative
Dentisrty 1995;15: 10-29.
301. Buser D, Dula K, Lang N.P & Nyman S. Long-term stability of osseointegration implants in bone
regenerated with the membrane technique. 5-year results of prospective study with 12 implants. Clinical
Oral Implants Research 1996;7: 175-183.
302. Hammerle C.H & Karring. Guided bone regeneration at oral implant sites. Periodontology 2000 1998;17:
151-175.
303. Rosen P.S & Reynolds M.A. Guided bone regeneration for dehiscence and fenestration defects on
implants using an absorbable polymer barrier. Journal of Periodontology 2001;72: 250-256.
304. Fugazzotto P.A. Implant placement at the time of maxillary molar extraction: technique and report of
preliminary results of 83 sites. Journal of Periodontology 2006;77: 302-309.
305. Hammerle C.H & Lang N.P. Single stage surgery combining transmucosal implant placement with
guided bone regeneration and bioresorbable materials. Clinical Oral Implants Research 2001;12: 9-18.

~ 331 ~
306. Juodzbalys G, Raustia A.M & Kubilius R. A 5-year follow-up study on one-stage implants inserted
concomitantly with localized alveolar ridge augmentation. Journal of Oral Rehabilitation 2007;34: 781-
789.
307. Becker W, Dahlin C, Becker B.E, Lekholm U, van Steenberghe D, Higuchi K & Jultje C. The use of e-
PTFE barrier membranes for bone promotion around titanium implants placed into extraction sockets: a
prospective multicenter study. The International Journal of Oral & Maxillofacial Implants 1994;9: 31-40.
308. Bragger U, Pasquali L, Kornman K.S. (1988) Remodelling of interdental alveolar bone after periodontal
flap procedures assessed by means of computer-assisted densitometric image analysis (CADIA). Journal
of Periodontology 15: 558-564.
309. Scarano, A., Piattelli, A., Assenza, B., Quaranta, A., Perrotti, V., Piarrelli, M. & Iezzi, G. (2010) Porcine
bone used in sinus augmentation procedures: a 5-year retrospective clinical evaluation. The International
Journal of Oral and Maxillofacial Surgery 68: 1869-1873.
310. Guarnieri, R., Pecora, G., Fini, M., Aldini, N.N., Giardino, R., Orsini, G. & Piattelli, A. (2004) Medical
grade calcium sulfate hemihydrate in healing of human extraction sockents: clinical and histological
observations at 3 months. Journal of Periodontology 75: 901-908.
311. Khan SN1, Cammisa FP Jr, Sandhu HS, Diwan AD, Girardi FP, Lane JM. The biology of bone grafting. J
Am Acad Orthop Surg. 2005 Jan-Feb;13(1):77-86.
312. Barone A, Todisco M, Ludovichetti M, Gualini F, Aggstaller H, Torrés-Lagares D, Rohrer MD, Prasad
HS, Kenealy JN. A prospective, randomized, controlled, multicenter evaluation of extraction socket
preservation comparing two bovine xenografts: clinical and histologic outcomes. Int J Periodontics
Restorative Dent. 2013 Nov-Dec;33(6):795-802
313. Wong M, Eulenberger J, Schenk R, Hunziker E. Effect of surface topology on the
osseointegration of implant materials in trabecular bone. J Biomed Mater Res
1995;29:1567-1575.
314. Brunette DM, Kenner GS, Gould TRL. Grooved titanium surfaces orient growth and
migration of cells from human gingival explants. J Dent Res 1983;62:1045-1048.
315. Albee FH. Bone graft surgery. Clin Orthop Relat Res 1996;(324):5-12.
316. Pikos MA. Alveolar ridge augmentation using mandibular block grafts: Clinical update.
Alpha Omegan 2000;93:14-21.
317. Marx RE. Biology of bone grafts. Oral Maxillofac Surg Knowl Update 1994;1:1-17.
318. Elves MW.Newer knowledge of the immunology of bone and cartilage. Clin Orthop
1976;120:232-259.
319. De Bruyn H, Collaert B.The effect of smoking on early implant failure. Clin Oral
Implants Res 1994;5:260-264.
320. Wallace RH.The relationship between cigarette smoking and dental implant failure.Eur
J Prosthodont Restor Dent 2000;8:103-106.
321. Smiler DG, Holmes RE.sinus lift procedure using porous hydroxyapatite: A
preliminary clinical report. J Oral implantol 1987; 13:239-253.
322. Ong JL, Prince CW, Raikar GN, Lucas LC. Effect of surface topography of titanium on
surface chemistry and cellular response. Implant Dent 1996;5:83-88.
323. Small SA, Zinner ID, Panno FV, Shapiro HJ. Augmenting the maxillary sinus for
implants: Report of 27 patients.Int J Oral Maxillofac Implants 1993; 8:523-528.
324. Jensen OT, Greer R. Immediate placement of osseointegrated implants into the
maxillary sinus augmented with mineralized cancellous allograft and Gore-Tex:
Second-stage surgical and histological findings. In: Laney WR, Tolman DE (eds).
Tissue Integration in Oral, Orthopedic and Maxillafacial Reconstruction. Chicago:
Quintessence, 1992:321-333.157)
325. Johansson B, Wannfors K, Ekenback J, smedberg JI,Hirsch J.Implants and sinus-inlay
bone grafts in a 1 stage procedure on severely atrophied maxillae: Surgical aspects of 3-
year follow-up study. Int Oral Maxillofac Implants 1999; 14:811-818.

~ 332 ~
326. Summers RB. The osteotome technique: Part 3. Less invasive methods of elevating the
sinus floor.Compend Contin Educ Dent 1994; 15:698-708.
327. Lambert PM, Morris HF, Ochi S. The influence of smoking on 3-year clinical success
of osseointegrated dental implants. Ann Periodontol 2000;5:79-89.
328. Schwartz-Arad D, Samet N, Mamlider A. Smoking and complications of endosseous
dental implants. J Periodontol 2002;73:153-157.
329. Trieger N. Antibiotics and anti-inflammatory agents in dental implantology. Implant
Dent 1999;8:343-346.
330. Zitzmann N, Scharer P. Sinus elevation procedures in the resorbed maxilla:
Comparison of the crestal and lateral approaches. Oral Surg Oral Med Oral Pathol Oral
Radiol Endod 1998; 85:8-17.
331. Keller EE, Tolman DE, Eckert SE. Maxillary antral-nasal inlay autogenous bone graft
reconstruction of compromised maxilla: A 12-year retrospective study.Int J Oral
Maxillofac Implants 1999; 14:707-721.
332. Papa,F, Cortese A, Maltarello MC, Sagliocco R, Felice P,Claudio PP.Outcome of 50
consecutive sinus lift operations. Brit J Oral Maxillofac Surg 2005; 43:3009-313.
333. Wiltfang J,Schultze-Mosgau S, Nkenke E, Thorwarth M, Neukam FW, Schlegel KA.
Onlay augmentation versus sinus lift procedure in the treatment of the severe resorbed
maxilla: A 5-year comparative longitudinal study. Int J Oral Maxillofac Surg 2005;
34:885-889.
334. Atamni F. Maxillary sinus grafting and simultaneous implant placement in patient with 4-6mm of
residual alveolar bone height. MedicinaStomatologica 2006; 1:101-104.
335. Atamni F. Single implant procedure with local sinus lifting in one stage procedure.Anale Stiintifice
2006; 4:375-378.
336. Glowacki J, Altobelli D, Mulliken JB. Fate of mineralized and demineralized osseous implants in cranial
defects. Calcif Tissue Int. 1981;33(1):71-6.
337. Mulliken JB, Glowacki J, Kaban LB, Folkman J, Murray JE. Use of demineralized allogeneic bone
implants for the correction of maxillocraniofacial deformities. Ann Surg. 1981 Sep;194(3):366-72.
338. Kuboki Y, Jin Q, Kikuchi M, Mamood J, Takita H. Geometry of artificial ECM: size of pores controlling
phenotype expression in BMP-induced osteogenesis and chondrogenesis. Connect Tissue Res 2002;
43:529–534.
339. Trueta J. The role of vessels in osteogenesis. J Bone Joint Surg 1963; 45:402–418.
340. Ripamonti U. The morphogenesis of bone in replicas of porous hydroxyapatite obtained from conversion
of calcium carbonate exoskeletons of coral. J Bone Joint Surg 1991; 73:692–703.
341. Ripamonti U. Osteoinduction in porous hydroxyapatite implanted in heterotopic sites of different animal
models. Biomaterials 1996; 17:31–35.
342. Fujibayashi S, Neo M, Kim HM, Kokubo T, Nakamura T. Osteoinduction of porous bioactive titanium
metal. Biomaterials 2004; 25:443–450.
343. Hall J, Miranda-Burgos P, Sennerby L. Stimulation of directed bone growth at oxidized titanium
implants by macroscopic grooves: an in vivo study. Clin Implant Dent Relat Res 2005; 7:76–82.
344. Van Eeden SP, Ripamonti U. Bone differentiation in porous hydroxyapatite in baboons is regulated by
the geometry of the substratum: implications for reconstructive craniofacial surgery. Plast Reconstr Surg
1996; 93:959–966.
345. Hammerle, C.H. & Jung, R.E. (2003) Bone augmentation by means of barrier membranes.
Periodontology 2000 33: 36-53.
346. Dahlin, D., Linde, A., Gottlow, J. & Nyman, S. (1988) Healing of bone defects by guided tissue
regeneration. Plastic and Reconstructive Surgery 81: 672-676.
347. Bassett, C.A., Campbell, J.B., Girado, J.M., Rossi, J.P. & Seymour, R.J. (1956) Application of
monomolecular filter tubes in bridging gaps in peripheral nerves and for prevention of neuroma
formation; a preliminary report. Journal of Neurosurgery 13: 635-637.

~ 333 ~
348. Ashley, F.L., Stone, R.S., Alonsoartieda, M., Syverud, J.M., Edwards, J.W., Sloan, R.F. & Mooney, S.A.
(1959) Experimental and clinical studies on the application of monomolecular cellulose filter tubes to
create artificial tendon sheaths in digits. Plastic and Reconstructive Surgery and the Transplantation
Bulletin 23: 526-534.
349. Murray, G., Holden, R. & Roshlau, W. (1957) Experimental and clinical study of new growth of bone in
a cavity. American Journal of Surgery 93: 385-387.
350. Hurley, L.A., Stinchfield, F.E., Bassett, A.L. & Lyon, W.H. (1959) The role of soft tissues in
osteogenesis. An experimental study of canine spine fusions. The Journal of Bone and Joint Surgery.
American volume 41-1: 1243-1254.
351. Boyne PJ, James RA. Grafting of the maxillary sinus floor with autogenous marrow and bone. J Oral
Surg. 1980 ;38:613-6.
352. Kahnberg, K.E. (1979) Restoration of mandibular jaw defects in the rabbit by subperiostcally implanted
Teflon mantle leaf. International Journal of Oral Surgery 8: 449-456.
353. Melcher, A.H. (1969) Role of the periosteum in repair of wounds of the parietal bone of the rat. Archives
of Oral Biology 14: 1101-1109.
354. Hammerle C.H, Schmid J, Fluckiger L, Gogolewski S, Winkler J.R & Lang N.P. The biological effect of
natural bone mineral on bone neoformation on the rabbit skull. Clinical Oral Implants Research 1997;8:
198-207.
355. Linde, A., Thoren, C., Dahlin, C. & Sandberg, R. (1993) Creation of new bone by an osteopromotive
membrane technique: an experimental study in rats. The International Journal of Oral and Maxillofacial
Surgery 51: 892-897.
356. Karring, T., Nyman, S., Gottlow, J. & Laurell, L. (1993( Development of the biological concept of
guided tissue regeneration-animal and human studies. Periodontology 2000 1: 26-35.
357. Davarpanah, M., Tecucianu, J. F., Slama, M. & Celletti, R. (1991) [bone regeneration in implantology.
The use of gore-tex membranes: Gtam]. Journal de Parodonologie 10: 169-176
358. Sandberg, E., Dahlin, C. & Linde, A. (1993) Bone regeneration by the osteopromotion technique using
bioabsorbable membranes: an experimental study in rats. The International Journal of Oral and
Maxillofacial Surgery 51: 1106-1114.
359. Simion, M., Dahlin, C., Blair, K. & Schenk, R.K. (1999) Effect of different microstructures of e-PTFE
membranes on bone regeneration and soft tissue response: a histologic study in canine mandible. Clinical
Oral Implants Research 10: 73-84.
360. Bartee, B.K. & Carr, J.A. (1995) Evaluation of high-density polytetrafluoroethylene (n-PTFE) membrane
as a barrier material to facilitate guided bone regeneration in the rat mandible. The Journal of Oral
Implantology 21: 88-95.
361. Lundgren, A.K., Sennerby, L. & Lundgren, D. (1998) Guided jaw-bone regeneration using an
experimental rabbit model the International Journal of Oral and Maxillofacial Surgery 27: 135-140.
362. Schenk, R.K., Buser, D., Hardwick, W.R. & Dahlin, C. (1994) Healing pattern of bone regeneration in
membrane-protected defects: a histologic study in the canine mandible. The International Journal of Oral
Maxillofacial Implants 9: 13-29.
363. Dahlin, C., Gottlow, J., Linde, A. & Nyman, S. (1990) Healing of maxillary and mandibular bone defects
using a membrane technique. An experimental study in monkeys. Scandinavian Journal of Plastic and
Reconstructive Surgery and Hand Surgery 24: 13-19.
364. Zellin G & Linde A. Effects of different osteopromotive membrane porosities on experimental bone
neogenesis in rats. Biomaterials 1996;17: 695-702.
365. Kostopoulos L, Karring T & Uraguchi R. Formation of jawbone tuberosities by guided tissue
regeneration. An expermintal study in the rat. Clinical Oral Implants Research 1994;5: 245-253.
366. Halaszyski TM, Juda R, Silverman DG. Optimizing postoperative outcomes with efficient preoperative
assessment and management. Crit Care Med 2004; 32: 76.
367. van Klei WA, Grobbee DE, Rutten CL, et al. Role of history and physical examination in preoperative
evaluation. Eur J Anaesthesiol 2003; 20: 612.
368. Older P, Hall A. Clinical review: how to identify high-risk surgical patients. Crit Care 2004; 8: 369.

~ 334 ~
369. Tawil G, Younan R, Azar P, Sleilati G. Conventional and advanced implant treatment in the type II
diabetic patient: Surgical protocol and long-term clinical results. Int J Oral Maxillofac Implant. 2008 Jul-
Aug;23(4): 744-752.
370. Bornstein MM, Cionca N, Mombelli A. systemic conditions and treatments as risk factors for implant
therapy. Int J Oral Maxillofac Implants 2009a;24 Suppl: 12-27.
371. Madrid C, Sanz M. What influence do anticoagulants have on oral implant therapy? A systematic review.
Clin Oral Implants Res 2009 Sep;20 Suppl 4: 96-106.
372. McDermott NE, Chuang SK, Woo VV, Dodson TB. Maxillary sinus augmentation as a risk factor for
implant failure. Int J Oral Maxillofac Implants 2006 May-Jun;21(3): 366-374.
373. Huynh-Ba G, Friedberg JR, Vogiatzy D, Ioannidou E. Implant failure predictors in the posterior maxilla:
A retrospective study of 273 consecutive implants. J Periodontol 2008 Dec;79(12): 2256-2261.
374. Heitz-Mayfield LJ, Huynh-Ba G. History of treated periodontitis and smoking as risks for implant
therapy. Int J Oral Maxillofac Implants 2009;24 Suppl: 39-68.
375. Li J, Wang Hl. Common implant-related advanced bone grafting complications: classification, etiology,
and management. Implant Dent 2008; Dec;17(4): 389-401.
376. Nemcovsky, C.E, & Moses, O. (2002) Rotated palatal flap: a surgical approach to increase keratinized
tissue width in maxillary implant uncovering: technique and clinical evaluation, The International
Journal of Periodontics & Restorative Dentistry 22: 607-612.
377. Gowen M, Mundy GR. Actions of recombinant interleukin 1, interleukin 2, and interferon-(Gamma
symbol) on bone resorption in vitro. J Immunol 1987;136:2478-2482.
378. Pfeilschifter J, Chenu C, Bird A, Mundy GR, Roodman GD. Interleukin-1 and tumor necrosis factor
stimulate the formation of human osteoclastlike cells in vitro. J Bone Miner Res 1989;4:113-118.
379. Feloutzis A, Lang NP, Tonetti MS, et al. IL-1 gene polymorphism and somking as risk factors for peri-
implant bone loss in a well-maintained population. Clin Oral Implants Res 2003;14:10-17.
380. Shimpuko H, Nosaka Y, Kawamura T, Tachi Y, Shinohara M, Ohura K. genetic polymorphisms of the
interleukin-1 gene and early marginal bone loss around endosseous dental implants. Clin Oral Implants
Res 2003;14:423-429.
381. Lin YH, Haung P, Lu X, et al. The relationship between IL-1 gene polymorphism and marginal bone loss
around dental implants. J Oral MaxillofacSurg 2007;65:2340-2344.
382. Holahan CM, Koka S, Kennel KA, et al. Effect of psteoporotic status on the survival of titanium dental
implants. Int J Oral Maxillofac Implants 2008; 5:905-910.
383. Slatger KW, Raghoebar GM, Vissink A. Osteoporosis and edentulous jaws. Int J Prosthodont 2008;
21:19-26
384. Glaser DL, Kaplan FS. Osteoporosis. Definition and clinical presentation. Spine 1997;22(24 suppl0:12S-
16S.
385. Elsubeihi ES, Zarb GA. Implant prosthodontics in medically challenged patients: The University of
Toronto experience. J Can Dent Assoc 2002;68:103-108.
386. Duarte PM, Neto JB, Goncalves PF, Sallum EA, Nociti FH. Estrogen deficiency affects bone healing
around titanium implants: A histometric study in rats. Implant Dent 2003;12:340-346.
387. Scott CK, Hightower JA. The matrix of endochondral bone differs from the matrix of intramembranous
bone. Calcif Tissue Int 1991;49:349-354.
388. Kloss FR, Gassner R. Bone and aging: Effects on the maxillofacial skeleton. ExpGerontol 2006;41:123-
129.
389. Dao TT, Anderson JD, Zarb GA. Is osteoporosis a risk factor for osseointegration of dental implants? Int
J Oral Maxillofac Implants 1993;8:137-144.
390. Friberg B, Ekestubbe A, Mellstrom D, Sennerby L. Branemark implants and osteoporosis: A clinical
exploratory study. Clin Implant Dent Relat Res 2001;3:50-56.
391. Mombelli A, Cionca N. Systemic diseases affecting osseointegration therapy. Clin Oral Implants Res
2006;17(suppl 2):97-103.
392. Turkylmaz, I. & McGlumphy, E.A. (2008) Influence of bone density on implant stability parameters and
implant success: a retrospective clinical study. BMC Oral Health 8: 32.

