INTRODUCTION

TISSUE IMPLANT BIOLOGIC SEAL

THE PERI IMPLANT MUCOSA
BIOLOGIC WIDTH AROUND DENTAL
IMPLANTS
PROBING THE PERIIMPLANT MUCOSA
COMPARISON OF TISSUES SURROUNDING
NATURAL DENTITION AND ORAL IMPLANTS
FACTORS AFFECTING SOFT TISSUES
AROUND IMPLANTS
BONE LOSS AND SOFT TISSUE HEALTH
PERI IMPLANT MICROBIOLOGY
CONTENTS
Oral implants pierce through the mucosa, thus establishing the
connection between the oral environment and the underlying
tissues.

The soft tissue connection to the transmucosal part is of crucial
importance as it relates to the stability of the peri implant
tissues and the prevention of the peri implant infection with
subsequent destruction of the peri implant structures.

Hermetic closure of the gingival tissues is important to
minimize the risk of infection and prevent the apical down
growth of the epithelium.

REGENERATION OF THE ATTACHED GINGIVA AND ITS ABILITY TO FORM A
GINGIVAL SULCUS LINED BY CREVICULAR EPITHELIUM
McKinney et al 1984
SYSTEMATIC SCIENTIFIC STUDY TO INVESTIGATE THE SEAL PHENOMENON
James and Kelln1974, 1981
NECESSITY FOR ATTACHED GINGIVA TO APPROPRIATELY ADAPT TO THE
IMPLANT
Lavelle 1981
CONCEPT OF A SEAL AROUND THE DENTAL IMPLANTS
Weinmann 1956
EARLY CIVILIZATIONS LATE 19
th
and EARLY 20
th
CENTURIES
Gramm CT (1898) Lewis (1889)
The concept of the gingival epithelium in
forming a biological seal is one of great
importance in implant dentistry
PERMUCOSAL PASSAGE
A WEAK LINK A zone where initial tissue
breakdown begins that can result in eventual
tissue necrosis and destruction around
implants.
The seal is a physiological barrier to prevent
ingress of bacterial plaque,toxins, oral debris..
1
INFLAMMATION OF SOFT TISSUES
2
OSTEOCLASTIC ACTIVITY
3
CHRONIC RESORPTION OF SUPPORTING BONE
4
FILL WITH GRANULATION TISSUE
5
IMPLANT MOBILITY
6
PERCOLATION OF BACTERIAL TOXINS AND DEGENERATIVE AGENTS FURTHER
INTO THE INTERNAL ENVIRONMENT SURROUNDING THE IMPLANT
7
ACUTE SUPPURATIVE INFLAMMATION
8
EXTENSIVE MOBILITY
9
RENDERING SUPPORT TO PROSTHESIS
IMPRACTICAL
10
IMPLANT TO BE REMOVED
PERIIMPLANT
MUCOSA
EPITHELIAL
COMPONENT
PERIIMPLANT
MUCOSA
CONNECTIVE
TISSUE

The interface between the epithelial cells and the titanium
surface is characterized by the presence of
hemidesmosomes and a basal lamina.



EA: Epithelial Attachment, LBI: Lamina Basalis Interna, LBE: Lamina Basalis Externa,
BC: Basal Complex, a junctional epithelium, b sulcular epithelium, c oral
epithelium; T/I : Titanium Implant, LL: Lamina Lucida, LD: Lamina Densa, HD:
Hemidesmosomes, D: Desmosomes
a junctional epithelium,
b sulcular epithelium,
c oral epithelium;
Im : Implant,
Ab: Abutment, MR: Margin of
gingiva, Bo: Bone, A/I :
Abutment/ Implant junction,
aAE : apical point of attached
epithelium
1. Implant Crown
2. Vertical alveologingival ct
fibers
3. Circular gingival fibers
4. Circular gingival fibers
5. Periosteal gingival ct
fibers

The connective tissue appears to be in direct contact with the
surface (TiO) of the implant.
The collagen fibers in this connective tissue form bundles which run
PARALLEL to the implant surface.
They can also have a cuff like circular orientation.
Higher amounts of collagen type V and VI were noticed.
Capillary loops under JE and SE



Moon et al (1999) reported that the attachment tissue close to the
implant contains only few blood vessels but a large number of
fibroblasts that were oriented with their long axes parallel with the
implant surface.
In more lateral compartments, there were fewer fibroblasts but
more collagen fibers and more vascular structures.


