CHRONIC INFECTIONS OF
JAWS
Presented by Dr. Mohammed haneef

 INTRODUCTION
 ANATOMY OF BONE
 TYPES OF INFECTIONS AFFECTING BONE
 PERIOSTITIS
 OSTEITIS
 OSTEOMYLTIS
 HISTORY
 CLASSIFICATION
 ETIOPATHOGENESIS
 PREDISPOSING FACTORS
 MICROBIOLOGY
 TYPES AND CLINICAL FEATURES
 INVESTIGATIONS
 MANAGEMENT

Bone is a connective tissue in which cells are arranged
at regular interval in a matrix.
 The matrix is impregnated with calcium phosphates
& Calcium hydroxide salts.
 Adult bone consists of
• 30-40 % Collagen.
• 60-70% minerals.(Excluding 25-30% of water).

• In Maxilla-
• Cortex is thin, In anterior
region Spongy part is well
Developed.
• Highly vascularised
• In Mandible-
• Well developed
• Periosteum and Cancellous
• A solid cortex.
• Two sources of blood supply

Bacterial, Trauma, Dental infection
(A)Acute Periostitis- Fulminating infection
Exudates separates the periosteum From
bone
OML
C/F- Localized-Periosteum over infected tooth involved.
Suppurative- Swelling of the face, Pain, Tenderness.
Sever stage- Trismus, loosening of teeth, Sinus tract &
Pus discharge, Chills, Fever.
Treatment:
Early Stage- Antibiotics, Extraction of offending teeth,
-Hot moist packs.
Late Stage- I & D.

(B) Chronic Periostitis / Garre’s Osteomyelitis:
Follows the Acute phase
Osteogenic activity may be stimulated
New bone formation, also called Periostitis Ossificans.
R/F: Increased radio-opacity, & thickening of periosteum, Bone
deposition at periphery.
Treatment:-Antibiotics & Hot moist Packs.
If adjacent bone is involved then Seqeustrum is removed.
• Debridement
• Drainage.

(A) Suppurative Osteitis:
Can arise from
• Odontogenic infection of carious tooth.
• Pericoronal Infection From Erupting 3rd
molar.
That's why classified as Dentoalveolar Abscess.
It may destroy the bone extensively but remains walled off & doesn’t
Spread.
R/F:
• Circumscribed osteolytic area,
• without definite cortical border.
• Sometimes irregular area of
Osteolysis.

• Bone formation as a result of inflammation.
• Infections & Circulatory Conditions are responsible (Heiss 1954)
• In some cases- process represents repair following the destruction of the
bone.
• In other cases- an initial bone production after osteoblast activation by
mild & chronic infection.
Cortical type of bone is produced.
in marrow space.
Elimination of spongiosa.
cellular infiltration in remaining marrow space.
(process is inflammatory)
(B) Sclerosing (Condensing) Osteitis:

R/f: Radiopaque irregular outline
with peripheral extensions.
C/f: Neurologic pain.
Boring character.
T/t: -Antibiotics
-Extraction of associated
tooth.
Sever pain –
• Decompression of the Inferior alveolar
• nerve.
• Excision of the sclerosed area.

In Greek osteon means bone
myelos means marrow
itis means inflammation
• OML is defined as an inflammatory condition of bone primarily involving
soft tissues{ARCHER 1975}
• Extensive inflammation of bone involving cancellous portion{LASKIN}
• Inflammation of bone marrow with a tendency to progression, involving
adjacent cortical plates & periosteum tissues.{Michael miloro}
• An inflammatory disease of bone that begins as a bacterial infection of
cancellous vascular spaces, comprising the haversian circulatory systems
& eventually extending to involve cortex & periosteum.{OMSCNA 1991}
“ Osteomyelitis may be defined as an inflammatory condition of bone, that
begins as an infection of medullary cavity and haversian systems and
extends to involve the periosteum of the affected area ”