~ 335 ~
393. Hua, Y., Nackaerts, O., Duyck, J., Maes, F. % Jacobs, R. (2009) bone quality assessment based on cone
beam computed tomography imaging. Clinical Oral Implants Reasearch 20: 767-771.
394. Naitoh, M., Katsumata, A., Mitsuya, S., Kamemoto, H. &Ariji, E. (2004) measurement of mandibles
with microfocus X-ray computerized tomography and compact computerized tomography for dental use.
The International Journal of Oran & Maxillifacial CImplants 19:239-246.
395. Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care
1997;20:1183-1197.
396. Accurse GE. Treatment outcomes with osseointegrated Branemark implants in diabetic patients: A
retrospective study [thesis]. Toronto: University of Toronto, 2000.
397. Bugea C, Luongo R, Di lorio D, Cocchetto R, Celletti R. Bone contact around osseointegrated implants:
Histologic analysis of a dual-acid-etched surface implant in a diabetic patient. Int J Periodontics
Restorative Dent 2008;28:145-151.
398. Miles T, Nauntofte B, Svensson P (eds). Clinical Oral Physiology. Copenhagen: Quintessence, 2004.
399. Isidor F, Brondum K, Hansen HJ, Jensen J, Sindet-Pedersen S. Outcome of treatment with implant-
retained dental prostheses in patients with Sjogren syndrome. Int J Oral Maxillofac Implants
1999;14:736-743.
400. Garagiola U, Maiorana C, Ghiglione V, Marzo G, Santoro F, Szabo G. osseointegration and guided bone
regeneration in ectodermal dysplasia patients. J Prosthet Dent 2002;88:21-25.
401. Guckes AD, Scurria MS, King TS. McCarthy GR, Brahim JS. Prospective clinical trial of dental
implants in persons with ectodermal dysplasia. J Prosthet Dent 2002;88:21-25.
402. Sweeney IP, Ferguson JW, Heggie AA, Lucas JO. Treatment outcomes for adolescent ectodermal
dysplasia patients treated with dental implants. Int J Paediatr Dent 2005;15:241-248.
403. Bergendal B, Ekman A, Nilsson P. Implant failure in young children with ectodermal dysplasia: A
retrospective evaluation of use and outcome of dental implant treatment in children in Sweden. Int J Oral
Maxillofac Implants 2008;23:520-524
404. Yap AK, Klineberg I. Dental implants in patients with ectodermal dysplasia and tooth agenesis: A
critical review of the literature. Int J Prosthodont 2009;22:268-276.
405. Linkevicius T, Apse P, Grybauskas S, Puisys A. The influence of soft tissue thickness on crestal bone
changes around implants: A 1-year prospective controlled clinical trial. Int J Oral Maxillofac Implants
2009;24:712-719.
406. Teughels W, Merheb J, Quirynen M. Critical horizontal dimensions of interproximal and buccal bone
around implants for optimal aesthetic outcomes. A systematic review. Clin Oral Implants Res
2009;20(suppl 4):134-145.
407. Lindh C, Petersson A, Rohlin M. Assessment of the trabecular pattern before endosseous implant
treatment: diagnostic outcome of periapical radiography in the mandible. Oral Surg Oral Med Oral
Pathol Oral Radiol Endod. 1996 Sep;82(3):335-43.
408. Ribeiro-Rotta RF, Pereira AC, Oliveira GH, Freire MC, Leles CR, Lindh C. An exploratory survey of
diagnostic methods for bone quality assessment used by Brazilian dental implant specialists. J Oral
Rehabil. 2010 Sep;37(9):698-703.
409. Bergkvist, G., Koh, K.J., Sahlholm, S., Klintstrom, E. & Lindh, C. (2010) Bone density at implant sites
and its relationship to assessment of bone quality and treatment outcome. International Journal of Oral
and Maxillofacial Implanta 25: 321-328.
410. Molly, L. (2006) Bone density and primary stability in implant therapy. Clinical Oral Implants Research
2:124-135.
411. de Oliveira RC, Leles CR, Normanha LM, Lindh C, Ribeiro Rotta RF. Assessments of trabecular bone
density at implant sites on CT images. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2008
Feb;105(2)231-238.
412. Turkyilmaz I, Tozum TF, Tumer C. Bone density assessments of oral implant sites using computerized
tomography. J Oral Rehabil. 2007 Apr;34(4):267-272.
413. Fuh LJ, Haung HL, Chen CS, Fu KL, Shen YW, Tu MG, Shen WC, Hsu JT. Variations in bone density
at dental implant sites in different regions of the jawbone. J Oral Rehabil. 2010 May 1;37(5):346-351.

~ 336 ~
414. Jensen SS, Terheyden H. Bone augmentation procedures in localized defects in the laveolar ridge:
Clinical results with different bone grafts and bone-substitute materials. Int J Oral Maxillofac Implants.
2009; 24 (Suppl.): 218-236.
415. Spray RJ, Black CG, Morris HF, Ochi S. The influence of bone thickness on facial marginal bone
response: Stage 1 placement through stage 2 uncovering. Ann Periodontol 2000;5:119-128.
416. Martin W, Lewis E, Nicol A. Local risk factors for implant therapy. Int J Oral Maxillofac Implants
2009;24(suppl):28-38.
417. ORBAN B. Clinical and histologic study of the surface characteristics of the gingiva. Oral Surg Oral
Med Oral Pathol. 1948 Sep;1(9):827-41.
418. Listgarten MA1, Lang NP, Schroeder HE, Schroeder A. Periodontal tissues and their counterparts around
endosseous implants [corrected and republished with original paging, article orginally printed in Clin
Oral Implants Res 1991 Jan-Mar;2(1):1-19]. Clin Oral Implants Res. 1991 Jul-Sep;2(3):1-19.
419. Bowers G. A study of the width of attached gingiva. Journal of Periodontology 34: 201-209.
420. Lindhe J1, Berglundh T. The interface between the mucosa and the implant. Periodontol 2000. 1998
Jun;17:47-54.
421. Berglundh T1, Lindhe J, Ericsson I, Marinello CP, Liljenberg B, Thomsen P. The soft tissue barrier at
implants and teeth. Clin Oral Implants Res. 1991 Apr-Jun;2(2):81-90.
422. Zigdon H1, Machtei EE. The dimensions of keratinized mucosa around implants affect clinical and
immunological parameters. Clin Oral Implants Res. 2008 Apr;19(4):38
423. Vervaeke S1, Dierens M, Besseler J, De Bruyn H. The influence of initial soft tissue thickness on peri-
implant bone remodeling. Clin Implant Dent Relat Res. 2014 Apr;16(2):238-47.
424. Bengazi F1, Wennström JL, Lekholm U. Recession of the soft tissue margin at oral implants. A 2-year
longitudinal prospective study. Clin Oral Implants Res. 1996 Dec;7(4):303-10.
425. Karring T, Ostergaard E, Löe H. Conservation of tissue specificity after heterotopic transplantation of
gingiva and alveolar mucosa. J Periodontal Res. 1971;6(4):282-93.
426. Apse P1, Zarb GA, Schmitt A, Lewis DW. The longitudinal effectiveness of osseointegrated dental
implants. The Toronto Study: peri-implant mucosal response. Int J Periodontics Restorative
Dent. 1991;11(2):94-111.
427. Mericske-Stern R1, Steinlin Schaffner T, Marti P, Geering AH. Peri-implant mucosal aspects of ITI
implants supporting overdentures. A five-year longitudinal study. Clin Oral Implants Res. 1994
Mar;5(1):9-18.
428. Cecchinato D1, Bengazi F, Blasi G, Botticelli D, Cardarelli I, Gualini F. Bone level alterations at
implants placed in the posterior segments of the dentition: outcome of submerged/non-submerged
healing. A 5-year multicenter, randomized, controlled clinical trial. Clin Oral Implants Res. 2008
Apr;19(4):429-31
429. Chang M1, Wennström JL. Peri-implant soft tissue and bone crest alterations at fixed dental prostheses: a
3-year prospective study. lin Oral Implants Res. 2010 May;21(5):527-34.
430. Bengazi F1, Botticelli D, Favero V, Perini A, Urbizo Velez J, Lang NP. Influence of presence or absence
of keratinized mucosa on the alveolar bony crest level as it relates to different buccal marginal bone
thicknesses. An experimental study in dogs. Clin Oral Implants Res. 2014 Sep;25(9):1065-71.
431. Wennström JL1, Derks J. Is there a need for keratinized mucosa around implants to maintain health and
tissue stability? Clin Oral Implants Res. 2012 Oct;23 Suppl 6:136-46.
432. Wennstrom JL, Bengazi F, Lekholm U. The influence of the masticatory mucosa on the peri-implant soft
tissue condition. Clin Oral Implants Res 1994;5:1-8.
433. Roos-JansakerAM, Renvert H, Lindahl C, Renver S. Nine- to fourteen-year follow-up of implant
treatment. Part III: Factors associated with peri-implant lesions. J ClinPeriodontol 2006;33:296-301.
434. Tan WL1, Wong TL, Wong MC, Lang NP. A systematic review of post-extractional alveolar hard and
soft tissue dimensional changes in humans. Clin Oral Implants Res. 2012 Feb;23 Suppl 5:1-21.
435. Brägger U1, Bürgin WB, Hämmerle CH, Lang NP. Associations between clinical parameters assessed
around implants and teeth. Clin Oral Implants Res. 1997 Oct;8(5):412-21.

~ 337 ~
436. Adibrad M1, Shahabuei M, Sahabi M. Significance of the width of keratinized mucosa on the health
status of the supporting tissue around implants supporting overdentures. J Oral
Implantol. 2009;35(5):232-7
437. Ericsson I1, Berglundh T, Marinello C, Liljenberg B, Lindhe J. Long-standing plaque and gingivitis at
implants and teeth in the dog. Clin Oral Implants Res. 1992 Sep;3(3):99-103.
438. Bouri A, Bissada N, Al-Zahrani MS, Faddoul F, Nouneh I. Width of keratinized gingiva and the health
status of the supporting tissues around dental implants. Int J Oral Maxillofac Implants 2008;23:323-326.
439. Olsson M, Lindhe J. Periodontal characteristics in individuals with varying form of the upper central
invisors. J ClinPeriodontol 1991;18:78-82.
440. Barboza EP, Caula AL, Carvalho WR. Crestal bone loss around submerged and exposed unloaded dental
implants: A radiographic and microbiological descripitive study. Implant Dent 2002;11:162-169.
441. De Rouck T, Eghbali R, Collys K, De Bruyn H, Cosyn J. The gingival biotype revisited: transparency of
the periodontal probe through the gingival margin as method to discriminate thin from thick gingiva. J
ClinPeriodontol 2009;36:428-433.
442. Shibli JA, Melo L, Ferrari DS, Figueiredo LC, Faveri M, Feres M. Composition of sipra- and subgingival
biofilm of subjects with healthy and diseased implants. Clin Oral Implants Res 2008;19:975-982.
443. Subramani K, Jung RE, Molenberg A, Hammerle CHF. Biofilm on dental implants: A review of the
literature Int J Oral Maxillofac Implants 2009;24:616-626.
444. Roccuzzo M1, Bonino L, Dalmasso P, Aglietta M. Long-term results of a three arms prospective cohort
study on implants in periodontally compromised patients: 10-year data around sandblasted and acid-
etched (SLA) surface.bClin Oral Implants Res. 2014 Oct;25(10):1105-12.
445. Ormianer Z1, Patel A. The use of tapered implants in the maxillae of periodontally susceptible patients:
10-year outcomes. Int J Oral Maxillofac Implants. 2012 Mar-Apr;27(2):442-8.
446. Lundgren D, Rylander H, Laurell L. To save or to extract, that is the question. Natural teeth or dental
implants in periodontitis-susceptible patients: clinical decision-making and treatment strategies
exemplified with patient case presentations. Periodontol 2000. 2008;47:27-50.
447. Hultin M, Komiyama A, Klinge B. Supportive therapy and the longevity of dental implants: A
systematic review of the literature. Clin Oral Implants Res 2007;18(suppl 3):50-62.
448. Karoussis IK, Slavi GE, Heitz-Mayfield LJ, Bragger U, Hammerle CH, Lang NP. Long-term implant
prognosis in patients with and without a history of chronic periodontitis. A 10-year prospective cohort
study of the ITI Dental Implant System. Clin Oral Implants Res 2003;14:329-339.
449. Machtei EE, Frankenthal S, Blumenfeld I, Gutmacher Z, Horwitz J. Dental implants for immediate fixed
restoration of partially edenetulous patients: A 1-year prospective pilot clinical trial in periodontally
susceptible patients. J Periodontol 2007;78:1188-1194.
450. Wennstrom JL, Ekestubbe A, Grondahl K, Karlsson S, Lindhe J. Oral rehabilitation with implant-
supported fixed partial dentures in periodontitis-susceptible subjects. A 5-year prospective study. J
ClinPeriodontol 2004;31:713-724.
451. Mengel R, Flores-deJacoby L. Implants in patients treated for generalized aggressive and chronic
periodontitis: A 3-year prospective longitudinal study. J Periodontol 2005;76:534-543.
452. Aloufi F, Bissada N, Ficara A, Faddoul F, Al-Zahrani MS. Clinical assessment of peri-implant tissues in
patients with varying severity of chronic periodontitis. Clin Implants Dent Relat Res 2009;11:37-40.
453. Mengel R, Behle M, Flores-de-Jacoby L. Osseointegrated implants in subjects treated for generalized
aggressive periodontitis: 10-year results of a prospective, long-term cohort study. J Periodontol
2007;78:2229-2237.
454. Karoussis IK, Kotsovilis S, Fourmousis I. A comprehensive and critical review of dental implant
prognosis on periodontally compromised partially edentulous patients. Clin Oral Implants Res
2007;18:669-679.
455. Al-Zahrani MS. Implant therapy in aggressive periodontitis patients: A systematic review and clinical
implications. Quintessence Int 2008;39:211-215.
456. Schou S. Implant treatment in periodontitis-susceptible patients: A systematic review. J Oral Rehabil
2008;35(suppl 1):9-22.