Berglundh et al (1994) observed that the vascular system of the peri
implant mucosa originates SOLELY from the LARGE
SUPRAPERIOSTEAL BLOOD VESSEL on the outside of the alveolar
ridge.

B.W.
Epithelial
attachment
Supracrestal
connective
tissue zone
3 to 4mm
2mm
1mm
A MINIMUM DIMENSION OF THE BIOLOGICAL WIDTH IS NEEDED
IN ORDER TO ACCOMMODATE FOR THE SOFT TISSUE HEALING
PROCESS; WHEN THIS DIMENSION IS NOT PRESENT, BONE
RESORPTION MAY OCCUR TO ALLOW FOR AN APPROPRIATE
BIOLOGICAL DIMENSION



DAY 0: COAGULUM OCCUPIES
SPACE BETWEEN MUCOSA AND
IMPLANT SURFACE
DAY 4: GRANULOCYTES INFILTRATE
CLOT; INITIAL SEAL
1 WEEK: FIBROBLASTS AND
COLLAGEN FIBERS
2 WEEKS: CONNECTIVE TISSUE RICH
IN CELLS AND VASCULARITY;
JUNCTIONAL EPI STARTS TO FORM
4 WEEKS: JUNCTIONAL EPITHELIUM
FORMS; MATURE CT
MORPHOGENESIS OF
PERI IMPLANT
MUCOSA
(BERGLUNDH et al
2007)
I n case of an implant probe goes
beyond the sulcus and reaches closer
to the bone
Ericsson and Lindhe (1993)
Probing caused both compression and lateral dislocation of
the peri implant mucosa, and the average histologic
probing depth was markedly deeper than at the tooth site:
2mm vs 0.7 mm.
The tip of the probe was consistently positioned deep in the
connective tissue/ abutment interface and apical of the
barrier epithelium.
Distance between probe tip and the bone crest was 0.2 mm.

The depth of the probe penetration reveals the thickness of
the mucoperiosteum through which the abutment/
restoration is emerging rather than a loss of attachment.
FLEXIBLE PLASTIC
PROBE FOR
PROBING AROUND
IMPLANTS
Recommended to not probe the
implant for at least 3 months following
abutment attachment to avoid disrupting
the permucosal seal
COMPARISON OF TOOTH AND IMPLANT SUPPORT STRUCTURES
STRUCTURE TOOTH IMPLANT
Connection Cementum, bone , periodontium Osseointegration , bone functional ankylosis
Junctional
epithelium
Hemidesmosomes and basal lamina (
lamina lucida and lucida , lamina
densa zones )
Hemidesmosomes and basal lamina ( lamina
, lamina densa and sublamina lucida zones )
Connective
tissue
13 groups : perpendicular to tooth
surfaces
Decreased collagen, increased
fibroblasts
Only 2 groups : parallel and circular fibers .
No attachment to the implant surface and
bone
Increased collagen and decreased fibroblasts
Biological
width
2.04 to 2.91 mm 3.08 mm

Vascularity Greater ; supraperiosteal and
periodontal ligament
Less ; periosteal
Probing
depth
3mm in health

