Osteomyelitis

"is often more than simply the presence of organisms in the

skeleton and often less than pain, swelling, and drainage.'‘

David Seligson Orthopedics in May 1994

 Presented by
Dr Jayesh
II year post graduate student
Dept of oral and maxillofacial surgery
 CONTENTS

Definition
Introduction
History
few different terms
Classification
Microbiology
Pathogenesis
Clinical presentations of various types of osteomyelitis
Imaging
Treatment principle
Antibiotic regimen
Surgical modalities
References
 Osteomyelitis of the jaws was once a frequently
encountered disease and was dreaded because of its
prolonged course and associated with disfigurement
and dysfunction due to loss of teeth and bone and
occasional facial scarring.
DEFINITION
 Osteomyelitis is an inflammatory condition of
bone that involves the medullary cavity and has
a tendency to progress along this space and
involve the adjacent cortex, periosteum, and soft
tissue.

From:- topazian 4° edition chapter 10

 Greek words
 Osteon – Bone, muelinos – marrow
 Infection of medullary portion of bone
introduction
 Fairly common disease in maxillofacial clinics

 Last 50 years – Profound change - Prevalence,

clinical course & management

 Introduction of - “Pencillin”
 Sophistication in medical & dental science
 Availability of adequate treatment
 Modern diagnostic imaging methods
 Inflammation of medullary space – also caused
by
 Traumatic injuries,
 Radiation,
 Chemicals etc.

 Term “osteomyelitis”- confined to infection caused

by pyogenic organisms (Marx 1991)
 Pre antibiotic era
 Classical presentation - acute form followed by
chronic
 Massive clinical symptoms – bone necrosis, neo-
osteogenesis, sequestrum formation, intra and
extra oral fistula formation and facial disfigurement
 Entry of antibiotics –
 Concealed acute phase
 Elimination of infection
 Sub acute & chronic forms more prominent
 Jaw osteomyelitis – Differ from long bones
 Presence of teeth
 Connects - oral cavity to PDL membrane
 Specific immunological & microbiological aspects
 Classifications – based on
 Clinical course
 Pathological-anatomical and/or radiological features
 Etiology
 Pathogenesis
Some terms
 Acute / Subacute osteomyelitis
 Rarely seen
 Duration – 1 month after onset of symptoms
 Subacute – used interchangeably with acute

 Chronic osteomyelitis
 Suppurative
 Nonsuppurative
 Chronic suppurative osteomyelitis / secondary
chronic osteomyelitis
 Commonest type
 Bacterial invasion from a contagious focus
 Pus, fistula & sequestration - typical findings
 Clini / Radiogr – Broad spectrum of phases
Aggressive osteolytic putrefactive phase ----- Dry
osteosclerotic phase
 Chronic nonsuppurative osteomyelitis
 Heterogeneous group - chronic sclerosing,
proliferative periostitis, actinomycotic and radiation
induced types (Topazian 1994, 2002)
 Lack – pus & fistula
 Hudson (1993) and Burnier(1995) – “A condition of
prolonged refractory osteomyelitis due to
inadequate treatment, a compromised host,
increased virulence and antibiotic resistance of the
involved microorganisms”
 SAPHO syndrome, Chronic Multifocal
Recurrent Osteomyelitis (CRMO)
 Synovitis, Acne, Pustulosis, Hyperostosis, Osteitis
S A P H O
 Few case reports linking association
 CRMO – characterized by periods exacerbations &
remissions
 Noted in adults & children
 Periostitis ossificans, (Garre’s osteomyelitis?)