~ 338 ~
457. Hermann F, Lerner H, Palti A. Factors Influencing the preservation of the periimplant marginal bone.
Implant Dent 2007;16:165-175.
458. Brook I. Sinusitis of odontogenic origin. Otolaryngol Head Neck Surg 2006 Sep;135(3): 349-355.
459. Abrahams JJ, Glassberg RM. Dental disease: a frequently unrecognized cause of maxillary sinus
abnormalities? AJR Am J Roentgenol 1996 May;166(5): 1219-1223.
460. Marx RE. Pamidronate (Aredia) and zoledronate (Zometa) induced avascular necrosis of the jaws: a
growing epidemic. J Oral Maxillofac Surg. 2003 Sep;61(9):1115-7.
461. Migliorati CA. Bisphosphanates and Oral Cavity Avascular Bone Necrosis. J Clin Oncol 2003; 21:4253-
4254.
462. Hoff AO1, Toth BB, Altundag K, Johnson MM, Warneke CL, Hu M, Nooka A, Sayegh G, Guarneri
V, Desrouleaux K, Cui J, Adamus A, Gagel RF, Hortobagyi GN. Frequency and risk factors associated
with osteonecrosis of the jaw in cancer patients treated with intravenous bisphosphonates. J Bone Miner
Res. 2008 Jun;23(6):826-36.
463. Marx RE1, Sawatari Y, Fortin M, Broumand V. Bisphosphonate-induced exposed bone
(osteonecrosis/osteopetrosis) of the jaws: risk factors, recognition, prevention, and treatment. J Oral
Maxillofac Surg. 2005 Nov;63(11):1567-75.
464. Jeffcoat MK1. Safety of oral bisphosphonates: controlled studies on alveolar bone. Int J Oral Maxillofac
Implants. 2006 May-Jun;21(3):349-53.
465. Bell BM1, Bell RE. Oral bisphosphonates and dental implants: a retrospective study. J Oral Maxillofac
Surg. 2008 May;66(5):1022-4
466. Madrid C1, Sanz M. What impact do systemically administrated bisphosphonates have on oral implant
therapy? A systematic review. Clin Oral Implants Res. 2009 Sep;20 Suppl 4:87-95
467. Ruggiero SL1, Dodson TB, Assael LA, Landesberg R, Marx RE, Mehrotra B; American Association of
Oral and Maxillofacial Surgeons. American Association of Oral and Maxillofacial Surgeons position
paper on bisphosphonate-related osteonecrosis of the jaws--2009 update. J Oral Maxillofac Surg. 2009
May;67(5 Suppl):2-12
468. Favia G1, Piattelli A, Sportelli P, Capodiferro S, Iezzi G. Osteonecrosis of the posterior mandible after
implant insertion: a clinical and histological case report. Clin Implant Dent Relat Res. 2011
Mar;13(1):58-63.
469. Edrawds BJ, Hellstein JW, Jacobsen PL, Kaltman S, Mariotti A, Migliorati CA. Uptaded
recommendations for managing the care of patients receiving oral bisphosphonate therapy: An advisory
statement from the American Dental Association Council on Scientific Affairs. J Am Dent Assoc
2008;139:1674-1677.
470. SarziAmade D, Tallarico M, Loreti MC, Montecchi PP, Niccoli A. Clinical guidelines for prevention of
osteonecrosis of the jaws in patients in treatment with bisphosphonates: Literature review and report of
three cases. Minerva Stomatol 2008;57:429-446.
471. Khan AA, Sandor GK, Dore E, et al. Canadian consensus practice guidelines for bisphosphonate
associated osteonecrosis of the jaw. J rheumatol 2008;35:1391-1397 [erratum 2008;35:1688].
472. Aapro M, Abrahamsson PA, Body JJ, et al. Guidance on the use of bisphosphonates in solid tumors:
Recommendations of an international expert panel. Ann Oncol 2008;19:420-432.
473. Ruggiero SL, Woo SB. Biophosphonate-related osteonecrosis of the jaws. Dent Clin North Am
2008;52:111-128.
474. Pariazanas M, Miller P, Blumentals WA, Bernal M, Kothawala P. A review of the literature on
osteonecrosis of the jaw in patients with osteoporosis treated with oral bisphosphonates: Prevalence, risk
factors, and clinical characteristics. ClinTher 2007;29:1548-1558.
475. Kyrgidis A, Vahtsevanos K, Koloustos G, et al. Bisphosphonate-related osteonecrosis of the jaws: A case
control study of risk factors in breast cancer patients. J ClinOncol 2008;26:4634-4638.
476. Manfredini D1, Lobbezoo F. Relationship between bruxism and temporomandibular disorders: a
systematic review of literature from 1998 to 2008. Oral Surg Oral Med Oral Pathol Oral Radiol
Endod. 2010 Jun;109(6):e26-50.

~ 339 ~
477. Lobbezoo F1, Brouwers JE, Cune MS, Naeije M. Dental implants in patients with bruxing habits. J Oral
Rehabil. 2006 Feb;33(2):152-9.
478. Paesani D. Bruxism: theory and practice. Berlin: Quintessence Publishing, 2010.
479. Lobbezoo F1, Van Der Zaag J, Naeije M. Bruxism: its multiple causes and its effects on dental implants -
an updated review. J Oral Rehabil. 2006 Apr;33(4):293-300.
480. Manfredini D1, Bucci MB, Sabattini VB, Lobbezoo F. Bruxism: overview of current knowledge and
suggestions for dental implants planning. Cranio. 2011 Oct;29(4):304-12.
481. Manfredini D1, Lobbezoo F. Role of psychosocial factors in the etiology of bruxism. J Orofac Pain. 2009
Spring;23(2):153-66.
482. Lobbezoo F1, Ahlberg J, Glaros AG, Kato T, Koyano K, Lavigne GJ, de Leeuw R, Manfredini
D, Svensson P, Winocur E. Bruxism defined and graded: an international consensus. J Oral
Rehabil. 2013 Jan;40(1):2-4.
483. Perettaa R, Manfredini D. Future perspectines in TMD physiopathology. In: Manfredini D, ed. Current
concepts on temporomandibular disorders. Berlin : Quintessence Publishing, 2010:153-168.
484. Lewis MB1, Klineberg I. Prosthodontic considerations designed to optimize outcomes for single-tooth
implants. A review of the literature. Aust Dent J. 2011 Jun;56(2):181-92.
485. Zinner ID, Shapiro HJ, Gold SD. Sinus graft complications. Problem solving. N Y State Dent J. 2008
Jun-Jul;74(4):40-43.
486. Christen AG. The clinical effects of tobacco on oral tissue. J Am Dent Assoc. 1970 Dec;81(6):1378-82.
487. Jones JK1, Triplett RG. The relationship of cigarette smoking to impaired intraoral wound healing: a
review of evidence and implications for patient care. J Oral Maxillofac Surg. 1992 Mar;50(3):237-9;
discussion 239-40.
488. Schwartz-Arad D1, Samet N, Samet N, Mamlider A. Smoking and complications of endosseous dental
implants. J Periodontol. 2002 Feb;73(2):153-7.
489. Jensen OT1, Shulman LB, Block MS, Iacono VJ. Report of the Sinus Consensus Conference of 1996. Int
J Oral Maxillofac Implants. 1998;13 Suppl:11-45.
490. Kan JY, Rungcharassaeng K, Kim J, Lozada JL, Goodacre CJ. Factors affecting the survival of implants
placed in grafted maxillary sinuses: a clinical report. J Prosthet Dent. 2002 May;87(5):485-489.
491. Bain CA1, Weng D, Meltzer A, Kohles SS, Stach RM. A meta-analysis evaluating the risk for implant
failure in patients who smoke. Compend Contin Educ Dent. 2002 Aug;23(8):695-9, 702, 704.
492. Kan JY1, Rungcharassaeng K, Lozada JL, Goodacre CJ. Effects of smoking on implant success in grafted
maxillary sinuses. J Prosthet Dent. 1999 Sep;82(3):307-11.
493. Silverstein P1. Smoking and wound healing. Am J Med. 1992 Jul 15;93(1A):22S-24S.
494. Peleg M1, Garg AK, Mazor Z. Healing in smokers versus nonsmokers: survival rates for sinus floor
augmentation with simultaneous implant placement. Int J Oral Maxillofac Implants. 2006 Jul-
Aug;21(4):551-9.
495. Nociti FH Jr1, César NJ, Carvalho MD, Sallum EA. Bone density around titanium implants may be
influenced by intermittent cigarette smoke inhalation: a histometric study in rats. Int J Oral Maxillofac
Implants. 2002 May-Jun;17(3):347-52.
496. César-Neto JB1, Duarte PM, Sallum EA, Barbieri D, Moreno H Jr, Nociti FH Jr. A comparative study on
the effect of nicotine administration and cigarette smoke inhalation on bone healing around titanium
implants. J Periodontol. 2003 Oct;74(10):1454-9.
497. César-Neto JB1, Benatti BB, Sallum EA, Sallum AW, Nociti FH Jr. Bone filling around titanium
implants may benefit from smoking cessation: a histologic study in rats. J Periodontol. 2005
Sep;76(9):1476-81.
498. Correa MG1, Gomes Campos ML, César-Neto JB, Casati MZ, Nociti FH, Sallum EA. Histometric
evaluation of bone around titanium implants with different surface treatments in rats exposed to cigarette
smoke inhalation. Clin Oral Implants Res. 2009 Jun;20(6):588-93.
499. Hinode D1, Tanabe S, Yokoyama M, Fujisawa K, Yamauchi E, Miyamoto Y. Influence of smoking on
osseointegrated implant failure: a meta-analysis. Clin Oral Implants Res. 2006 Aug;17(4):473-8.

~ 340 ~
500. Strietzel FP1, Reichart PA, Kale A, Kulkarni M, Wegner B, Küchler I. Smoking interferes with the
prognosis of dental implant treatment: a systematic review and meta-analysis. J Clin Periodontol. 2007
Jun;34(6):523-44.
501. Pjetursson BE, Tan WC, Zwahlen M, Lang NP. A systematic review of the success of sinus floor
elevation and survival of implants inserted in combination with sinus floor elevation. [Part I: Lateral
approach.] J Clin Periodontol. 2008 Sep;35(8 Suppl):216-240.
502. Klokkevold PR, Han TJ. How do smoking, diabetes, and periodontitis affect outcomes of implant
treatment? Int J Oral Maxillofac Implants 2007;22(suppl):173-202.
503. Penarrocha M, Palomar M, Sanchis JM, Guarinos J, Balaguer J. Radiologic study of marginal bone loss
around 108 dental implants and its relationship to smoking, implant location, and morphology. Int J Oral
Maxillofac Implants 2004;19:861-867.
504. Nitzan D, Mamlider A, Levin L, Schwartz-Arad D. Impact of smoking on marginal bone loss. Int J Oral
Maxillofac Implants 2005;20:605-609.
505. Ross-JansakerAM, Lindahl C, Renvert H, Renvert S. Nine- to fourteen-year follow-up of implant
treatment. Part I: Implant loss and associations to various factors. J ClinPeriodontol 2006;33:283-289.
506. Sanchez-Perez A, Moya-Villaescusa MJ, Caffesse RG. Tobacco as a risk factor for survival of dental
implants. J Periodontol 2007;78:351-359.
507. Galindo-Moreno P, Fauri M, Avila-Ortiz G, Fernandez-Barbero JE, Cabrera-Leon A, Sanchez-Fernandez
E. Influence of alcohol and tobacco habits on peri-implant matginal bone loss: A prospective study. Clin
Oral Implants Res 2005;16:579-586.
508. Fransson C, Wennstrom J, Berglundh T. Clinical characteristics at implants with a history of progressive
bone loss. Clin Oral Implants Res 2008;19:142-147.
509. Carmeli G, Artzi Z, Avital K, Yoram S, Landsberg R. Antral computerized tomography pre-operative
evaluation : relationship between mucosal thickening and maxillary sinus function. Clin. Oral Impl. Res.
22, 2011: 78-82.
510. Hallman M1, Nordin T Sinus floor augmentation with bovine hydroxyapatite mixed with fibrin glue and
later placement of nonsubmerged implants: a retrospective study in 50 patients. Int J Oral Maxillofac
Implants. 2004 Mar-Apr;19(2):222-7.
511. Becker W, Becker BE, Alsuwyed A, Al-Mubarak S. Long-term evaluation of 282 implants in maxillary
and mandibular molar positions: A prospective study. J Periodontol 1999;70:896-901.
512. Lindquist LW, Carlsson GE, Jemt T. Association between marginal bone loss around osseointegrated
mandibular implants and smoking habits: A 10-year follow-up study. J Dent Res 1997;76:1667-1674.
513. Ferreira SD, Silva GL, Cortelli JR, Costa FO. Prevalence and risk variables for peri-implant disease in
Brazilian subjects. J ClinPeriodontol 2006;33:929-935.
514. Ludlow JB1, Davies-Ludlow LE, Brooks SL. Dosimetry of two extraoral direct digital imaging devices:
NewTom cone beam CT and Orthophos Plus DS panoramic unit. Dentomaxillofac Radiol. 2003
Jul;32(4):229-34.
515. Borg E1, Gröndahl K, Gröndahl HG. Marginal bone level buccal to mandibular molars in digital
radiographs from charge-coupled device and storage phosphor systems. An in vitro study. J Clin
Periodontol. 1997 May;24(5):306-12.
516. Kavadella A1, Karayiannis A, Nicopoulou-Karayianni K. Detectability of experimental peri-implant
cancellous bone lesions using conventional and direct digital radiography. Aust Dent J. 2006
Jun;51(2):180-6.
517. Dave M1, Davies J, Wilson R, Palmer R. A comparison of cone beam computed tomography and
conventional periapical radiography at detecting peri-implant bone defects. Clin Oral Implants Res. 2013
Jun;24(6):671-8.
518. Jacobs R, Vam Steenberghe D. Imaging procedures for pre-operative assessement. In: Jacobs R & Van
Steenberghe D., eds. Radiographic Planning and Assesment of Endosseous Oral Implants, 7-30. Berlin:
Springer.

~ 341 ~
519. Vazquez L, Nizam Al Din Y, Christoph Belser U, Combescure C, Bernard JP. Reliability of the vertical
magnification factor on panoramic radiographs: clinical implications for posterior mandibular implants.
Clin Oral Implants Res. 2011 Dec;22(12):1420-5.
520. Mischkowski RA1, Ritter L, Neugebauer J, Dreiseidler T, Keeve E, Zöller JE. Diagnostic quality of
panoramic views obtained by a newly developed digital volume tomography device for maxillofacial
imaging. Quintessence Int. 2007 Oct;38(9):763-72.
521. Angelopoulos C1, Thomas SL, Hechler S, Parissis N, Hlavacek M. Comparison between digital
panoramic radiography and cone-beam computed tomography for the identification of the mandibular
canal as part of presurgical dental implant assessment. J Oral Maxillofac Surg. 2008 Oct;66(10):2130-5.
522. Tal H1, Moses O. A comparison of panoramic radiography with computed tomography in the planning of
implant surgery. Dentomaxillofac Radiol. 1991 Feb;20(1):40-2.
523. Hatcher DC1, Dial C, Mayorga C. Cone beam CT for pre-surgical assessment of implant sites. J Calif
Dent Assoc. 2003 Nov;31(11):825-33.
524. Watanabe H1, Honda E, Tetsumura A, Kurabayashi T. A comparative study for spatial resolution and
subjective image characteristics of a multi-slice CT and a cone-beam CT for dental use. Eur J
Radiol. 2011 Mar;77(3):397-402.
525. Shannon, C.E., (1949) Communication in the presence of noise. Proceedings of the Institute of Radio
Engineers 37: 10-21.
526. Monje A1, Monje F, González-García R, Galindo-Moreno P, Rodriguez-Salvanes F, Wang HL.
Comparison between microcomputed tomography and cone beam computed tomography radiologic bone
to assess atrophic posterior maxilla density and microarchitecture. Clin Oral Implants Res. 2014
Jun;25(6):723-8.
527. Harris D, Horner K, Grondahl K, Jacobs R, Helmrot E, Benic GI, Bornstein MM, Dawood A, Quirynen
M. E.A.O. guidelines for the use of diagnostic imaging in implant dentistry 2011. A consensus workshop
organized by the European Association for Osseointegration at the Medical University of Warsaw. Clin
Oral Impl Res 2012; 23:1243-1253.
528. Feldkamp LA1, Goldstein SA, Parfitt AM, Jesion G, Kleerekoper M. The direct examination of three-
dimensional bone architecture in vitro by computed tomography. J Bone Miner Res. 1989 Feb;4(1):3-11.
529. Ito M1. Assessment of bone quality using micro-computed tomography (micro-CT) and synchrotron
micro-CT. J Bone Miner Metab. 2005;23 Suppl:115-21.
530. Rüegsegger P1, Koller B, Müller R. A microtomographic system for the nondestructive evaluation of
bone architecture. Calcif Tissue Int. 1996 Jan;58(1):24-9.
531. Thomsen JS1, Laib A, Koller B, Prohaska S, Mosekilde L, Gowin W. Stereological measures of
trabecular bone structure: comparison of 3D micro computed tomography with 2D histological sections
in human proximal tibial bone biopsies. J Microsc. 2005 May;218(Pt 2):171-9.
532. Fanuscu M, Chang TL. Three-dimensional morphometric analysis of human cadaver bone:
microstructural data from maxilla and mandible. Clinical Oral Implants Research (Impact Factor:
3.12). 05/2004; 15(2):213-8.
533. Morinaga K1, Kido H, Sato A, Watazu A, Matsuura M. Chronological changes in the ultrastructure of
titanium-bone interfaces: analysis by light microscopy, transmission electron microscopy, and micro-
computed tomography. Clin Implant Dent Relat Res. 2009 Mar;11(1):59-68.
534. Cha JY1, Lim JK, Song JW, Sato D, Kenmotsu M, Inoue T, Park YC. Influence of the length of the
loading period after placement of orthodontic mini-implants on changes in bone histomorphology:
microcomputed tomographic and histologic analysis. Int J Oral Maxillofac Implants. 2009 Sep-
Oct;24(5):842-9.
535. Kühl S1, Götz H, Hansen T, Kreisler M, Behneke A, Heil U, Duschner H, d'Hoedt B. Three-dimensional
analysis of bone formation after maxillary sinus augmentation by means of microcomputed tomography:
a pilot study. Int J Oral Maxillofac Implants. 2010 Sep-Oct;25(5):930-8.
536. Kon K1, Shiota M, Ozeki M, Yamashita Y, Kasugai S. Bone augmentation ability of autogenous bone
graft particles with different sizes: a histological and micro-computed tomography study. Clin Oral
Implants Res. 2009 Nov;20(11):1240-6.