2.5 to 5.0mm ( depending on soft tissue
depth )
Bleeding on
probing
More reliable Less reliable
Attachment between the
periodontal tissue and the
root surface
Attachment between the
peri-implant tissue and an
implant surface
Periotest was originally devised by Dr. Schulte to measure tooth
mobility.
Teerlinck, et al.(1991) used this method to overcome destructive
methods in measuring the implant stability.
Periotest evaluates the damping capacity of the periodontium. It
is designed to identify the damping capacity and the stiffness of
the natural tooth or implant by measuring the contact time of an
electronically driven and electronically monitored rod after
percussing the test surface.
Periotest value(PTV) is marked from -8(low mobility) to +50(high
mobility). PTV of -8 to -6 is considered good stability.
Control Box +Probe
PROBE APPLI ED
HORI ZONTALLY
MUCOSAL THICKNESS
SURGICAL PROCEDURE
LOADING
TITANIUM SURFACES AND ABUTMENT
MATERIALS

IMPLANT STRUCTURE AND POSITION

IMMEDIATE POST EXTRACTIVE INSERTION

THIN BIOTYPE
OCHSENBEIN &ROSS
THICK BIOTYPE
DELICATE AND
FRIABLE
REACTS TO INJURY BY
RECESSION
AMOUNT OF
KERATINIZED MUCOSA
USUALLY QUITE SMALL
DENSER AND MORE
FIBROTIC GINGIVA
MIMICKING THE
FLATTER AND THICKER
UNDERLYING OSSEOUS
ARCHITECTURE
MORE RESISTANT TO
INJURY

PROBE VISIBLE THROUGH THE
THIN GINGIVA
THIN
BIOTYPE
MORE PRONE TO
CRESTAL BONE
RESORPTION
AVOID SUPRACRESTAL
PLACEMENT
THICK BIOTYPE
LESS CRESTAL BONE
RESORPTION
SUPRACRESTAL
PLACEMENT
MINIMIZES BONE
LOSS
A minimum of 3 mm of peri implant mucosa is required for
a stable epithelial connective tissue attachment to form.




Linkevicious et al in a human study done to compare the
effects of tissue thickness at the time of surgery on crestal
bone changes around non submerged implants after one year
follow up found that positioning an implant 2mm supra
crestally did not prevent crestal bone loss, if THIN GINGIVAL
TISSUES are present at the time of implant placement.
Implants with thin tissue underwent additional bone loss
interproximally than the group with thick tissue pattern which
had significantly less bone loss.



Initial tissue thickness if less than 2.5 mm leads to an
expected bone loss of 1.45 mm within the first year of
function.



In thick tissues, >2.5 mm or more, marginal bone recession
can be avoided if the implant abutment junction is 2mm or
above the bone level, minimal 0.2 mm



Thin Biotypes
Thick maintain
papillary height
GINGIVAL
RECESSION
Apical and lingual
direction
Facial plate loss
GRAYISH COLOR
ALVEOLAR
BONE
RESORPTION



PROSTHETIC
DESIGN
CONCAVE ABUTMENT
/CROWN PROFILE
IMPLANT DESIGN
SMALLER DIAMETER,
PLATFORM SWITCHING
STRAIGHT/ PARALLEL
WALLED IMPLANT
IMPLANT
POSITION
(PALATAL/APICAL)

ESTHETIC MANAGEMENT TRIAD
Abrahamsson et al 1996 :
Evaluated the influence of the surgical protocol (one
stage vs. two stage) on the soft tissue healing around
3 different implant systems.
Histological results demonstrated similar dimensions
and composition of the epithelial and connective
tissue components.



Abrahamsson et al 1999
THE SURGICAL PROTOCOL (i.e. one or two stage surgical
protocol) do not influence the dimensions and composition of
the biological width.
It was observed that the mucosa that formed at implants
placed in a submerged or a non submerged procedure had
many features in common
THE DEEPER THE IMPLANT SHOULDER POSITION IN BONE THE
LONGER THE BIOLOGICAL WIDTH.



Cochran et al. 1997
Evaluated the dimensions of the implanto gingival junction
around non submerged loaded and not loaded implants at 3
and 12 months after implant placement.