 Descriptive term for a condition, caused by several

entities

 Periosteal inflammatory reaction to non specific stimuli

-----formation of new immature type of bone outside
the normal cortical layer

 Garre’s osteomyelitis - most confusing & misinterpreted

term, (term discarded by medical pathologists)
 Synonyms – Periostitis ossificans, Chronic non suppurative
osteomyelitis of Garre, Garre’s proliferative periostitis,
Chronic sclerosing inflammation of the jaws, Chronic
osteomyelitis with proliferative periostitis and many more
 Carl Garre in 1893 – in his historical article,
 Described special forms & complications of – acute infective
osteomyelitis.
 Did not describe new type of osteomyelitis.
 Enjoyed great acceptance in medical & dental literature till
recently (1994)
 Alveolar osteitis or Dry socket
 Localized form
 3 types – alveolitis simplex, alveolitis granulomatosa,
alveolitis sicca
 In alveolar osteomyelitis – absence of invasion in to bone
& hence not considered as form of osteomyelitis
 Due to breakdown of clot by fibrinolysins released by
bacteria or trauma
 Bacteria remain on the surface of exposed bone & do not
invade
 Osteoradionecrosis & Radioosteomyelitis

 Still an observed condition, (in spite of advances)

 Initiated by bacteria - hence the term – ‘radiation induced

osteomyelitis or radioosteomyelitis’

 Marx in 1983 – as radiation induced avascular necrosis of

bone due to 3- H - Hypoxic, Hypocellular and Hypovascular
tissue -------- chronic non healing wound ----super
infection ---------- osteomyelits
 Osteochemonecrosis
 Caused by drugs (anti cancer, corticosteroids & others)
chemicals (phossy jaw or phosphorous necrosis due to
white P in matchbox industry)

 Recent years – “Bisphosphonate induced osteo-

chemo necrosis of jaws” – Due to Bisphosphonates
drugs, used for osteoporosis, Paget’s disease, bone
cancer metastasis, multiple myeloma etc.
 “Juvenile chronic osteomyelitis” – Resembles Garre’s
, peaks in puberty, with voluminous expansion of
bone, periosteal apposition, & mixed sceroticolytic
appearance
classification
 Waldvogel is credited with the first classification
system for osteomyelitis.This system categorizes based
upon pathogenesis. He describes three categories of
osteomyelitis:

 1) hematogenous osteomyelitis
 2) osteomyelitis secondary to a contiguous focus of
infection and
 3) osteomyelitis associated with peripheral vascular
disease.
 Classification of Osteomyelitis of the jaws

Suppurative Osteomyelitis
Non suppurative osteomyelitis

 Acute suppurative osteomyelitis Diffuse sclerosing osteomyelitis

 Chronic suppurative osteomyelitis Focal sclerosing osteomyelitis
Primary – no acute phase Proliferative periostitis
preceding Osteoradionecrosis
Secondary – Follows acute
phase
 Infantile osteomyelitis

 From:- topazian 4° edition chapter 10

 Classification based on clinical picture and radiology
 I. Acute forms of
osteomyelitis (suppurative
or nonsuppurative)
 A. Contagious focus
 1. Trauma
 2. Surgery
 3. Odontogenic Infection
 B. Progressive
 1. Burns
 2. Sinusitis
 3. Vascular insu!ciency
 C. Hematogenous(metastatic)
 1. Developing skeleton
(children)
II. Chronic forms of osteomyelitis
A. Recurrent multifocal
1. Developing skeleton (children)
2. Escalated osteogenic (activity< age 25 years)
B. Garrè's
1. Unique proliferative
subperiosteal reaction
2. Developing skeleton (children
and young adults)
C. Suppurative or nonsuppurative
1. Inadequately treated forms
2. Systemically compromised
forms
3. Refractory forms (chronic recur-
rent multifocal osteomyelitis
CROM)
D. Diffuse sclerosing
1. Fastidious microorganisms
2. Compromised host/pathogen
interface
 Classification based on clinical picture,
radiology, pathology, and etiology

 I. Acute suppurative sclerosing osteomyelitis

osteomyelitis (rarefactional
osteomyelitis)
 II. Chronic suppurative
osteomyelitis
 (sclerosing osteomyelitis)
 V. Chronic osteomyelitis
with proliferative periostitis
(Garre's chronic nonsuppurative
sclerosing osteitis,ossifying
periostitis)