~ 342 ~
537. Rosenfeld AL, Mecall RA. The use of interactive computed tomography predict the esthetic and
functional demands of implants-supported prostheses. Compend Contin Educ Dent 1996;17: 1125-
1128,1130-1132.
538. Besimo C, Lambrech J.T, Nidecker A. Dental implant treatment planning with reformatted computed
tomography. Dentomaxillofac. Radiol 1995;24: 264-7.
539. Bolin A, Eliasson S. Panoramic and tomographic dimensional determinations for maxillary
osseointegrated implants. Comparison of the morphologic information potential of two and three
dimensional radiographic systems. Swed. Dent. J 1995;19: 65-71.
540. Testori T, Sacerdoti S, Barenghi A et.al. La tomografia assiale computerizzata nella moderna
implantologia: reali vantaggi per una corretta progrommazione chirurgico-protesica; dose assorbita dal
paziente. Ital J. Osseointegration 1993;1: 19-28.
541. Dula K, Buser D, Porcellini B, Berthold H, Schwartz M. Computed tomography/oral implantology (I).
Dental CT: a program for the computed tomographic imaging of the jaws: the principles and exposure
technic. Schweiz Monatsschr Zahnmed 1994;104: 450-9.
542. Dula K, Buser D. Computed tomography/oral implantology. Dental-CT: a program for the computed
tomographic imaging of the jaws. The indications for perimplantological clarification. Schweiz
Monatsschr Zahnmed 1996;106: 550-63.
543. Seipel S, Wagner I.V, Koch S, Schneider W. A virtual reality environment for enhanced oral
implantology. Medinfo 1995;8 Pt 2: 1710.
544. Ekestubbe A1, Gröndahl K, Gröndahl HG. The use of tomography for dental implant planning.
Dentomaxillofac Radiol. 1997 Jul;26(4):206-1.
545. Sakakura CE1, Morais JA, Loffredo LC, Scaf G. A survey of radiographic prescription in dental implant
assessment. Dentomaxillofac Radiol. 2003 Nov;32(6):397-400.
546. Tyndall DA1, Brooks SL. Selection criteria for dental implant site imaging: a position paper of the
American Academy of Oral and Maxillofacial radiology. Oral Surg Oral Med Oral Pathol Oral Radiol
Endod. 2000 May;89(5):630-7.
547. Baciut M1, Hedesiu M, Bran S, Jacobs R, Nackaerts O, Baciut G. Pre- and postoperative assessment of
sinus grafting procedures using cone-beam computed tomography compared with panoramic
radiographs. Clin Oral Implants Res. 2013 May;24(5):512-6.
548. Mengel R, Candir M, Shiratori K, Flores-de-Jacoby L. Digital volume tomography in the diagnosis of
periodontal defects: an in vitro study on native pig and human mandibles. J Periodontol 2005
May;76(5):665-73
549. Isoda K1, Ayukawa Y, Tsukiyama Y, Sogo M, Matsushita Y, Koyano K. Relationship between the bone
density estimated by cone-beam computed tomography and the primary stability of dental implants. Clin
Oral Implants Res. 2012 Jul;23(7):832-6.
550. Aranyarachkul P1, Caruso J, Gantes B, Schulz E, Riggs M, Dus I, Yamada JM, Crigger M. Bone density
assessments of dental implant sites: 2. Quantitative cone-beam computerized tomography. Int J Oral
Maxillofac Implants. 2005 May-Jun;20(3):416-24.
551. Naitoh M1, Hirukawa A, Katsumata A, Ariji E. Evaluation of voxel values in mandibular cancellous
bone: relationship between cone-beam computed tomography and multislice helical computed
tomography. Clin Oral Implants Res. 2009 May;20(5):503-6
552. Nomura Y1, Watanabe H, Honda E, Kurabayashi T. Reliability of voxel values from cone-beam
computed tomography for dental use in evaluating bone mineral density. Clin Oral Implants Res. 2010
May;21(5):558-62.
553. Arisan V1, Karabuda ZC, Avsever H, Özdemir T. Conventional multi-slice computed tomography (CT)
and cone-beam CT (CBCT) for computer-assisted implantplacement. Part I: relationship of radiographic
gray density and implant stability. Clin Implant Dent Relat Res. 2013 Dec;15(6):893-906.
554. Cassetta M1, Stefanelli LV, Pacifici A, Pacifici L, Barbato E. How accurate is CBCT in measuring bone
density? A comparative CBCT-CT in vitro study. Clin Implant Dent Relat Res. 2014 Aug;16(4):471-8.

~ 343 ~
555. Merheb J1, Van Assche N, Coucke W, Jacobs R, Naert I, Quirynen M. Relationship between cortical
bone thickness or computerized tomography-derived bone density values andimplant stability. Clin Oral
Implants Res. 2010 Jun;21(6):612-7.
556. Rodrigo D1, Aracil L, Martin C, Sanz M. Diagnosis of implant stability and its impact
on implant survival: a prospective case series study. Clin Oral Implants Res. 2010 Mar;21(3):255-61
557. Cehreli MC1, Kökat AM, Comert A, Akkocaoğlu M, Tekdemir I, Akça K. Implant stability and bone
density: assessment of correlation in fresh cadavers using conventional and osteotome implant sockets.
Clin Oral Implants Res. 2009 Oct;20(10):1163-9.
558. Coutant JC, Seguela V, Hauret L, Caix P, Ella B. Assessment of
the correlation between implant stability and bone density by computed tomography and resonance
frequency analysis in fresh cadavers. Int J Oral Maxillofac Implants. 2014 Nov-Dec;29(6):1264-70.
559. Bischof M1, Nedir R, Szmukler-Moncler S, Bernard JP, Samson J.
Implant stability measurement of delayed and immediately loaded implants during healing. Clin Oral
Implants Res. 2004 Oct;15(5):529-39.
560. Simunek A1, Strnad J, Kopecka D, Brazda T, Pilathadka S, Chauhan R, Slezak R, Capek L. Changes in
stability after healing of immediately loaded dental implants. Int J Oral Maxillofac Implants. 2010 Nov-
Dec;25(6):1085-92.
561. Khayat PG1, Arnal HM, Tourbah BI, Sennerby L. Clinical outcome of dental implants placed with high
insertion torques (up to 176 Ncm). Clin Implant Dent Relat Res. 2013 Apr;15(2):227-33.
562. Ottoni JM, Oliveira ZF, Mansini R, Cabral AM. Correlation between placement-torque and survival of
single-tooth implants. Int J Oral Maxillofac Implants 2005; 20:769-776.
563. Glauser R. Immediate Loadinsg of Branemark implants [pre congress symposium]. in: 125 Jahrestagung
der Deutsch. Ges. f. Zahn-, Mund- und Kieferheilkunde Jahrestagung der. Deutsch. Ges. f.Implantologie;
10 Nov 2001, Mannheim, Germany.
564. Truhlar RS, Morris HF, Ochi S. Stability of the bone-implant complex. Results of longitudinal testing to
60 months with the Periotest device on endosseous dental implants. Ann Periodontol 2000; 5:42-55.
565. Walker L, Morris HF, Ochi S. Periotest values of dental implants in the first 2 years after second-stage
surgery: DICRG interim report no. 8. Dental Implant Clinical Research Group. Implant Dent 1997;
6:207-212.
566. Aparicio C. The use of the Periotest value as the initial success criteria of an implant: 8 year report. Int J
Periodontics Restorative Dent 1997; 17:150-161.
567. Sennerby L, Meredith N. Implant stability measurements using resonance frequency analysis: biological
and biomechanical aspects and clinical implications. Periodontol 2000. 2008;47:51-66.
568. Olivé J, Aparicio C. Periotest method as a measure of osseointegrated oral implant stability. Int J Oral
Maxillofac Implants. 1990 Winter;5(4):390-400.
569. Hobkirk JA, Wiskott HWA. Biomechanical aspects of oral implants Consensus report of Working Group
1. 10.1111/j.1600-0501.2006.01358.x.
570. Baltayan S, Mardirosian M, El-Ghareeb M, Aghaloo T, Pi-Anfruns J, Moy P. The Predictive Value of
Resonance Frequency Analysis in the Surgical Placement and Loading of Endosseus Implants. AAID
Poster 2011
571. Ostman P.O, Hellman M, Sennerby L. Direct implant loading in the edentulous maxilla using a bone
density-adapted surgical protocol and primary implant stability criteria for inclusion 2005 ;7(Suppl 1) :
S90-9.
572. Ostman P.O, Hellman M, Sennerby L. Immediate occlusal loading of implants in the partially edentate
mandible : a prospective 1-year radiographic and 4-year clinical study. International Journal of Oral and
Maxillofac Implant s 2008 ;23 : 315-322.
573. Sennerby L, Meredith N. Implant stability measurments using resonance frequency analysis : biological
and biomechanical aspects and clinical implications. Periodontology 2000 ;47 : 51-66.
574. Friberg B1, Sennerby L, Meredith N, Lekholm U. A comparison between cutting torque and resonance
frequency measurements of maxillary implants. A 20-month clinical study. Int J Oral Maxillofac
Surg. 1999 Aug;28(4):297-303.

~ 344 ~
575. Degidi M1, Daprile G, Piattelli A, Carinci F. Evaluation of factors influencing resonance frequency
analysis values, at insertion surgery, of implants placed in sinus-augmented and nongrafted sites.
Clin Implant Dent Relat Res. 2007 Sep;9(3):144-9.
576. Huwiler MA1, Pjetursson BE, Bosshardt DD, Salvi GE, Lang NP. Resonance frequency analysis in
relation to jawbone characteristics and during early healing of implantinstallation. Clin Oral Implants
Res. 2007 Jun;18(3):275-80.
577. Glauser R, Ruhstaller P, Gottlow J, Sennerby L, Portmann M, Hammerle CH. Immediate occlusal
loading of Branemark TiUnite implants placed predominantly in soft bone: 1-year results of a
prospective clinical study. Clin Implant Dent Relat Ress 2003;5:47-56.
578. Glauser R1, Sennerby L, Meredith N, Rée A, Lundgren A, Gottlow J, Hämmerle CH. Resonance
frequency analysis of implants subjected to immediate or early functional occlusal loading. Successful
vs. failing implants. Clin Oral Implants Res. 2004 Aug;15(4):428-34.
579. Balshi SF1, Allen FD, Wolfinger GJ, Balshi TJ. A resonance frequency analysis assessment of maxillary
and mandibular immediately loaded implants. Int J Oral Maxillofac Implants. 2005 Jul-Aug;20(4):584-
94.
580. Al-Nawas B1, Wagner W, Grötz KA. Insertion torque and resonance frequency analysis of
dental implant systems in an animal model with loaded implants. Int J Oral Maxillofac Implants. 2006
Sep-Oct;21(5):726-32.
581. Berglundh T1, Abrahamsson I, Lang NP, Lindhe J. De novo alveolar bone formation adjacent to
endosseous implants. Clin Oral Implants Res. 2003 Jun;14(3):251-62.
582. Perren SM1. Evolution of the internal fixation of long bone fractures. The scientific basis of biological
internal fixation: choosing a new balance between stability and biology. J Bone Joint Surg Br. 2002
Nov;84(8):1093-110.
583. Trisi P, Carlesi T, Colagiovanni M, Perfetti G. Implant Stability Quotient (ISQ) vs Direct in Vitro
Measurement of Primary Stability (Micromotion): Effect of Bone Density and Insertion Torque. Journal
of Osteology and Biomaterials, Volume 1, Number 3, 2010
584. Johansson C, Albrektsson T. Integration of screw implants in the rabbit: A 1-year follow-up of removal
torque of titanium implants. Int J Oral Maxillofac Implants 1987; 2:69-75.
585. Sullivan DY1, Sherwood RL, Collins TA, Krogh PH. The reverse-torque test: a clinical report. Int J Oral
Maxillofac Implants. 1996 Mar-Apr;11(2):179-85.
586. Misch CE: Maxillary sinus augmentation for endosteal implants: organized alternative treatment plans,
Int J Oral Implant 4:49-58, 1987.
587. Zarb GA, Schmitt A. the longitudinal clinical effectiveness of osseointegrated dental Implants in
posterior partially edentulous patients. Int J Prosthodont 1993; 6:189-196.
588. Blomqvist JE, Alberius P, Isaksson S. Retrospective analysis of one-stage maxillary sinus augmentation
with endosseous implants. Int J Oral Maxillofac Implants. 1996 11:512-21.
589. Khoury F. Augmentation of the sinus floor with mandibular bone block and simultaneous implantation: a
6-year clinical investigation. Int J Oral Maxillofac Implants. 1999;14:557-64.
590. Wannfors K, Johansson B, Hallman M, Strandkvist T. A prospective randomized study of 1- and 2-stage
sinus inlay bone grafts: 1-year follow-up. Int J Oral Maxillofac Implants. 2000; 15:625-32.
591. Kahnberg KE, Ekestubbe A, Gröndahl K, Nilsson P, Hirsch JM. Sinus lifting procedure. I. One-stage
surgery with bone transplant and implants. Clin Oral Implants Res. 2001; 12:479-87.
592. Munoz-Guerra MF, Naval-Gias L, Escorial V, Sastre-Perez J. Dentin dysplasia type I treated with onlay
bone grafting, sinus augmentation, and osseointegrated implants. Implant Dent 2006;15:248-253.
593. Keller EE, van Roekel NB, Desjardins RR et al: Prosthetic surgical reconstruction of severely resorbed
maxilla with iliac bone grafting and tissue integrated prostheses, Int J Oral Maxillofac Impl 2:155, 1987.
594. Sailer HF: A new method of inserting endosseous implants in totally atrophic maxillae, J Cranio
Maxillofac Surg 17:299-305, 1989.
595. Schenk RK, Buser D. Osseointegration: A reality. Periodontal 2000 1998;17:22-35.
596. Tatum H Jr. Maxillary and sinus implant reconstructions. Dent Clin North Am 1986;30(2):207-29.