SD: 0.50 mm
JE: 1.44 mm
CT: 1.01 mm
LOADED
SD: 0.49mm
JE: 1.16 mm
CT: 1.36 mm
UNLOADED
Abrahamsson et al.
Analyzed soft tissue healing to abutments made of titanium,
gold alloy, dental porcelain and AlO ceramic



Failed to form an attachment
Gold alloy
and
porcelains
Formed attachment with similar
dimensions and tissue
structures
Titanium and
ceramic
Abrahamsson et al. 2002
Demonstrated that surface characteristics (smooth vs
rough titanium surfaces) do not influence the
biologic width dimension.


ABUTMENT IMPLANT INTERFACE
MICROGAP
LEVEL BONE CREST
LEVEL OF THE INTERFACE
SUBMERGED AND NON SUBMERGED
CRESTAL BONE LOSS IN VARIOUS CASES
SUBMERGED
Implant placed into
the bone and the top
of the implant placed
at or below the bone
crest
Soft tissues are closed
over the bone and
implant thereby
submerging it
NON SUBMERGED
Implant extends
coronally beyond the
alveolar crest where
the soft tissue flap is
placed around the
implant body
Second
intervention not
needed
Hermann et al 2000
Study on 6 types of implants
A C NON SUBMERGED
D F SUBMERGED
A : 6mm R/S at bone crest
B: 5mm; R/S 1mm below
A,B: ONE PIECE; No interface
C, D: 4.5 mm interface at bone crest
E,F : 4.5 mm interface 1 mm above
and 1mm below the crest


MEASUREMENTS:
1. Distance between the top of the implant (top) and
first bone to implant contact (fBIC) for A and B.
2. Distance between interface (microgap) of the
implant (IF) and fBIC
3. Top and R/S for A and B.
4. IF R/S (for C F).




TYPE TOP - fBIC R/S - fBIC MICROGAP - fBIC
A 2.98 mm 0.19 mm
B 3.88 mm 0.01 mm
C 1.68 mm 0.39 mm
D 0.28 mm 1.57 mm
E 0.06 mm 2.64 mm
F 0.89 mm 1.25 mm
GREATEST BONE LOSS
WAS OBSERVED
AROUND TYPE F
(2.25mm)
TYPES C, D F: SEVERE
SIGNS OF CLINICAL
INFLAMMATION
TYPE A AND B : SLIGHT
INFLAMMATION
R/S fBIC

IN ALL 2 PIECE IMPLANTS, THE LOCATION OF THE
INTERFACE (MICROGAP) WHEN LOCATED AT OR
BELOW THE ALVEOLAR CREST DETERMINES THE
AMOUNT OF BONE RESORPTION





A and B showed minimal signs of clinical
inflammation
C, D F Moderate to Severe signs of disease





2 piece implants
Abutment implant junction:
Microgap
Crestal bone resorption
FURTHER BIOLOGICAL WIDTH CHANGES,
INCREASED SUBGINGIVAL BACTERIAL
COLONIZATION LEADING TO FURTHER
BONE LOSS
INEVITABLE
1.5 mm during first
year
0.1 mm in subsequent
years
The greatest crestal bone loss occurs with 2 piece
implants when the interface located below the crest
rather than at or above the crestal bone level.
Osseous changes influence the location of the gingival
margin and the dimensions of the biologic width.





SIGNIFICANT CRESTAL BONE LOSS OCCURS IN 2 PIECE
IMPLANT CONFIGURATIONS EVEN WITH THE
SMALLEST SIZE OF THE MICROGAP (<10m) IN
COMBINATION WITH POSSIBLE MOVEMENTS
BETWEEN IMPLANT COMPONENTS





Schultes and Gaggl 2001
Compared healing at implants placed in a healed ridge
and implants immediately placed in fresh extraction
sockets at 8 months have reported a LARGER
DIMENSION OF SOFT TISSUE BARRIER IN IMPLANTS
PLACED IMMEDIATELY





Both of these are characterized by an inflammatory reaction in the tissues
surrounding an implant.

Peri-implant mucositis has been described as a disease in which the
presence of inflammation is confined to the soft tissues surrounding a
dental implant with no signs of loss of supporting bone following initial
bone remodeling during healing.