 III. Chronic focal sclerosing  VI. Specific osteomyelitis

osteomyelitis  1. Tuberculous osteomyelitis
 2. Syphilitic osteomyelitis
 (pseudo-paget, condensing
osteomyelitis)  3. Actinomycotic osteomyelitis

 IV. Chronic diffuse

 CLASSIFICATION BASED ON PATHOGENESIS

 I. Hematogenous osteomyelitis
 II. Osteomyelitis secondary to a contigu-
 ous focus of infection
 III. Osteomyelitis associated with or with-
 out peripheral vascular disease
 Dual classification based on pathological
anatomy and pathophysiology

Stage IV: diffuse osteomyelitis –

I. Anatomic Types
o defect greater than 2 cm. Pathologic
 Stage I: medullar osteomyelitis –
fracture, infection, nonunion
involved medullar bone without
cortical involvement; usually
hematogenous II. Physiological class
Stage II: super$cial osteomyelitis –
 A host: normal host
• less than 2 cm bony defect without
 B host: systemic compromised host,
cancellous bone
 local compromised host
Stage III: localized osteomyelitis –
 C host: treatment worse than disease
o less than 2 cm bony defect on
radiograph, defect does not appear
to involve both cortices
MICROBIOLOGY
 Staphylococcus aureus account for 80% of the cases of osteomyelitis
of the jaws.
 Others include

 Streptococcus epidermis

 Staphylococcus albus and Salmonella.

 In addition Mycobacterium tuberculosis, Treponema palladium and

Actinomyces israelli produce certain specific forms of osteomyelitis.
Osteomyelitis Clinical Rheumatology
Vol. 20, No. 6, pp.1065e1081, 2006
pATHOGENESIS
 It is usually initiated from a contiguous focus of infection or by
hematogenous spread.

 This is primarily caused by odontogenic infection originating

from the pulpal or periodontal tissues. It is polymicrobial in nature as
compared with that of long bone osteomyelitis, in which classically
Staphylococcus aureus is the infecting organism.

 Trauma, especially compound fractures is the second leading

cause.
 Acute inflammation following infection
⇃
Hyperemia
⇃
Capillary permeability ↑and infiltration of granulocytes
⇃
Tissue necrosis
⇃
Destruction of bacteria, vascular thrombosis & Pus forms
⇃
intramedullary pressure ↑ as pus accumulates -> anesthesia compression
⇃
Vascular collapse, venous stasis and ischemia
⇃
Pus accumulates with Stripping of periosteum
⇃
vascular supply reduced
⇃
periosteum penetration and mucosal fistulas
⇃
chronic Inflammation - >granulation tissue & lysis of bone
⇃
separation of necrotic bone (sequestra)
⇃
sheath of new bone (involucrum)
CLINICAL PRESENTATION
• Pain
• Swelling and erythema of overlying tissues
• Adenopathy
• Fever
• Paresthesia of the inferior alveolar nerve
• Trismus
• Malaise
 Acute suppurative osteomyelitis

 It may have appearance of typical odontogenic infection.

 It can be localised or widespread

 Aetiology :
 Odontogenic infections
 Compond fractures of jaws
 Local traumatic injuries
 Peritonsillar abscess
 Clinical Features
 Generalised constitutional symptoms
 Deep seated boring, continuous and intense pain
 Facial cellulitis
 Trismus

Established cases may present with

 Fetid odour
 Purulent discharge with sinuses
 Dehydration, acidosis and toxemia
 Regional lymphadenopathy is usually present
Chronic focal sclerosing
osteomyelitis
 It is an unusual reaction of bone
to infection, occurring in instances of
extremely high tissue resistance or in
cases of a low grade infection.

This form of osteomyelitis arises

most commonly in young persons
below 20yrs.
 The tooth most commonly involved is
first molar, which presents as a large
carious lesion.
 There may be no signs or symptoms of
the disease other than mild pain
associated with an infected pulp.
 Periapical radiograph show
 Well-circumscribed radio-opaque mass of
sclerotic bone surrounding and extending
below the apex of involved tooth.
 The border of this lesion, abutting the
normal bone, may be smooth and distinct
or appear to blend into the surrounding
bone.