~ 345 ~
597. Wallace SS, Froum SJ. Effect of maxillary sinus augmentation on the survival of endosseous dental
implants. A systematic review Ann. 2003; 8: 328-43.
598. Hallmann M. Sennerby L. Lundgren S. A clinical and histologic evaluation of implant integration in the
posterior maxilla after sinus floor augmentation with autogenous bone, bovine hydroxyapatite, or a 20:80
mixture, int J Oral Maxillofac. Implants 2002;17:635-43.
599. Valentini P, Abensur D, Densari D, Graziani JN, Hämmerle C. Histological evaluation of Bio-Oss in a 2-
stage sinus floor elevation and implantation procedure. A human case report. Clin Oral Implants Res.
1998;9:59-64.
600. Toffler M. Osteotome-mediated sinus floor elevation: A clinical report. Int J Oral Maxillofac Implants
2004;19:266-273.
601. Peleg M, Mazor Z, Chaushu G, Garg AK. Sinus floor augmentation with simultaneous implant
placement in the severely atrophic maxilla. J Periodontol 1998;69:1397-1403.
602. Peleg M, Mazor Z, Garg AK. Augmentation grafting of the maxillary sinus and simultaneous implant
placement in patients with 3 to 5 mm of residual alveolar bone height. Int J Oral Maxillofac Implants
1999;14:549-556.
603. Mazor Z, Peleg M, Gross M. Sinus augmentation for single-tooth replacement in the posterior maxilla:
A 3-year follow-up clinical report. Int J Oral Maxillofac Implants 1999; 14:55-60.
604. Feigel A, Maker M: The significance of sinus elevation for blade implantology: report of an autopsy
case, J Oral Implant 15:232-247, 1989.
605. Aghaloo TL, Moy PK. Which hard tissue augmentation techniques are the most successful in furnishing
bony support for implant placement? Int J Oral Maxillofac Implants. 2007;22 Suppl:49-70
606. Geiger SA, Pesch HJ. Animal experimental studies on the healing around ceramic implantation in bone
lesions in the maxillary sinus region. Dtsch Zahnarztl Z. 1977 May;32(5):396-9.
607. Tatum OH: The Omni implant system. In Hardin JF, editor: Clarke’s clinical dentistry, Philadelphia,
1984, Lippincott.
608. Kent J, Block M. simultaneous maxillary sinus floor bone grafting and placement of hydroxylapatite-
coated implants. J Oral Maxillofac Surg 1989;47:238-242.
609. Daelemans P, Hermans M, Godet F, Malavez C. Autologous bone graft to augment the maxillary sinus in
conjunction with immediate endosseous implants: A retrospective study up to 5 years. Int J Periodontics
Restorative Dent 1997;17:27-39.
610. Lazzara RJ. The Sinus elevation procedure in endosseous implant therapy. Curr Opin Periodontol
1996;3:178-183.
611. PJ. The use of bone graft systems in maxillary implant surgery. Proceedings of the 50thAnnual. Meeting
of the American institute of Oral Biology, Palm Springs, CA, Oct 29-Nov 2. Madison, WI: Omni,
1993:107-114.
612. Triplett RG, Schow SR. Autologous bone grafts and endosseous implants: Complementary techniques. J
Oral Maxillofac Surg 1996;54:486-494.
613. Del Fabbro M, Testori T, Francetti L, Weinstein R. Systematic review of survival rates for implants
placed in the grafted maxillary sinus. Int J. Periodontics Restorative Dent. 2004; 24(6): 565-77.
614. Tetsch J1, Tetsch P, Lysek DA. Long-term results after lateral and osteotome technique sinus floor
elevation: a retrospective analysis of 2190 implants over a time period of 15 years. Clin Oral Implants
Res. 2010 May;21(5):497-503.
615. Busenlechner D1, Huber CD, Vasak C, Dobsak A, Gruber R, Watzek G. Sinus augmentation analysis
revised: the gradient of graft consolidation. Clin Oral Implants Res. 2009 Oct;20(10):1078-83.
616. Tadjoedin ES1, de Lange GL, Bronckers AL, Lyaruu DM, Burger EH. Deproteinized cancellous bovine
bone (Bio-Oss) as bone substitute for sinus floor elevation. A retrospective, histomorphometrical study
of five cases. J Clin Periodontol. 2003 Mar;30(3):261-70.
617. Chanavez M. Maxillary sinus. Anatomy, physiology, surgery, and bone grafting relating to implantology
– Eleven years of clinical experience (1979-1990). J Oral Implantol 1990;16:199-209.
618. Regev E, Smith RA, Perrot DH, Pogrel MA. Maxillary sinus complications related to endosseous
implants. Int J Oral Maxillofac Implants 1995;10:451-461.

~ 346 ~
619. Zimbler MS, Lebowitz RA, Glickman R. Antral augmentation osseointegration and sinusitis: The
otolaryngologist perspective. Am J Rhinol 1998; 12:311-316.
620. Watelet JB, Van Cauwenberge P. Applied anatomy and physiology of the nose and paranasal sinuses.
Allergy 1999;54:14-25.
621. Peleg M, Chaushu G, Mazor Z, et al. Radiological findings of the post-sinusitis lift maxillary sinus: A
computerized tomography follow-up. Periodontol 1999;70:1564-1573.
622. Mantovani, M. (2009) Otolaryngological contraindications in augmentation of the maxillary sinus.
In:Testori, T., Del Fabbro, M. & Weinstein, R. et al.,eds. Maxillary Sinus Surgery and alternatives, 1st
edition,42–52. Chicago: Quintessence Publishing.
623. Stammberger, H. (1986) Endoscopic endonasal surgery–concepts in treatment of recurring rhinosinusitis.
Part II. Surgical technique. Otolaryngology Head and Neck Surgery 94: 147–156.
624. Uchida Y1, Goto M, Katsuki T, Soejima Y. Measurement of maxillary sinus volume using computerized
tomographic images. Int J Oral Maxillofac Implants. 1998 Nov-Dec;13(6):811-8.
625. Krennmair G1, Krainhöfner M, Maier H, Weinländer M, Piehslinger E.Computerized tomography-
assisted calculation of sinus augmentation volume. Int J Oral Maxillofac Implants. 2006 Nov-
Dec;21(6):907-13.
626. Fenner M1, Vairaktaris E, Fischer K, Schlegel KA, Neukam FW, Nkenke E. Influence of residual
alveolar bone height on osseointegration of implants in the maxilla: a pilot study. Clin Oral Implants
Res. 2009 Jun;20(6):555-9.
627. Fenner M1, Vairaktaris E, Stockmann P, Schlegel KA, Neukam FW, Nkenke E. Influence of residual
alveolar bone height on implant stability in the maxilla: an experimental animal study. Clin Oral Implants
Res. 2009 Aug;20(8):751-5.
628. Nkenke E1, Stelzle F. Clinical outcomes of sinus floor augmentation for implant placement using
autogenous bone or bone substitutes: a systematic review. Clin Oral Implants Res. 2009 Sep;20 Suppl
4:124-33.
629. Rodriguez A1, Anastassov GE, Lee H, Buchbinder D, Wettan H. Maxillary sinus augmentation with
deproteinated bovine bone and platelet rich plasma with simultaneous insertion of endosseous implants. J
Oral Maxillofac Surg. 2003 Feb;61(2):157-63.
630. Mardinger O1, Nissan J, Chaushu G. Sinus floor augmentation with simultaneous implant placement in
the severely atrophic maxilla: technical problems and complications. J Periodontol. 2007
Oct;78(10):1872-7.
631. Rios HF, Avila G, Galindo P, Bratu E, Wang HL. The influence of remaining alveolar bone upon lateral
window sinus augmentation implant survival. Implant Dentistry 2009; 18(5): 402-412.
632. Urban IA1, Lozada JL. A prospective study of implants placed in augmented sinuses with minimal and
moderate residual crestal bone: results after 1 to 5 years. Int J Oral Maxillofac Implants. 2010 Nov-
Dec;25(6):1203-12.
633. Tong DC, Rioux K, Drangsholt M, Beirne OR. A review of survival rates for implants placed in grafted
maxillary sinuses using meta-analysis. Int J Oral Maxillofac Implants 1998; 13: 175-82
634. Jensen OT1, Sennerby L. Histologic analysis of clinically retrieved titanium microimplants placed in
conjunction with maxillary sinus floor augmentation. Int J Oral Maxillofac Implants. 1998;13:513-21.
635. Hallman M1, Sennerby L, Zetterqvist L, Lundgren S.A 3-year prospective follow-up study of implant-
supported fixed prostheses in patients subjected to maxillarysinus floor augmentation with a 80:20
mixture of deproteinized bovine bone and autogenous bone Clinical, radiographic and resonance
frequency analysis.Int J Oral Maxillofac Surg. 2005 May;34(3):273-80.
636. Pikos MA. In: Jensen OT, ED. The sinus bone graft, 2nd ed. Chicago, IL: Quintessence, 2006: 103-14.
637. Lindhe J1, Meyle J; Group D of European Workshop on Periodontology. Peri-implant diseases:
Consensus Report of the Sixth European Workshop on Periodontology. J Clin Periodontol. 2008
Sep;35(8 Suppl):282-5.

~ 347 ~
638. Wallace SS1, Mazor Z, Froum SJ, Cho SC, Tarnow DP. Schneiderian membrane perforation rate
during sinus elevation using piezosurgery: clinical results of 100 consecutive cases. Int J Periodontics
Restorative Dent. 2007 Oct;27(5):413-9.
639. Rickert D1, Vissink A, Slater JJ, Meijer HJ, Raghoebar GM. Rickert D1, Vissink A, Slater JJ, Meijer
HJ, Raghoebar GM. Comparison between conventional and piezoelectric surgical tools for maxillary
sinus floor elevation. A randomized controlled clinical trial. Clin Implant Dent Relat Res. 2013
Apr;15(2):297-302.
640. Schwartz-Arad D1, Herzberg R, Dolev E. The prevalence of surgical complications of the sinus graft
procedure and their impact on implant survival. J Periodontol. 2004 Apr;75(4):511-6.
641. Katranji A1, Fotek P, Wang HL. Sinus augmentation complications: etiology and treatment. Implant
Dent. 2008 Sep;17(3):339-49.
642. Ferrigno N1, Laureti M, Fanali S. Dental implants placement in conjunction with osteotome sinus floor
elevation: a 12-year life-table analysis from a prospective study on 588 ITI implants. Clin Oral Implants
Res. 2006 Apr;17(2):194-205.
643. Herrmann I1, Lekholm U, Holm S, Kultje C. Evaluation of patient and implant characteristics as potential
prognostic factors for oral implant failures. Int J Oral Maxillofac Implants. 2005 Mar-Apr;20(2):220-30.
644. Barone A1, Ricci M, Grassi RF, Nannmark U, Quaranta A, Covani U. A 6-month histological analysis on
maxillary sinus augmentation with and without use of collagen membranes over the osteotomy window:
randomized clinical trial. Clin Oral Implants Res. 2013 Jan;24(1):1-6.
645. Choi KS1, Kan JY, Boyne PJ, Goodacre CJ, Lozada JL, Rungcharassaeng K. The effects of resorbable
membrane on human maxillary sinus graft: a pilot study. Int J Oral Maxillofac Implants. 2009 Jan-
Feb;24(1):73-80.
646. Mardinger O1, Moses O, Chaushu G, Manor Y, Tulchinsky Z, Nissan J. Challenges associated with
reentry maxillary sinus augmentation. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2010
Sep;110(3):287-91.
647. Krennmair G, Ulm CW, Lugmayr H, Solar P. The incidience, location, and height of maxillary sinus
septa in the edentulous and dentate maxilla. J Oral Maxillofac Surg 1999 Jun;57: 667-671.
648. Haas R, Mensdorff-Pouilly N, Mailath G, Watzek G. Success of 1,920 IMZ implants. Followed for up to
100 months.Int J Oral Maxillofac Implants 1996; 11:581-588.
649. Cecchinato D1, Parpaiola A, Lindhe J. A cross-sectional study on the prevalence of marginal bone loss
among implant patients. Clin Oral Implants Res. 2013 Jan;24(1):87-90.
650. Cecchinato D1, Parpaiola A, Lindhe J. Mucosal inflammation and incidence of crestal bone loss among
implant patients: a 10-year study. Clin Oral Implants Res. 2014 Jul;25(7):791-6.
651. Sanz M, Chapple IL, on behalf of Working Group 4 of the VIII European Workshop on Periodontology.
Clinical research on peri-implant diseases: consensus report of Working Group 4. J Clin Periodontol
2012; 39 (Suppl. 12): 202–206.
652. J Periodontol. 2002 Mar;73(3):322-33.
653. Manz MC1. Factors associated with radiographic vertical bone loss around implants placed in a clinical
study. Ann Periodontol. 2000 Dec;5(1):137-51.
654. Esposito M1, Hirsch JM, Lekholm U, Thomsen P. Biological factors contributing to failures of
osseointegrated oral implants. (I). Success criteria and epidemiology. Eur J Oral Sci. 1998
Feb;106(1):527-51.
655. Kronström M1, Svenson B, Hellman M, Persson GR. Early implant failures in patients treated with
Brånemark System titanium dental implants: a retrospective study. Int J Oral Maxillofac Implants. 2001
Mar-Apr;16(2):201-7.
656. Carlsson GE1, Lindquist LW, Jemt T. Long-term marginal periimplant bone loss in edentulous patients.
Int J Prosthodont. 2000 Jul-Aug;13(4):295-302.
657. Rompen E1, Touati B, Van Dooren E. Factors influencing marginal tissue remodeling around implants.
Pract Proced Aesthet Dent. 2003 Nov-Dec;15(10):754-7, 759, 761.
658. Herzberg R1, Dolev E, Schwartz-Arad D. Implant marginal bone loss in maxillary sinus grafts. Int J Oral
Maxillofac Implants. 2006 Jan-Feb;21(1):103-10.

~ 348 ~
659. Shin YK1, Han CH, Heo SJ, Kim S, Chun HJ. Radiographic evaluation of marginal bone level around
implants with different neck designs after 1 year. Int J Oral Maxillofac Implants. 2006 Sep-
Oct;21(5):789-94.
660. Pontes AE1, Ribeiro FS, da Silva VC, Margonar R, Piattelli A, Cirelli JA, Marcantonio E Jr. Clinical and
radiographic changes around dental implants inserted in different levels in relation to the crestal bone,
under different restoration protocols, in the dog model. J Periodontol. 2008 Mar;79(3):486-94.
661. Jung RE1, Jones AA, Higginbottom FL, Wilson TG, Schoolfield J, Buser D, Hämmerle CH, Cochran DL.
The influence of non-matching implant and abutment diameters on radiographic crestal bone levels in
dogs. J Periodontol. 2008 Feb;79(2):260-70.
662. Abrahamsson I1, Berglundh T. Effects of different implant surfaces and designs on marginal bone-level
alterations: a review. Clin Oral Implants Res. 2009 Sep;20 Suppl 4:207-15.
663. Hansson S1. Implant-abutment interface: biomechanical study of flat top versus conical. Clin Implant
Dent Relat Res. 2000;2(1):33-41.
664. Novaes AB Jr1, Papalexiou V, Muglia V, Taba M Jr. Influence of interimplant distance on gingival
papilla formation and bone resorption: clinical-radiographic study in dogs. Int J Oral Maxillofac
Implants. 2006 Jan-Feb;21(1):45-51.
665. Hansson S1, Werke M. The implant thread as a retention element in cortical bone: the effect of thread size
and thread profile: a finite element study. J Biomech. 2003 Sep;36(9):1247-58.
666. Hansson S1, Norton M. The relation between surface roughness and interfacial shear strength for bone-
anchored implants. A mathematical model. J Biomech. 1999 Aug;32(8):829-36.
667. Aloy-Prósper A1, Maestre-Ferrín L, Peñarrocha-Oltra D, Peñarrocha-Diago M. Marginal bone loss in
relation to the implant neck surface: an update. Med Oral Patol Oral Cir Bucal. 2011 May 1;16(3):e365-8.
668. Vela-Nebot X1, Rodríguez-Ciurana X, Rodado-Alonso C, Segalà-Torres M. Benefits of an implant
platform modification technique to reduce crestal bone resorption. Implant Dent. 2006 Sep;15(3):313-20.
669. Canullo L1, Fedele GR, Iannello G, Jepsen S. Platform switching and marginal bone-level alterations: the
results of a randomized-controlled trial. Clin Oral Implants Res. 2010 Jan;21(1):115-21.
670. Serrano-Sánchez P1, Calvo-Guirado JL, Manzanera-Pastor E, Lorrio-Castro C, Bretones-López P, Pérez-
Llanes JA. The influence of platform switching in dental implants. A literature review. Med Oral Patol
Oral Cir Bucal. 2011 May 1;16(3):e400-5.
671. Piattelli A1, Degidi M, Paolantonio M, Mangano C, Scarano A. Residual aluminum oxide on the surface
of titanium implants has no effect on osseointegration. Biomaterials. 2003 Oct;24(22):4081-9.
672. Cappiello M1, Luongo R, Di Iorio D, Bugea C, Cocchetto R, Celletti R. Evaluation of peri-implant bone
loss around platform-switched implants. Int J Periodontics Restorative Dent. 2008 Aug;28(4):347-55.
673. Tarnow DP1, Cho SC, Wallace SS. The effect of inter-implant distance on the height of inter-implant
bone crest. J Periodontol. 2000 Apr;71(4):546-9.
674. Traini T1, Novaes AB, Piattelli A, Papalexiou V, Muglia VA. The relationship between interimplant
distances and vascularization of the interimplant bone. Clin Oral Implants Res. 2010 Aug;21(8):822-9.
675. Broggini N1, McManus LM, Hermann JS, Medina R, Schenk RK, Buser D, Cochran DL. Peri-implant
inflammation defined by the implant-abutment interface. J Dent Res. 2006 May;85(5):473-8.
676. Rodríguez-Ciurana X1, Vela-Nebot X, Segalà-Torres M, Calvo-Guirado JL, Cambra J, Méndez-Blanco
V, Tarnow DP. The effect of interimplant distance on the height of the interimplant bone crest when using
platform-switched implants. Int J Periodontics Restorative Dent. 2009 Apr;29(2):141-51.
677. Galindo-Moreno P1, Fernández-Jiménez A, Avila-Ortiz G, Silvestre FJ, Hernández-Cortés P, Wang HL.
Marginal bone loss around implants placed in maxillary native bone or grafted sinuses: a retrospective
cohort study. Clin Oral Implants Res. 2014 Mar;25(3):378-84.
678. Vigolo P1, Givani A. Platform-switched restorations on wide-diameter implants: a 5-year clinical
prospective study. Int J Oral Maxillofac Implants. 2009 Jan-Feb;24(1):103-9.
679. Chvartzsaid D, Koka S, Zarb G. Osseointegration failure. In: Zarb G, Albrektsson T, Eckert S, Stanford
C, Tarnow D, Wennerberg A, eds. Osseointegration – on continuing synergies in surgery, prosthodontics,
biomaterials. Chicago, IL: Quiintessence 2008, 2009:157–164.