Peri-implantitis has been characterized by an inflammatory process
around an implant, which includes both soft tissue inflammation and
progressive loss of supporting bone beyond biological bone remodeling
Peri-implant diseases present in two forms
PERI-IMPLANT MUCOSITIS
PERI-IMPLANTITIS
The term peri-implantitis was introduced in the 1980s
(Mombelli A,1987)

Formerly used terms as implant histoclasia and peri
implantoclasia accepted in the 1963 edition of Current Clinical Dental
Terminology.

Peri implantitis was defined as an inflammatory reaction with loss of
supporting bone in tissues surrounding a functioning implant
Albrektsson T et al, Proceedings of the 1
st
European Workshop on
Periodontology, 1994

While peri-implant mucositis is a reversible inflammatory condition
confined to the peri-implant soft-tissue unit, peri-implantitis is
characterised by progressive inflammatory destruction of the crest
of the alveolar bone supporting the implant, by increased peri-
implant probing depths, and by bleeding and/or suppuration on
probing.

Additionally, peri-implant mucositis may be successfully treated
using non-surgical efforts if detected early, whereas peri-implantitis
usually requires surgical treatment.

Main Diagnostic Differences Between
Peri-implant Mucositis And Peri-
implantitis

Clinical parameter Peri-implant mucositis Peri-implantitis

Increased probing depth +/- +
BOP + +
Suppuration +/- +
Mobility - +/-
Radiographic bone loss - +
(a)Peri-implant mucositis presenting with
changes in color, form, and texture

(b)Peri-implant mucositis presents
radiographically with no change in crestal
bone
(a) Peri-implantitis presenting with
changes in color, form, texture, and
associated bone loss resulting in
increased probing depth

(b) Peri implantitis radiographically
demonstrates crestal bone resorption

Saucer shaped destruction of the crestal bone or wedge-shaped
defects along the implant.
Bone destruction may proceed without any notable signs of
implant mobility until osseointegration is completely lost.
Vertical bone destruction is associated with the formation of a
peri-implant pocket.
Bleeding after gentle probing with a blunt instrument
There may be suppuration from the pocket.
Tissues may or may not be swollen.
Hyperplasia is frequently seen
Pain is not a typical feature of peri-implantitis.


MICROBIOLOGY OF PERI-
IMPLANT AREA

INITIAL COLONIZATION
The microflora associated with stable osseointegrated implants
serving successfully as abutments for overdentures was
investigated in 18 edentulous patients.
50% FACULTATI VELY ANAEROBI C COCCI
17% FACULTATI VELY ANAEROBI C RODS
7% GRAM NEGATI VE ANAEROBI C RODS
9% F.nucleatum, P.intermedia
Porphyromonas gingivalis and Spirochetes not found

PARTIALLY EDENTULOUS RIDGES
Higher percentages of black pigmenting Gram negative
anaerobes and wet spreaders (Capnocytophaga)
MI CROBI AL STATUS OF THE REMAINI NG TEETH
I NFLUENCES THE FATE OF NEWLY I NCORPORATED
I MPLANTS

Thus the teeth microbiota are the primary source of putative
pathogens.


MICROBIOLOGY OF DISEASED IMPLANTS
Microbiology plays important role in etiology of peri-
implantitis

The main cause of peri- implantitis is dental plaque (Meffert
R.M.)

Aggretebacter actinomycetemcomitans
Porphyromonas gingivalis
Bacteroides forsythus
Fusobacterium nucleatum
Campylobacter
Peptostreptococcus micros
Prevotella intermedia
( Tanner A et al, 1997)
From an experimental study it was reported that: For teeth, 3 weeks to 3 months of
undisturbed plaque accumulation resulted in no further extension of the
inflammatory lesion. However, for implants, under identical experimental
conditions, a further spread in apical direction of the inflammatory cell infiltrate
was consistently observed.


This implies that the defense mechanism of the gingiva may be more effective
than that of the peri-implant mucosa in preventing further apical propagation
of the pocket microbiota.