 Treatment consists of endodontic therapy

or extraction of involved tooth following
which the bony lesion may remodel or
remain distinct.
Chronic diffuse sclerosing
osteomyelitis
 Chronic diffuse sclerosing
osteomyelitis also represents a
proliferative reaction of bone to low
grade infection.

 Here the portal of entry of

infection is mainly through the
periodontium.

 This might occur at any age, but

most commonly in older persons,
especially in edentulous mandibular
jaws. It is more common in females.
 Radiographically there is diffuse sclerosis of bone. Radio-opaque
lesions may be extensive. Border between normal bone and sclerotic bone is
indistinct.
 Treatment of chronic diffuse sclerosing osteomyelitis is mainly
conservative. It consists of removal of source of infection and antibiotic
administration.
Garre’s osteomyelitis
 This was first described
by Carl Garre in 1893 as a
focal gross thickening of the
periosteum of long bones, with
peripheral reactive bone
formation resulting from mild
irritation or infection

 This is seen primarily in

children and young adults.
Clinically it is characterised by
a localized, hard, non-tender
swelling over the mandible.
 Intra-oral periapical radiograph will often
reveal a carious tooth opposite the hard bony
mass.
 Occlusal view will show a focal overgrowth of
bone on the outer surface of the cortex, which
may be described as a duplication of the
cortical layer of bone. This mass of bone is
smooth and rather well calcified.
 Treatment is by removal of the involved
tooth along with biopsy of the lesion to confirm
the diagnosis. Remodeling of the bone occurs
gradually following removal of the offending
tooth.
INFANTILE OSTEOMYELITIS

Osteomyelitis of the jaws in infants is not a common disease.

It is seen a few weeks after birth and usually involves maxilla.
It is thought to occur via hematogenous route or from
perinatal trauma of the oral mucosa from the obstetrician’s finger or the
mucosa suction bulb used to clear the airway immediately after birth.
Infections involving the maxillary sinus and infected human or artificial
nipples have also been implicated as sources of infant infection.
 Clinically the patient presents with a Facial
cellulitis centered about the orbit.

Irritability and malaise precede frank cellulitis, which

are followed by hyperpyrexia, anorexia and dehydration.
Convulsions and vomiting may occur.

 Intra-orally
 The maxilla on the affected side is swollen both bucally and
palatally
 Fluctuance is often present and
 Fistulas may exist in the alveolar mucosa.

During the early acute phase, little radiographic changes are noted and
leucocytosis is generally present.
ACTINOMYCOTIC
OSTEOMYELITIS
 Actinomycosis is a chronic infection manifests both with granulomatous
and suppurative features involving soft tissues and bone of cervicofacial
region. It is caused by Actinomycosis israelii.

 Actinomycotic osteomyelitis of jaws are rare but may present as

 A periostitis as a result of the involvement of the adjacent soft
tissues.
 An Actinomycotic osteomyelitis in which the mandible is
thickened and honeycombed by narrow tracts in which the micro-
organisms is embedded in granulation tissue. Eventually sequestration of
the bone occurs.
 A chronic infection of a fracture of the jaw bone and produce a
chronic facial sinus.
 Diagnosis is by microscopic examination of the pus. Sulphur granules are
rarely present when the patient has already received antibiotic therapy.

 Treatment entails prolonged antibiotic therapy with penicillin 500mg 6th

hourly or amoxycillin 500mg 8th hourly orally for 6-8 weeks Surgical
intervention will be required to remove any sequestra, which have formed.
TUBERCULOUS OSTEOMYELITIS
 This condition of the jaws is rare. Infection of bone
by Mycobacterium tuberculosis is usually brought
about by hematogenous spread and is almost always
secondary to a primary focus in respiratory or
alimentary tract.