~ 349 ~
680. Jimbo R, Albrektsson T. On marginal bone loss and clinical results of long term followed up oral implant
systems. (submitted).
681. Mardinger O1, Chaushu G, Sigalov S, Herzberg R, Shlomi B, Schwartz-Arad D. Factors affecting changes
in sinus graft height between and above the placed implants. Oral Surg Oral Med Oral Pathol Oral Radiol
Endod. 2011 Jan;111(1):e6-11.
682. Iwaniec UT1, Wronski TJ, Turner RT. Histological analysis of bone. Methods Mol Biol. 2008;447:325-
41.
683. Uchida Y1, Goto M, Katsuki T, Soejima Y. Measurement of maxillary sinus volume using computerized
tomographic images. Int J Oral Maxillofac Implants. 1998 Nov-Dec;13(6):811-8.
684. Johansson B1, Grepe A, Wannfors K, Aberg P, Hirsch JM. Volumetry of simulated bone grafts in the
edentulous maxilla by computed tomography: an experimental study. Dentomaxillofac Radiol. 2001
May;30(3):153-6.
685. Tepper G1, Haas R, Zechner W, Krach W, Watzek G. Three-dimensional finite element analysis of
implant stability in the atrophic posterior maxilla: a mathematical study of the sinus floor augmentation.
Clin Oral Implants Res. 2002 Dec;13(6):657-65.
686. Krennmair G1, Krainhöfner M, Maier H, Weinländer M, Piehslinger E.Computerized tomography-
assisted calculation of sinus augmentation volume. Int J Oral Maxillofac Implants. 2006 Nov-
Dec;21(6):907-13.
687. Jensen T1, Schou S, Svendsen PA, Forman JL, Gundersen HJ, Terheyden H, Holmstrup P. Volumetric
changes of the graft after maxillary sinus floor augmentation with Bio-Oss and autogenous bone in
different ratios: a radiographic study in minipigs. Clin Oral Implants Res. 2012 Aug;23(8):902-10.
688. Peleg M1, Chaushu G, Mazor Z, Ardekian L, Bakoon M. Radiological findings of the post-sinus lift
maxillary sinus: a computerized tomography follow-up. J Periodontol. 1999 Dec;70(12):1564-73.
689. Hallman M1, Hedin M, Sennerby L, Lundgren S. A prospective 1-year clinical and radiographic study of
implants placed after maxillary sinus floor augmentation with bovine hydroxyapatite and autogenous
bone. J Oral Maxillofac Surg. 2002 Mar;60(3):277-84; discussion 285-6.
690. Davies JE1. Understanding peri-implant endosseous healing. J Dent Educ. 2003 Aug;67(8):932-49.
691. Block MS1, Kent JN, Kallukaran FU, Thunthy K, Weinberg R. Bone maintenance 5 to 10 years after
sinus grafting. J Oral Maxillofac Surg. 1998 Jun;56(6):706-14; discussion 714-5.
692. Hatano N1, Shimizu Y, Ooya K. A clinical long-term radiographic evaluation of graft height changes
after maxillary sinus floor augmentation with a 2:1 autogenous bone/xenograft mixture and simultaneous
placement of dental implants. Clin Oral Implants Res. 2004 Jun;15(3):339-45.
693. Zijderveld SA1, Schulten EA, Aartman IH, ten Bruggenkate CM. Long-term changes in graft height after
maxillary sinus floor elevation with different grafting materials: radiographic evaluation with a minimum
follow-up of 4.5 years. Clin Oral Implants Res. 2009 Jul;20(7):691-700.
694. Kühl S1, Payer M, Kirmeier R, Wildburger A, Wegscheider W, Jakse N. The influence of bone marrow
aspirates and concentrates on the early volume stability of maxillary sinus grafts with deproteinized
bovine bone mineral - first results of a RCT. Clin Oral Implants Res. 2014 Feb;25(2):221-5.
695. Chang SC1, Chuang H, Chen YR, Yang LC, Chen JK, Mardini S, Chung HY, Lu YL, Ma WC, Lou J.
Cranial repair using BMP-2 gene engineered bone marrow stromal cells. J Surg Res. 2004 Jun
1;119(1):85-91.
696. Huang W1, Carlsen B, Wulur I, Rudkin G, Ishida K, Wu B, Yamaguchi DT, Miller TA. BMP-2 exerts
differential effects on differentiation of rabbit bone marrow stromal cells grown in two-dimensional and
three-dimensional systems and is required for in vitro bone formation in a PLGA scaffold. Exp Cell
Res. 2004 Oct 1;299(2):325-34.
697. Mangano FG1, Tettamanti L, Sammons RL, Azzi L, Caprioglio A, Macchi A, Mangano C. Maxillary
sinus augmentation with adult mesenchymal stem cells: a review of the current literature. Oral Surg Oral
Med Oral Pathol Oral Radiol. 2013 Jun;115(6):717-23.
698. Clavero J1, Lundgren S. Ramus or chin grafts for maxillary sinus inlay and local onlay augmentation:
comparison of donor site morbidity and complications. Clin Implant Dent Relat Res. 2003;5(3):154-60.

~ 350 ~
699. Raghoebar GM1, Louwerse C, Kalk WW, Vissink A. Morbidity of chin bone harvesting. Clin Oral
Implants Res. 2001 Oct;12(5):503-7.
700. Kalk WW1, Raghoebar GM, Jansma J, Boering G. Morbidity from iliac crest bone harvesting. J Oral
Maxillofac Surg. 1996 Dec;54(12):1424-9; discussion 1430.
701. Iezzi G1, Degidi M, Scarano A, Petrone G, Piattelli A. Anorganic bone matrix retrieved 14 years after a
sinus augmentation procedure: a histologic and histomorphometric evaluation. J Periodontol. 2007
Oct;78(10):2057-61.
702. Bellhouse DR. Area Estimation by Point-Counting Techniques. Biometrics 37:303-3012.
703. Artzi Z1, Tal H, Dayan D. Porous bovine bone mineral in healing of human extraction sockets: 2.
Histochemical observations at 9 months. J Periodontol. 2001 Feb;72(2):152-9.
704. Keller EE, Eckert SE, Tolman DE Maxillary antral and nasal one-stage inlay composite bone graft:
preliminary report on 30 recipient sites. J Oral Maxillofac Surg. 1994 ;52:438-47
705. Keller EE, Tolman DE, Eckert SE. Int J Oral Maxillofac Implants. Maxillary antral-nasal inlay
autogenous bone graft reconstruction of compromised maxilla: a 12-year retrospective study. 1999
14:707-21.
706. Tadjoedin ES, de Lange GL, Holzmann PJ, Kulper L, Burger EH. Histological observations on biopsies
harvested following sinus floor elevation using a bioactive glass material of narrow size range. Clin Oral
Implants Res. 2000; 11:334-44.
707. Tadjoedin ES, de Lange GL, Lyaruu DM, Kuiper L, Burger EH. High concentrations of bioactive glass
material (BioGran) vs. autogenous bone for sinus floor elevation. Clin Oral Implants Res. 2002; 13:428-
36.
708. Valentini P1, Abensur D, Wenz B, Peetz M, Schenk R. Sinus grafting with porous bone mineral (Bio-
Oss) for implant placement: a 5-year study on 15 patients. Int J Periodontics Restorative Dent. 2000;
20:245-53.
709. Froum SJ, Tarnow DP, Wallace SS, Rohrer MD, Cho SC. Sinus floor elevation using anorganic bovine
bone matrix (OsteoGraf/N) with and without autogenous bone: a clinical, histologic, radiographic, and
histomorphometric analysis--Part 2 of an ongoing prospective study. Int J Periodontics Restorative Dent.
1998;18:528-43.
710. Moy PK, Lundgren S, Holmes RE. Maxillary sinus augmentation: histomorphometric analysis of graft
materials for maxillary sinus floor augmentation. J Oral Maxillofac Surg. 1993;51:857-62.
711. Garg AK. Current concepts in augmentation grafting of the maxillary sinus for placement of dental
implants. Dent Implantol Update. 2001;12:17-22
712. Zitzmann NU, Schärer P, Marinello CP. Long-term results of implants treated with guided bone
regeneration: a 5-year prospective study. Int J Oral Maxillofac Implants. 2001 May-Jun;16(3):355-66.
713. Tidwell JK1, Blijdorp PA, Stoelinga PJ, Brouns JB, Hinderks F. Composite grafting of the maxillary
sinus for placement of endosteal implants. A preliminary report of 48 patients. Int J Oral Maxillofac
Surg. 1992 Aug;21(4):204-9.
714. Klijn RJ1, Meijer GJ, Bronkhorst EM, Jansen JA.Sinus floor augmentation surgery using autologous
bone grafts from various donor sites: a meta-analysis of the total bone volume. Tissue Eng Part B
Rev. 2010 Jun;16(3):295-303.
715. Jensen T1, Schou S, Stavropoulos A, Terheyden H, Holmstrup P. Maxillary sinus floor augmentation
with Bio-Oss or Bio-Oss mixed with autogenous bone as graft: a systematic review. Clin Oral Implants
Res. 2012 Mar;23(3):263-73.
716. Sbordone L1, Levin L, Guidetti F, Sbordone C, Glikman A, Schwartz-Arad D. Apical and marginal bone
alterations around implants in maxillary sinus augmentation grafted with autogenous bone or bovine
bone material and simultaneous or delayed dental implant positioning. Clin Oral Implants Res. 2011
May;22(5):485-91.
717. Truedsson A1, Hjalte K, Sunzel B, Warfvinge G. Maxillary sinus augmentation with iliac autograft - a
health-economic analysis. Clin Oral Implants Res. 2013 Oct;24(10):1088-93.
718. Langer B, Langer L. Use of allografts for sinus grafting. In: Jensen OT (ed). The Sinus Bone Graft.
Chicago: Quintessence, 1999: 69-78.

~ 351 ~
719. Froum SJ, Wallace SS, Elian N, Cho SC, Tarnow DP. Comparison of mineralized cancellous bone
allograft (Puros) and anorganic bovine bone matrix (Bio-Oss) for sinus augmentation: histomorphometry
at 26 to 32 weeks after grafting. Int J Periodontics Restorative Dent. 2006;26:543-51.
720. Boyan BD1, Ranly DM, McMillan J, Sunwoo M, Roche K, Schwartz Z. Osteoinductive ability of human
allograft formulations. J Periodontol. 2006 Sep;77(9):1555-63.
721. Hising P. Bolin A. Branting C. Reconstruction of severely resorbed alveolar crests with dental implants
using a bovine mineral for augmentation. Int J Oral Maxillofac. Implants 2001;16:90-97.
722. Orsini G, Scarano A, Degidi M, Caputi S, Iezzi G, Piattelli A. Histological and ultrastructural evaluation
of bone around Bio-Oss particles in sinus augmentation. Oral Dis. 2007;13:586-93.
723. Traini T1, Valentini P, Iezzi G, Piattelli A. A histologic and histomorphometric evaluation of anorganic
bovine bone retrieved 9 years after a sinus augmentation procedure.J Periodontol. 2007;78:955-61.
724. Rosenlicht JL, Tarnow DP. J Oral Implantol. Human histologic evidence of integration of functionally
loaded hydroxyapatite-coated implants placed simultaneously with sinus augmentation: a case report 2
1/2 years postplacement. 1999;25:7-10.
725. Scarano A, Pecora G, Piattelli M, Piattelli A. Osseointegration in a sinus augmented with bovine porous
bone mineral: histological results in an implant retrieved 4 years after insertion. A case report. J
Periodontol. 2004;75:1161-6.
726. Yildirim M, Spiekermann H, Biesterfeld S, Edelhoff D. Maxillary sinus augmentation using xenogenic
bone substitute material Bio-Oss in combination with venous blood. A histologic and histomorphometric
study in humans. Clin Oral Implants Res. 2000 Jun;11(3):217-29.
727. Yildirim M, Spiekermann H, Handt S, Edelhoff D. Maxillary sinus augmentation with the xenograft Bio-
Oss and autogenous intraoral bone for qualitative improvement of the implant site: a histologic and
histomorphometric clinical study in humans. Int J Oral Maxillofac Implants. 2001;16:23-33.
728. Klongnoi B1, Rupprecht S, Kessler P, Zimmermann R, Thorwarth M, Pongsiri S, Neukam FW, Wiltfang
J, Schlegel KA. Lack of beneficial effects of platelet-rich plasma on sinus augmentation using a
fluorohydroxyapatite or autogenous bone: an explorative study. J Clin Periodontol. 2006 Jul;33(7):500-9.
729. Chackartchi T1, Iezzi G, Goldstein M, Klinger A, Soskolne A, Piattelli A, Shapira L. Sinus floor
augmentation using large (1-2 mm) or small (0.25-1 mm) bovine bone mineral particles: a prospective,
intra-individual controlled clinical, micro-computerized tomography and histomorphometric study. Clin
Oral Implants Res. 2011 May;22(5):473-80.
730. Esposito M1, Grusovin MG, Coulthard P, Worthington HV. The efficacy of various bone augmentation
procedures for dental implants: a Cochrane systematic review of randomized controlled clinical trials. Int
J Oral Maxillofac Implants. 2006 Sep-Oct;21(5):696-710.
731. Lee DZ1, Chen ST, Darby IB. Maxillary sinus floor elevation and grafting with deproteinized bovine
bone mineral: a clinical and histomorphometric study. Clin Oral Implants Res. 2012 Aug;23(8):918-24.
732. Haas R1, Donath K, Födinger M, Watzek G. Bovine hydroxyapatite for maxillary sinus grafting:
comparative histomorphometric findings in sheep. Clin Oral Implants Res. 1998 Apr;9(2):107-16.
733. McAllister BS1, Margolin MD, Cogan AG, Buck D, Hollinger JO, Lynch SE. Eighteen-month
radiographic and histologic evaluation of sinus grafting with anorganic bovine bone in the chimpanzee.
Int J Oral Maxillofac Implants. 1999 May-Jun;14(3):361-8.
734. Johansson LA1, Isaksson S, Lindh C, Becktor JP, Sennerby L. Berglundh T1, Lindhe J. Healing around
implants placed in bone defects treated with Bio-Oss. An experimental study in the dog. Clin Oral
Implants Res. 1997 Apr;8(2):117-24.
735. Berglundh T1, Lindhe J. Maxillary sinus floor augmentation and simultaneous implant placement using
locally harvested autogenous bone chips and bone debris: a prospective clinical study. J Oral Maxillofac
Surg. 2010 Apr;68(4):837-44.
736. Wetzel AC1, Stich H, Caffesse RG. Bone apposition onto oral implants in the sinus area filled with
different grafting materials. A histological study in beagle dogs. Clin Oral Implants Res. 1995
Sep;6(3):155-63.