 Localised osteomyelitis may follow tooth extraction

performed on tuberculous patient. Active
tuberculosis infection of the tooth socket is seen
both in patients with pulmonary TB with a positive
sputum and in patients with active infection in
cervical lymphnodes.

Primary tuberculous osteomyelitis of the mandible: a case report

Dentomaxillofacial Radiology (2008) 37, 415–420
 The diagnosis is confirmed on biopsy.
If the infection of mandible is left
untreated it may spread into soft tissues
and form an indolent, chronic facial
sinus.
 Treatment consists of local
surgery and anti-tuberculous therapy
(a) Part of an enhanced panoramic
radiograph of the left side of the
mandible showing healing of the bony
lesion 6 months after the initiation of
antituberculous chemotherapy (arrows).
(b) Occlusal view of the left side of the
mandible showing healing of the bone
6 months after the initiation of
antituberculous chemotherapy
Syphilitic osteomyelitis
 Infection by Treponema palladium may affect the bones in
syphilis in both the secondary and tertiary stages and also in
cases of congenital syphilis

 At the site of the lesion there is a chronic, inflammatory

granulomatous and necrotising periarterial infiltrate
accompanied by partial destruction of bone. As the disease
progress the vascularity of the area become diminished and the
bone tends to become sclerosed. Osteosclerosis with new bone
formation is more common than osteoporosis and rarefaction
 In neonatal syphilis the involvement of the skeleton takes place
approximately at the end of the fifth month of intrauterine life
and the characteristic bone changes are seen at birth.
Gummatous destruction of the nasal septum and hard palate are
common. This result in saddle shaped nose due to subsidence
of the bridge of the nose and perforations of the palate.
 Radiologically, the cranium has a worm-eaten appearance due
to subperiosteal gummas. In the absence of treatment,
separation of the circular sequestra from the base of ulcerating
gummatous lesions may lead to complete perforation of the
bone
 In acquired syphilis bony changes are seldom seen before
tertiary stage. The palate, nose, skull and tibia are the bone
most commonly affected. The changes seen are in the form of
periosteal or central gumma. Bone is resorbed at the site of the
gumma producing radiolucency with a poorly defined margin
 Syphilitic osteomyelitis of the jaws cannot be distinguished
from pyogenic osteomyelitis on clinical and radiologic
examination. Diagnosis may be missed, unless a gumma is
seen or evidence of tertiary syphilis is found elsewhere in the
body or a serological test to show presence of syphilis. The
condition rapidly improves with use of penicillin or
erythromycin.
DIAGNOSTIC IMAGING

The increasing availability of 3-dimensional imaging, magnetic

resonance imaging (MRI), scintigraphy, and, now, PET/CT imaging has
made it much easier to precisely delineate the extent of the disease process
in a timely manner.

The newest imaging modalities, such as scintigraphy and PET scan,

are able to highlight biological as well as anatomic activity

Alveolar Osteitis and Osteomyelitis of the jaws

Oral and Maxillofacial Surg Clin N Am 23 2011 401-413
Conventional Radiography
 Although the standard for many
decades, the role of this modality is limited
in detection of and therapy for osteomyelitis
because it only shows changes after
extensive bone abnormality has been
present for prolonged periods.
 However, it is readily available and
exposes patients to minimal radiation.
Panoramic projection is most useful in most
maxillofacial cases

Alveolar Osteitis and Osteomyelitis of the jaws

Oral and Maxillofacial Surg Clin N Am 23 2011 401-413
 Once osteomyelitis has become well established,
radiographic changes usually demonstrate one of the
following sets of characteristics (Worth 1969)
 Scattered areas of bone destruction - a moth-
eaten appearance

 Bone destruction of varied extent in which there are

islands that is sequestra. A sheath of new bone
(involucrum) is often found separated from sequestra
by a zone of radiolucency.

 Stippled or granular densification of bone

caused by subperiosteal deposition of new bone.
COMPUTED TOMOGRAPHY
 The addition of cone beam
computerized tomography,
which is highly useful for
imaging hard tissues of the head
and neck in multiplanar slices, is
ideal for visualizing
decortications and periosteal
changes. Soft tissue changes can
also be visualized in medical-
grade CT scans by adding
contrast medium .

Alveolar Osteitis and Osteomyelitis of the jaws

Oral and Maxillofacial Surg Clin N Am 23 2011 401-413
mri
Use of gadolinium as a contrast agent can show early osteomyelitis
changes in tissue by highlighting nonspecific disturbances in tissue-blood
interfaces, which are common in infection, inflammation, trauma, or
tumors. The changes are most often noted in the soft tissues and can also
be noticed in the medullary portion of the affected bone

Alveolar Osteitis and Osteomyelitis of the jaws

Oral and Maxillofacial Surg Clin N Am 23 2011 401-413
scintigraphy
The radioactive substances used to
identify altered bone physiology are
technetium 99m— labeled methylene
diphosphonate, gallium 67, and indium
111.
 The most common scintigraphic agent
is technetium 99m , which is used to
delineate increased bone turnover, and
it is often coupled with the gallium 67
to distinguish the osteomyelitis lesions
from tumor and trauma because
gallium is sensitive to inflammatory
changes

Alveolar Osteitis and Osteomyelitis of the jaws

Oral and Maxillofacial Surg Clin N Am 23 2011 401-413
Recent advances
Pet/ct
The application of PET scan using fludeoxyglucose F 18 has shown
promise in the identification of osteo myelitis in the jaws especially when
applied with traditional CT. The 2 scanning modalities fuse together
anatomic findings and a metabolic state finding in a real-time frame.

Alveolar Osteitis and Osteomyelitis of the jaws

Oral and Maxillofacial Surg Clin N Am 23 2011 401-413
Treatment principle
1.Early Diagnosis
2. Elimination of the source of infection
3.Establishment of surgical drainage
4. Bacteriologic identification and antibiotic sensitivity testing
5. Appropriate antibiotic coverage
6. Surgical debridement
7. Supportive care
8. Reconstruction.

How can we diagnose and treat osteomyelitis of the jaws as early as possible?
Oral and Maxillofac Surg Clin N Am (23) 2011 557-567
Antibiotics
 Aqueous Peicillin-2 million units every 4 hourly or
Oxacillin 1g IV every 4 hourly
When patient has been asymptomatic for 48-72 hours then
switch to Dicloxacillin 250mg 4 hourly orally for 4 to 6 weeks.
If patient is allergic to penicillin
2nd choice – Clindamycin 600mg 6 hourly
3rd Choice- Cephalosporins
4th Choice – Erythromycin 500 mg every 6 hourly
Hyperbaric O2 in treatment of OML

Hyperbaric oxygen therapy consists of breathing 100% oxygen through a face

mask or hood in a monoplace or a large chamber at 2.4 absolute
atmospheres pressure for 90 min session or dives for as many as 5 days a
week totaling 30 or more sessions often followed by another 10 or more
sessions
Action of HBO therapy:
1.Enhancement of lysosomal degradation potential of polymorphonuclear
leukocytes and O2 radicals.Formation of these enzymes is decreased in
hypoxic environment as in OML.
2. Free radicals of O2 are toxic to many anaerobes(bactericidal).
2)Exotoxin liberated by microorganisms are rendered inert by
exposure to elevated partial pressure of O2
3)Tissue hypoxia is reversed by HBO
4)Postive enhancement of neoangiogenesis

Clinical effects
 It aids in healing of draining sinus
 Improves osteogenesis in lytic areas
 Reduces destruction of bone and soft tissues
 Sequestra undergo rapid dissolution without suppuration &
healing eliminates the need for surgical intervention.
Marx protocol
•30 (100% O2 for 90 min at 2.4ATA)
•Examine the exposed bone

Stage – 1

•10(100% 02 for 90 min at 2.4

Response
ATA) (stage 1 responder) •Surgery
•10(100% 02 for 90min at 2.4 ATA)
Stage-2