~ 352 ~
737. Schenk RK1, Buser D, Hardwick WR, Dahlin C. Healing pattern of bone regeneration in membrane-
protected defects: a histologic study in the canine mandible. Int J Oral Maxillofac Implants. 1994 Jan-
Feb;9(1):13-29.
738. Avila G1, Wang HL, Galindo-Moreno P, Misch CE, Bagramian RA, Rudek I, Benavides E, Moreno-
Riestra I, Braun T, Neiva R. The influence of the bucco-palatal distance on sinus augmentation
outcomes. J Periodontol. 2010 Jul;81(7):1041-50.
739. Hallman M, Thor A. Bone substitutes and growth factors as an alternative/complement to autogenous
bone for grafting in implant dentistry. Periodontology 2000 2008;47:172-192.
740. Hallman M, Lundgren S, Sennerby L. Histologic analysis of clinical biopsies taken 6 months and 3 years
after maxillary sinus floor augmentation with 80% bovine hydroxyapatite and 20% autogenous bone
mixed with fibrin glue. Clin Implant Dent Relat Res 2001;3:87-96.
741. Schlegel AK, Donath K. BIO-OSS--a resorbable bone substitute? Journal of long-term effects of medical
implants 1998;8:201-209.
742. Schlegel KA, Fichtner G, Schultze-Mosgau S, Wiltfang J. Histologic findings in sinus augmentation with
autogenous bone chips versus a bovine bone substitute. Int J Oral Maxillofac Implants 2003;18:53-58.
743. Mordenfeld A, Hallman M, Johansson C.B, Albrektsson T. Histological and histomorphometrical
analyses of biopsies harvested 11 years after maxillary sinus floor augmentation with deproteinized
bovine and autogenous bone. Clin Oral Implants Res. 2010 Sep;21(9):961-70.
744. Lopez SP, Froum S, Khouly I. Histomorphological analysis of a biopsy harvested 10 years after maxillary
sinus augmentation with anorganic bovine bone matrix and plasma rich in growth factors: a case report.
Implant Den 2015;24;480-486.
745. Meyer C1, Chatelain B, Benarroch M, Garnier JF, Ricbourg B, Camponovo T. [Massive sinus-lift
procedures with beta-tricalcium phosphate: long-term results]. Rev Stomatol Chir Maxillofac. 2009
Apr;110(2):69-75.
746. Zerbo IR1, Bronckers AL, de Lange G, Burger EH. Localisation of osteogenic and osteoclastic cells in
porous beta-tricalcium phosphate particles used for human maxillary sinus floor elevation.
Biomaterials. 2005 Apr;26(12):1445-51.
747. Szabó G1, Huys L, Coulthard P, Maiorana C, Garagiola U, Barabás J, Németh Z, Hrabák K, Suba Z. A
prospective multicenter randomized clinical trial of autogenous bone versus beta-tricalcium phosphate
graft alone for bilateral sinus elevation: histologic and histomorphometric evaluation. Int J Oral
Maxillofac Implants. 2005 May-Jun;20(3):371-81.
748. Esposito M1, Grusovin MG, Kwan S, Worthington HV, Coulthard P. Interventions for replacing missing
teeth: bone augmentation techniques for dental implant treatment. Cochrane Database Syst Rev. 2008 Jul
16;(3):CD003607.
749. Artzi Z1, Kozlovsky A, Nemcovsky CE, Weinreb M. The amount of newly formed bone in sinus grafting
procedures depends on tissue depth as well as the type and residual amount of the grafted material. J Clin
Periodontol. 2005 Feb;32(2):193-9.
750. von Arx T1, Cochran DL, Hermann JS, Schenk RK, Higginbottom FL, Buser D. Lateral ridge
augmentation and implant placement: an experimental study evaluating implant osseointegration in
different augmentation materials in the canine mandible. Int J Oral Maxillofac Implants. 2001 May-
Jun;16(3):343-54.
751. Zerbo IR1, Zijderveld SA, de Boer A, Bronckers AL, de Lange G, ten Bruggenkate CM, Burger EH.
Histomorphometry of human sinus floor augmentation using a porous beta-tricalcium phosphate: a
prospective study. Clin Oral Implants Res. 2004 Dec;15(6):724-32.
752. Wheeler DL1, Eschbach EJ, Hoellrich RG, Montfort MJ, Chamberland DL. Assessment of resorbable
bioactive material for grafting of critical-size cancellous defects. J Orthop Res. 2000 Jan;18(1):140-8.
753. Vogel M1, Voigt C, Gross UM, Müller-Mai CM. In vivo comparison of bioactive glass particles in
rabbits. Biomaterials. 2001 Feb;22(4):357-62.
754. Galindo-Moreno P1, Avila G, Fernández-Barbero JE, Mesa F, O'Valle-Ravassa F, Wang HL. Clinical
and histologic comparison of two different composite grafts for sinus augmentation: a pilot clinical trial.
Clin Oral Implants Res. 2008 Aug;19(8):755-9.

~ 353 ~
755. Gatti AM1, Simonetti LA, Monari E, Guidi S, Greenspan D. Bone augmentation with bioactive glass in
three cases of dental implant placement. J Biomater Appl. 2006 Apr;20(4):325-39. Epub 2006 Jan 27.
756. De Kok IJ1, Peter SJ, Archambault M, van den Bos C, Kadiyala S, Aukhil I, Cooper LF. Investigation of
allogeneic mesenchymal stem cell-based alveolar bone formation: preliminary findings. Clin Oral
Implants Res. 2003 Aug;14(4):481-9.
757. Mankani MH1, Kuznetsov SA, Shannon B, Nalla RK, Ritchie RO, Qin Y, Robey PG. Canine cranial
reconstruction using autologous bone marrow stromal cells. Am J Pathol. 2006 Feb;168(2):542-50.
758. Trojani C1, Boukhechba F, Scimeca JC, Vandenbos F, Michiels JF, Daculsi G, Boileau P, Weiss P, Carle
GF, Rochet N. Ectopic bone formation using an injectable biphasic calcium phosphate/Si-HPMC
hydrogel composite loaded with undifferentiated bone marrow stromal cells. Biomaterials. 2006
Jun;27(17):3256-64. Epub 2006 Feb 28.
759. Daculsi G1, Laboux O, Malard O, Weiss P. Current state of the art of biphasic calcium phosphate
bioceramics. J Mater Sci Mater Med. 2003 Mar;14(3):195-200.
760. Artzi Z1, Nemcovsky CE, Dayan D. Nonceramic hydroxyapatite bone derivative in sinus augmentation
procedures: clinical and histomorphometric observations in 10 consecutive cases. Int J Periodontics
Restorative Dent. 2003 Aug;23(4):381-9.
761. Arinzeh TL1, Tran T, Mcalary J, Daculsi G. A comparative study of biphasic calcium phosphate
ceramics for human mesenchymal stem-cell-induced bone formation. Biomaterials. 2005
Jun;26(17):3631-8.
762. Jensen SS1, Broggini N, Hjørting-Hansen E, Schenk R, Buser D. Bone healing and graft resorption of
autograft, anorganic bovine bone and beta-tricalcium phosphate. A histologic and histomorphometric
study in the mandibles of minipigs. Clin Oral Implants Res. 2006 Jun;17(3):237-43.
763. Jensen SS1, Yeo A, Dard M, Hunziker E, Schenk R, Buser D. Evaluation of a novel biphasic calcium
phosphate in standardized bone defects: a histologic and histomorphometric study in the mandibles of
minipigs. Clin Oral Implants Res. 2007 Dec;18(6):752-60. Epub 2007 Sep 20.
764. Detsch R1, Mayr H, Ziegler G. Formation of osteoclast-like cells on HA and TCP ceramics. Acta
Biomater. 2008 Jan;4(1):139-48. Epub 2007 Jul 15.
765. Daculsi G1, Weiss P, Bouler JM, Gauthier O, Millot F, Aguado E. Biphasic calcium
phosphate/hydrosoluble polymer composites: a new concept for bone and dental substitution
biomaterials. Bone. 1999 Aug;25(2 Suppl):59S-61S.
766. Anitua E1, Sánchez M, Nurden AT, Nurden P, Orive G, Andía I. New insights into and novel
applications for platelet-rich fibrin therapies. Trends Biotechnol. 2006 May;24(5):227-34. Epub 2006
Mar 15.
767. Anitua E1, Sánchez M, Orive G, Andía I. The potential impact of the preparation rich in growth factors
(PRGF) in different medical fields. Biomaterials. 2007 Nov;28(31):4551-60. Epub 2007 Jul 30.
768. Anitua E1, Carda C, Andia I. A novel drilling procedure and subsequent bone autograft preparation: a
technical note. Int J Oral Maxillofac Implants. 2007 Jan-Feb;22(1):138-45.
769. Anitua E1, Prado R, Orive G. Bilateral sinus elevation evaluating plasma rich in growth factors
technology: a report of five cases. Clin Implant Dent Relat Res. 2012 Mar;14(1):51-60.
770. Boyapati L1, Wang HL. The role of platelet-rich plasma in sinus augmentation: a critical review. Implant
Dent. 2006 Jun;15(2):160-70.
771. Jensen T1, Schou S, Gundersen HJ, Forman JL, Terheyden H, Holmstrup P. Bone-to-implant contact
after maxillary sinus floor augmentation with Bio-Oss and autogenous bone in different ratios in mini
pigs. Clin Oral Implants Res. 2013 Jun;24(6):635-44.
772. Klijn RJ1, Meijer GJ, Bronkhorst EM, Jansen JA. A meta-analysis of histomorphometric results and graft
healing time of various biomaterials compared to autologous bone used as sinus floor augmentation
material in humans. Tissue Eng Part B Rev. 2010 Oct;16(5):493-507.
773. John HD1, Wenz B. Histomorphometric analysis of natural bone mineral for maxillary sinus
augmentation. Int J Oral Maxillofac Implants. 2004 Mar-Apr;19(2):199-207.
774. Khaled EG1, Saleh M, Hindocha S, Griffin M, Khan WS. Tissue engineering for bone production- stem
cells, gene therapy and scaffolds. Open Orthop J. 2011;5 Suppl 2:289-95.

~ 354 ~
775. Rickert D1, Sauerbier S, Nagursky H, Menne D, Vissink A, Raghoebar GM. Maxillary sinus floor
elevation with bovine bone mineral combined with either autogenous bone or autogenous stem cells: a
prospective randomized clinical trial. Clin Oral Implants Res. 2011 Mar;22(3):251-8.
776. Cunningham CD 3rd1, Slattery WH 3rd, Luxford WM. Postoperative infection in cochlear implant
patients. Otolaryngol Head Neck Surg. 2004 Jul;131(1):109-14.
777. Poetker DM1, Pytynia KB, Meyer GA, Wackym PA. Complication rate of transtemporal hydroxyapatite
cement cranioplasties: a case series review of 76 cranioplasties. Otol Neurotol. 2004 Jul;25(4):604-9.
778. Niedergethmann M1, Farag Soliman M, Post S. Postoperative complications of pancreatic cancer surgery.
Minerva Chir. 2004 Apr;59(2):175-83.
779. Beretta M1, Cicciù M, Bramanti E, Maiorana C.
Schneider membrane elevation in presence of sinus septa: anatomic features and surgical management.
Int J Dent. 2012;2012:261905.
780. Zijderveld SA, van den Bergh, JPA, Schulten EAJM, ten Bruggenkate CM. Anatomical and surgical
findings and complications in 100 consectutive maxillary sinug floor elevations. J Oral Maxillofac Surg
2008;66: 1426-38.
781. Cho SC, Wallace SS, Froum SJ, Tarnow DP. Influence of anatomy on Schneiderian membrane
perforations during sinus elevation surgery: three-dimensional analysis. Pract Proced Aesthet Dent. 2001
Mar;13(2):160-3.
782. Barone A, Santini S, Sbordone L, Crespi R, Covani U. A clinical study of the outcomes and
complications associated with maxillary sinus augmentation. Int J Oral Maxillofac Implants 2006;21: 81-
5.
783. Ardekian L1, Oved-Peleg E, Mactei EE, Peled M. The clinical significance of sinus membrane
perforation during augmentation of the maxillary sinus. J Oral Maxillofac Surg. 2006 Feb;64(2):277-82.
784. Testori T1, Wallace SS, Del Fabbro M, Taschieri S, Trisi P, Capelli M, Weinstein RL. Repair of
large sinus membrane perforations using stabilized collagen barrier membranes: surgical techniques with
histologic and radiographic evidence of success. Int J Periodontics Restorative Dent. 2008 Feb;28(1):9-
17.
785. Hernández-Alfaro F1, Torradeflot MM, Marti C. Prevalence and management of
Schneiderian membrane perforations during sinus-lift procedures. Clin Oral Implants Res. 2008
Jan;19(1):91-8. Epub 2007 Oct 23.
786. Oh E1, Kraut RA. Effect of sinus membrane perforation on dental implant integration: a retrospective
study on 128 patients. Implant Dent. 2011 Feb;20(1):13-9.
787. Becker ST1, Terheyden H, Steinriede A, Behrens E, Springer I, Wiltfang J. Prospective observation of 41
perforations of the Schneiderian membrane during sinus floor elevation. Clin Oral Implants Res. 2008
Dec;19(12):1285-9.
788. Yilmaz HG1, Tözüm TF. Are gingival phenotype, residual ridge height, and membrane thickness critical
for the perforation of maxillarysinus? J Periodontol. 2012 Apr;83(4):420-5.
789. Proussaefs P1, Lozada J, Kim J, Rohrer MD. Repair of the perforated sinus membrane with a resorbable
collagen membrane: a human study. Int J Oral Maxillofac Implants. 2004 May-Jun;19(3):413-20.
790. Karabuda C1, Arisan V, Özyuvaci H. Effects of sinus membrane perforations on the success of dental
implants placed in the augmented sinus. J Periodontol. 2006 Dec;77(12):1991-7.
791. Toscano NJ1, Holtzclaw D, Rosen PS. The effect of piezoelectric use on open sinus lift perforation: a
retrospective evaluation of 56 consecutively treated cases from private practices. J Periodontol. 2010
Jan;81(1):167-71.
792. Barone A1, Santini S, Marconcini S, Giacomelli L, Gherlone E, Covani U. Osteotomy and membrane
elevation during the maxillary sinus augmentation procedure. A comparative study: piezoelectric device
vs. conventional rotative instruments. Clin Oral Implants Res. 2008 May;19(5):511-5.
793. Malkinson S, Irinakis T. The influence of interfering septa on the incidence of Schneiderian membrane
perforations during maxillary sinus elevation surgery: a retrospective study of 52 consecutive lateral
window procedures. Oral Surg 2009;2:19-25.

~ 355 ~
794. von Arx T, Fodich I, Bornstein MM, Jensen SS. Perforation of the sinus membrane during sinus floor
elevation: a retrospective study of frequency and possible risk factors. Int J Oral Maxillofac
Implants. 2014 May-Jun;29(3):718-26.
795. Schneider AC1, Bragger U, Sendi P, Caversaccio MD, Buser D, Bornstein MM. Characteristics and
dimensions of the sinus membrane in patients referred for single-implant treatment in the posterior
maxilla: a cone beam computed tomographic analysis. Int J Oral Maxillofac Implants. 2013 Mar-
Apr;28(2):587-96.
796. Cakur B, Sumbllu MA, Durna D. Relationship among shceiderian membrane, Underwood’s septa, and
the maxillary sinus inferior border. DOI 10.1111/j.1798-8208.2011.
797. Blus C1, Szmukler-Moncler S, Salama M, Salama H, Garber D. Sinus bone grafting procedures using
ultrasonic bone surgery: 5-year experience. Int J Periodontics Restorative Dent. 2008 Jun;28(3):221-9.
798. Shlomi B1, Horowitz I, Kahn A, Dobriyan A, Chaushu G. The effect of sinus membrane perforation and
repair with Lambone on the outcome of maxillary sinus floor augmentation: a radiographic assessment.
Int J Oral Maxillofac Implants. 2004 Jul-Aug;19(4):559-62.
799. Fugazzotto PA, Vlassis J. A simplified classification and repair system for sinus membrane perforations. J
Periodontol. 2003 Oct;74(10):1534-41.
800. Fugazzotto PA, Vlassis J. Long-term success of sinus augmentation using various surgical approaches
and grafting materials. Int J Oral Maxillofac Implants 1998; 13:52-58.
801. van den Bergh JP1, ten Bruggenkate CM, Groeneveld HH, Burger EH, Tuinzing DB. Recombinant human
bone morphogenetic protein-7 in maxillary sinus floor elevation surgery in 3 patients compared to
autogenous bone grafts. A clinical pilot study. J Clin Periodontol. 2000 Sep;27(9):627-36.
802. Pjeturrson B, Lang N, Karring T (eds). Clinical Periodontology and Implant Dentistry, ed 5. Oxford:
Blackwell Munksgaard, 2008:1106.
803. Jensen SS1, Terheyden H. Bone augmentation procedures in localized defects in the alveolar ridge:
clinical results with different bonegrafts and bone-substitute materials. Int J Oral Maxillofac
Implants. 2009;24 Suppl:218-36.
804. Kahnberg KE1, Vannas-Löfqvist L. Sinus lift procedure using a 2-stage surgical technique: I. Clinical
and radiographic report up to 5 years. Int J Oral Maxillofac Implants. 2008 Sep-Oct;23(5):876-84.
805. Lee HW1, Lin WS, Morton D. A retrospective study of complications associated with 100 consecutive
maxillary sinus augmentations via the lateral window approach. Int J Oral Maxillofac Implants. 2013
May-Jun;28(3):860-8.
806. Timmenga NM1, Raghoebar GM, van Weissenbruch R, Vissink A. Maxillary sinusitis after augmentation
of the maxillary sinus floor: a report of 2 cases. J Oral Maxillofac Surg. 2001 Feb;59(2):200-4.
807. Timmenga NM1, Raghoebar GM, Boering G, van Weissenbruch R. Maxillary sinus function after sinus
lifts for the insertion of dental implants. J Oral Maxillofac Surg. 1997 Sep;55(9):936-9;discussion 940.
808. Kaptein ML1, de Putter C, de Lange GL, Blijdorp PA. Survival of cylindrical implants in composite
grafted maxillary sinuses. J Oral Maxillofac Surg. 1998 Dec;56(12):1376-80; discussion 1380-1.
809. Raghoebar GM1, Timmenga NM, Reintsema H, Stegenga B, Vissink A. Maxillary bone grafting for
insertion of endosseous implants: results after 12-124 months. Clin Oral Implants Res. 2001
Jun;12(3):279-86.
810. Quiney RE1, Brimble E, Hodge M. Maxillary sinusitis from dental osseointegrated implants. J Laryngol
Otol. 1990 Apr;104(4):333-4.
811. Raghoebar GM1, Batenburg RH, Timmenga NM, Vissink A, Reintsema H. Morbidity and complications
of bone grafting of the floor of the maxillary sinus for the placement of endosseous implants. Mund
Kiefer Gesichtschir. 1999 May;3 Suppl 1:S65-9.
812. Maksoud MA1. Complications after maxillary sinus augmentation: a case report. Implant
Dent. 2001;10(3):168-71.
813. el-Hakim IE1, el-Fakharany AM. The use of the pedicled buccal fat pad (BFP) and palatal rotating flaps
in closure of oroantral communication and palatal defects. J Laryngol Otol. 1999 Sep;113(9):834-8.