HealingResponse
without exposed •Excision of nonviable bone
bone (stage 2 responder) •Fixation of mandibular segment
Stage-3
•10(100%0 2 for 90 min at 2.4 ATA)

•Reconstruction after 3 months

•No further HBO required
CONTRAINDICATIONS OF HBO THERAPY

Pneumothorax
COPD
Optic neuritis
Acute viral infection
Congenital spherocytosis
Malignancy
Pregnancy
Surgical debridement of the osteomyelitic jaw may encompass a series of
procedures. The removal of infected and devitalized teeth and associated
soft tissue is a preliminary treatment of osteomyelitis.

The removal of necrotic and chronically infected bone is essential to

the successful management of the infection. Multiple procedures over a
period of days or weeks may be required to eradicate the infection from the
affected jaw. The procedures include Sequestrectomy, Saucerization,
Decortication, Resection, and Reconstruction.

How can we diagnose and treat osteomyelitis of the jaws as early as possible?
Oral and Maxillofac Surg Clin N Am (23) 2011 557-567
SURGICAL treatment
Sequestrectomy
 Sequestrectomy is the removal of
infected devitalized bony fragments in the
infected area of the jaw. The sequestrum
is often surrounded by a sheath or
membrane of new bone, termed an
involucrum. The removal of sequestra is
important because it enables the
penetration of high concentrations of
antibiotics into an area of previously poor
vascularity
How can we diagnose and treat osteomyelitis of the jaws as early as possible?
Oral and Maxillofac Surg Clin N Am (23) 2011 557-567
SAUCERIZATION
Saucerization is frequently performed in conjunction with
sequestrectomy. This procedure removes the margins of necrotic bone to
expose the medullary spaces for further exploration and removal of necrotic
tissue.
The procedure is usually performed intraorally, giving direct
access to the infected bone. After the procedure the wound may be packed
open to allow irrigation and examination during the early healing of the
defect. Once a bed of healthy granulation tissue is formed, the packing may
be removed.
How can we diagnose and treat osteomyelitis of the jaws as early as possible?
Oral and Maxillofac Surg Clin N Am (23) 2011 557-567
decortication
Decortication is the removal of lateral and inferior cortical plates of bone to
gain access to the infected medullary cavity. Avascular bone is removed
until a 1- to 2-cm margin of vital bone is achieved.

How can we diagnose and treat osteomyelitis of the jaws as early as possible?
Oral and Maxillofac Surg Clin N Am (23) 2011 557-567
resection
Long-term osteomyelitic infections
may lead to pathologic fractures,
continuing infection after decortication, . In
such cases, resection and eventual
reconstruction may be indicated to
eradicate the disease.
The resection margins should be in a
viable bone 1 to 2 cm from the site of
infection.

How can we diagnose and treat osteomyelitis of the jaws as early as possible?
Oral and Maxillofac Surg Clin N Am (23) 2011 557-567
CLOSED WOUND IRRIGATION
SYSTEM
Recent advances
 Calcitonin and parathyroid hormone regulate
bone turnover, and therefore maintain calcium
balance and homeostasis.
 It is used for relief of bone pain in Paget’s
disease, neoplastic bone disease and post-
menopausal osteoporosis.
 Its analgesic properties result from inhibition of
prostaglandins and stimulation of production of
endorphins.
 Radiographs have shown good healing, but
further clinical studies are required to asses the
true effect of calcitonin and its use as an
adjunct to antimicrobial and surgical treatment
Long term antibiotics and calcitonin in the treatment
of chronic osteomyelitis of the mandible: Case report
British Journal of Oral and Maxillofacial Surgery 46 (2008) 400–402
references
 Topazian 4° edition
 Osteomyeltis of jaw mark baltensperger
 Radiographic imaging in osteomyelitis: the role of plain radiography,
computed tomography, ultrasonography, magnetic resonance imaging, and
scintigraphy
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