~ 356 ~
814. Andric M1, Saranovic V, Drazic R, Brkovic B, Todorovic L. Functional endoscopic sinus surgery as an
adjunctive treatment for closure of oroantral fistulae: a retrospective analysis. Oral Surg Oral Med Oral
Pathol Oral Radiol Endod. 2010 Apr;109(4):510-6.
815. Schaefer SD1, Manning S, Close LG. Endoscopic paranasal sinus surgery: indications and considerations.
Laryngoscope. 1989 Jan;99(1):1-5.
816. Stammberger H1. History of rhinology: anatomy of the paranasal sinuses. Rhinology. 1989
Sep;27(3):197-210.
817. Busaba NY1, Kieff D. Endoscopic sinus surgery for inflammatory maxillary sinus disease.
Laryngoscope. 2002 Aug;112(8 Pt 1):1378-83.
818. Hirschman A. uber endoskopic der nuse und deren Nebemhohler. Eine neue Untersuchungsmetnode.
Arch Langol Rhimol (Berlin) 1903;14:195.
819. Kennedy DW: Functional endoscopic sinus surgery. Tech Arch Otolaryngol 1985; 111:643- 9.
820. Pagella F1, Emanuelli E, Castelnuovo P. Endoscopic extraction of a metal foreign body from the
maxillary sinus. Laryngoscope. 1999 Feb;109(2 Pt 1):339-42.
821. Sugiura N1, Ochi K, Komatsuzaki Y. Endoscopic extraction of a foreign body from the maxillary sinus.
Otolaryngol Head Neck Surg. 2004 Feb;130(2):279-80.
822. Nakamura N1, Mitsuyasu T, Ohishi M. Endoscopic removal of a dental implant displaced into the
maxillary sinus: technical note. Int J Oral Maxillofac Surg. 2004 Mar;33(2):195-7.
823. Shumrick KA1, Ryzenman JM. Endoscopic management of facial fractures. Facial Plast Surg Clin North
Am. 2001 Aug;9(3):469-74.
824. Troulis MJ Endoscopic open reduction and internal rigid fixation of subcondylar fractures. J Oral
Maxillofac Surg. 2004 Oct;62(10):1269-71.
825. Varol A1, Türker N, Göker K, Basa S. Endoscopic retrieval of dental implants from the maxillary sinus.
Int J Oral Maxillofac Implants. 2006 Sep-Oct;21(5):801-4.
826. Nosaka Y. Sinus Floor Elevation: avoiding pitfalls using cone-beam CT. 2010 Quintessence Puplishing
Co. Ltd., Tokio.
827. Tsodoulos S, Karabouta I, Voulgaropoulou M, Georgiou C. Atraumatic removal of an asymptomatic
migrated dental implant into the maxillary sinus: a case report. J Oral Implantol. 2012 Apr;38(2):189-93.
828. Chiapasco M1, Felisati G, Maccari A, Borloni R, Gatti F, Di Leo F. The management of complications
following displacement of oral implants in the paranasal sinuses: a multicenter clinical report and
proposed treatment protocols. Int J Oral Maxillofac Surg. 2009 Dec;38(12):1273-8.
829. Ridaura-Ruiz L1, Figueiredo R, Guinot-Moya R, Piñera-Penalva M, Sanchez-Garcés MA, Valmaseda-
Castellón E, Gay-Escoda C. Accidental displacement of dental implants into the maxillary sinus: a report
of nine cases. Clin Implant Dent Relat Res. 2009 Oct;11 Suppl 1:e38-45.
830. Galindo-Moreno P1, Moreno-Riestra I, Avila G, Fernández-Barbero JE, Mesa F, Aguilar M, Wang
HL, O'Valle F. Histomorphometric comparison of maxillary pristine bone and composite bone graft
biopsies obtained after sinus augmentation. Clin Oral Implants Res. 2010 Jan;21(1):122-8.
831. Whitehouse J1. Technology helps an "amateur" place implants. Dent Today. 2008 Nov;27(11):120, 122,
124.
832. Bradley PJ, Manning KP, Shaw MD. Brain abscess secondary to paranasal sinusitis. J Laryngol
Otol. 1984 Jul;98(7):719-25.
833. Giannoni CM1, Stewart MG, Alford EL. Intracranial complications of sinusitis. Laryngoscope. 1997
Jul;107(7):863-7.
834. Kastner J1, Taudy M, Lisy J, Grabec P, Betka J. Orbital and intracranial complications after acute
rhinosinusitis. Rhinology. 2010 Dec;48(4):457-61.
835. Iida S1, Tanaka N, Kogo M, Matsuya T. Migration of a dental implant into the maxillary sinus. A case
report. Int J Oral Maxillofac Surg. 2000 Oct;29(5):358-9.
836. Caldwell G. Diseases of the accessory sinuses of the nose and an improved method of treatment for
suppuration of the maxillary antrum. The Journal of the Medical Society of New Jersey. 1893 58:526.
837. Sahin YF1, Muderris T, Bercin S, Sevil E, Kırıs M. Chronic maxillary sinusitis associated with
an unusual foreign body: a case report. Case Rep Otolaryngol. 2012;2012:903714.

~ 357 ~
838. Lindorf HH. Osteoplastic surgery of the sinus maxillaris--the "bone lid"-method. J Maxillofac Surg. 1984
Dec;12(6):271-6.
839. Widmark G1, Ekholm S, Borrman H, Grangård U, Holmberg K. The use of a bone lid to close the
anterior wall defect after surgery in the maxillary sinus. Swed Dent J. 1992;16(5):173-82.
840. Biglioli F1, Goisis M. Access to the maxillary sinus using a bone flap on a mucosal pedicle: preliminary
report. J Craniomaxillofac Surg. 2002 Aug;30(4):255-9.
841. Stammberger H, Zinreich SJ, Kopp W, Kennedy DW, Johns ME, Rosenbaum AE. [Surgical treatment
of chronic recurrent sinusitis--the Caldwell-Luc versus a functional endoscopic technic]. HNO. 1987
Mar;35(3):93-105.
842. Pjetursson BE1, Rast C, Brägger U, Schmidlin K, Zwahlen M, Lang NP. Maxillary sinus floor elevation
using the (transalveolar) osteotome technique with or without grafting material. Part I: Implant survival
and patients' perception. Clin Oral Implants Res. 2009 Jul;20(7):667-76.
843. Testori T. complications: Diagnosis and management. In Testoi T (ed). Maxillary Sinus and Alternatives
in Treatement. London: Quintessence. 2009:311-324.
844. Rosen P. Complications with the bone-added osteotome sinus floor elevation: Etiology, prevention and
treatmen. In: Froum SJ (ed). Dental Implant Complications: Etiology, Prevention and Treatment.
Chichester, UK: Wiley-Blackwell, 2010:210-324.
845. Testori T, Mandelli F, Valentini P, Wallace S. A novel technique to prevent the loss of graft material
through the antrostomy after sinus surgery: technical note. Int J Oral Maxillofac Implants. 2014 May-
Jun;29(3):e272-4.
846. Tal H1. Spontaneous early exposure of submerged implants: I. Classification and clinical observations. J
Periodontol. 1999 Feb;70(2):213-9.
847. Jovanovic SA1, Spiekermann H, Richter EJ. Bone regeneration around titanium dental implants in
dehisced defect sites: a clinical study. Int J Oral Maxillofac Implants. 1992 Summer;7(2):233-45.
848. Koka S1, Zarb G. On osseointegration: the healing adaptation principle in the context of
osseosufficiency, osseoseparation, and dental implant failure. Int J Prosthodont. 2012 Jan-Feb;25(1):48-
52.
849. Mombelli A1, Müller N, Cionca N. The epidemiology of peri-implantitis. Clin Oral Implants Res. 2012
Oct;23 Suppl 6:67-76.
850. Berglundh T1, Lindhe J, Marinello C, Ericsson I, Liljenberg B. Soft tissue reaction to de novo plaque
formation on implants and teeth. An experimental study in the dog. Clin Oral Implants Res. 1992
Mar;3(1):1-8.
851. Ericsson I1, Giargia M, Lindhe J, Neiderud AM. Progression of periodontal tissue destruction at
splinted/non-splinted teeth. An experimental study in the dog. J Clin Periodontol. 1993 Nov;20(10):693-
8.
852. Pontoriero R1, Tonelli MP, Carnevale G, Mombelli A, Nyman SR, Lang NP. Experimentally induced
peri-implant mucositis. A clinical study in humans. Clin Oral Implants Res. 1994 De’c;5(4):254-9.
853. Koldsland OC1, Scheie AA, Aass AM. Prevalence of peri-implantitis related to severity of the disease
with different degrees of bone loss. J Periodontol. 2010 Feb;81(2):231-8.
854. Melis M, Lobo SL, Ceneviz, et al. Atypical odontalgia: A review of the literature. Headache
2003;43:1060-1074.
855. McElin TW, Horton DT. Atypical facial pain: A statistical consideration of 65 cases. Ann Intern Med
1947;27:749-753.
856. Klausner JJ1. Epidemiology of chronic facial pain: diagnostic usefulness in patient care. J Am Dent
Assoc. 1994 Dec;125(12):1604-11.
857. Brooke RI. Atypical odontalgia. A report of twenty-two cases. Oral Surg Oral Med Oral Pathol. 1980
Mar;49(3):196-9.
858. Marbach JJ1. Is phantom tooth pain a deafferentation (neuropathic) syndrome? Part II: Psychosocial
considerations. Oral Surg Oral Med Oral Pathol. 1993 Feb;75(2):225-32.
859. Pertes RA1, Bailey DR, Milone AS. Atypical odontalgia--a nondental toothache. J N J Dent Assoc. 1995
Winter;66(1):29-31, 33.

~ 358 ~
860. Okeson, J.P. Neuropathic pain. in: Bell's orofacial pains , ed 5. Chicago: Quintessence; 1995:403–455.
861. Bates RE Jr1, Stewart CM. Atypical odontalgia: phantom tooth pain. Oral Surg Oral Med Oral
Pathol. 1991 Oct;72(4):479-83.
862. Gross SG. Atypical odontalgia: a cause for dental failure. J Conn State Dent Assoc. 1991
Winter;67(2):36-7.
863. Marbach JJ1, Raphael KG. Phantom tooth pain: a new look at an old dilemma. Pain Med. 2000
Mar;1(1):68-77.
864. Queral-Godoy E1, Vazquez-Delgado E, Okeson JP, Gay-Escoda C. Persistent idiopathic facial pain
following dental implant placement: a case report. Int J Oral Maxillofac Implants. 2006 Jan-
Feb;21(1):136-40.
865. al-Amer AF1, Walia HS, Madda JP. Cholesterol granuloma of the peritoneum. Can J Surg. 1990
Oct;33(5):410-3.
866. Graham J, Michaels L. Cholesterol granuloma of the maxillary antrum. Clin Otolaryngol Allied
Sci. 1978 May;3(2):155-60.
867. Leon ME1, Chavez C, Fyfe B, Nagorsky MJ, Garcia FU. Cholesterol granuloma of the maxillary sinus.
Arch Pathol Lab Med. 2002 Feb;126(2):217-9.
868. Bhattacharyya N1, Baugh RF, Orvidas L. Clinical practice guideline: benign paroxysmal positional
vertigo. Otolaryngol Head Neck Surg. 2008 Nov;139(5 Suppl 4):S47-81.
869. Katsarkas A1. Benign paroxysmal positional vertigo (BPPV): idiopathic versus post-traumatic. Acta
Otolaryngol. 1999;119(7):745-9.
870. Parnes LS1, Agrawal SK, Atlas J. Diagnosis and management of benign paroxysmal positional vertigo
(BPPV). CMAJ. 2003 Sep 30;169(7):681-93.
871. Cakir BO1, Ercan I, Cakir ZA, Civelek S, Sayin I, Turgut S. What is the true incidence of horizontal
semicircular canal benign paroxysmal positional vertigo? Otolaryngol Head Neck Surg. 2006
Mar;134(3):451-4.
872. Sakata E, Uchida Y, Nakano Y, Takahashi K. Pathophysiology of positional vertigo of the malignant
paroxysmal type. Auris Nasus Larynx. 1984;11(2):79-90.
873. Reddy K S1, Shivu ME, Billimaga A. Benign paroxysmal positional vertigo during lateral window sinus
lift procedure: a case report and review. Implant Dent. 2015 Feb;24(1):106-9.
874. Käyser AF. Shortened dental arches and oral function. J Oral Rehabil. 1981 Sep;8(5):457-62.
875. Fontijn-Tekamp FA1, Slagter AP, Van Der Bilt A, Van 'T Hof MA, Witter DJ, Kalk W, Jansen JA.
Biting and chewing in overdentures, full dentures, and natural dentitions. J Dent Res. 2000
Jul;79(7):1519-24.
876. Laney W.R. Glossary of oral and maxillofacial implants. Quintessence Publishing Ct 2007.
877. Rose LF, Mealy BL, Genco RJ, Cohen DW. Periodontics medicine, surgery, and implants. St. Louis: CV
Mosby Co. Inc. 2004
878. Lindhe J, Karring T, Lang MP. Clinical periodontology and implant dentistry, 4th ed. Oxford: Blackwell
publishing Ltd., 2003.
879. Lang N.P., Hammerle, C.H., Bragger, U., Legmann, B. & Nyman, S.R. (1994) Guided tissue
regeneration in jawbone defects prior to implant placement. Clinical Oral Implants Research 5: 92-97.
880. Boyne PJ, James RA. Grafting of the maxillary sinus floor with autogenous marrow and bone. J Oral
Surg 1980;38(8):613-6.
881. Tatum H Jr. Maxillary and sinus implant reconstructions. Dent Clin North Am 1986;30(2):207-29.
882. Summers RB. A new concept in maxillary implant surgery: the osteotome technique. Compendium
1994;15(2): 152;154-6; 158; 162.
883. Branemark PI, Zarb GA, Albrektsson T. Tissue-integrated prosthesis: osseointegration in clinical density.
Chicago: Quintessence Publishing Co., Inc., 1985.
884. Schnek RK, Hjorting-Hansen E, Buser D. Bone integration of implants. Forum Implantologicum 2006;2:
14-23.
885. Schroeder A, Sutter F, Krekeler G. Oral implantology. New York: Thieme Verlag Stuttgart, 1991.

~ 359 ~
886. Rosen PS, Summer R, Mellado JR, Salkin LM, Shanaman RH, Marks MH, Fugazzotto PA. The bone-
added osteotome sinus floor elevation technique: multicenter retrospective report of consecutively treated
patients. Int J Oral Maxillofac Implants 1999;14(6): 853-8.
887. Falkner M, Woolfaardt J, Chan A. Measuring abutment/implant joint integrity with the Periotest
instrument. Int J Oral Maxillofac Implants 1999;14: 681-688.
888. Vrielinck L, Politis C, Schepers S, Pauwels M, Naert I. Image-based planning and clinical validation of
zygoma and pterygoid implant placement in patients with severe bone atrophy using customized drill
guides. Preliminary results from a prospective clinical follow-up study. Int J Oral Maxillofac Surg
2003;32(1): 7-14.
889. Graves SL. The pterygoid plate implant: a solution for restoring the posterior maxilla. Int J Periodontics
Restorative Dent 1994;14(6): 512-23.
890. Wolff J. Das Gesetz der Transformation der Knochen. Berlin A Hirschwald, 1891.
891. Salter R. Textbook of disorders and injuries of the musculoskeletal system. Baltimore: Williams and
Wilkens, 1970.

~ 360 ~