Reference Classification Classification
Criteria
Topazian RG
Osteomyelitis of
the Jaws. In
Topizan RG,
Goldberg MH
(eds): Oral and
Maxillofacial
Infections.
Philadelphia, WB
Saunders 1994,
Chapter 7, pp
251-88
I. Suppurative osteomyelitis
1. Acute Suppurative osteomyelitis
2.Chronic Suppurative osteomyelitis.
-Primary chronic Suppurative OML
-Sec. chronic Suppurative OML
3. Infantile osteomyelitis.
II. Nonsuppurative osteomyelitis
1. Chronic sclerosing osteomyelitis
– Focal sclerosing osteomyelitis
– Diffuse sclerosing osteomyelitis
2. Garrè's sclerosing osteomyelitis
3. Actinomycotic osteomyelitis
4. Radiation osteomyelitis and necrosis.
Classification based on
clinical picture,
radiology, and etiology
(specific forms such as
syphilitic,
tuberculous, brucellar,
viral, chemical,
Escherichia coli and
Salmonella
osteomyelitis not
integrated in
classification)

Reference Classification Classification
criteria
Hudson JW
Osteomyelitis
of the jaws: a
50-year
perspective.
J Oral
Maxillofac
Surg 1993
Dec;51(12):12
94-301
I. Hematogenous osteomyelitis
II. Osteomyelitis secondary to
a contiguous focus of
infection.
III. Osteomyelitis associated with
or without peripheral vascular
disease.
Classification
based on
pathogenesis.
From Vibhagool
1993

Reference Classification Classificatio
n criteria
Hudson JW
Osteomyelitis
of the jaws: a
50-year
perspective.
J Oral
Maxillofac
Surg 1993
Dec;51(12):12
94-301
I. Anatomic Types
Stage I: medullar osteomyelitis
–involves medullar bone without
cortical involvement; usually Hematogenous.
Stage II: superficial osteomyelitis
–less than 2 cm bony defect without
cancellous bone
Stage III: localized osteomyelitis
– less than 2 cm bony defect on
radiograph, defect does not appear
to involve both cortices.
Stage IV: diffuse osteomyelitis
defect greater than 2 cm. Pathologic
fracture, infection, nonunion.
II. Physiological class
A host: normal host
B host: systemic compromised host,
local compromised host
C host: treatment worse than disease.
Dual
classification
based on
pathological
anatomy and
pathophysiolog
y
From
Vibhagool
1993 and
Cierny 1985

• Lytic
• Sclerotic
• Mixed &
• Sequestrum pattern .
(Indian Journal Of Radiology & Imaging1993)

The patients were classified based on 5 disease stages:
• stage 0, potential osteomyelitis with bone contamination;
• stage I, early or acute osteomyelitis;
• stage II, intermediate osteomyelitis with subperiosteal abscess;
• stage III, late or chronic osteomyelitis with sequestrum and
subdivided into curable (IIIa), controllable (IIIb) and complicated
(IIIc); and
• stage IV, compound osteomyelitis either anatomical (IVa) or
physiological (IVb).
(East African Medical Journal, 2003 (Vol. 80) (No. 7) 373-378

IMMUNOCOMPROMISED
PATIENTS
• Diabetes
• Leukemia
• Severe anemia,
• Malnutrition,
• Chronic alcoholism,
• Sickle cell anemia and
• Febrile illness such as
Typhoid.)
• Agranulocytosis
ALTERATION IN JAW
VASCULARITY
• Radiation,
• Osteoporosis,
• Paget`s disease,
• Fibrous dysplasia,
• Bone Malignancy
and Bone Necrosis
caused by Mercury,
Bismuth and
Arsenic

Acute inflammation ( edema, pus)
Increased intermedullary pressure
Vascular collapse (stasis, ischemia of bone)
Avascular bone
Pus organism extention
Haversian system/ nutrient canal involvement
Elevation of periosteum
Disruption of periosteal blood supply
Avascular infected bone

• Pathogenesis can be divided into 4 phases:
• Microbial adherence and invasion:
• Mechanisms of tissue destruction and bone death:
• Mechanism of microbial persistence:
• Responses to infection
• Osteomyelitis --- opportunistic disease as presented
by the host to the pathogenic microbe.
• Odontogenic infections.
• Trauma.
• Infections of orofacial regions.
• Hematogenous spread.

•Caused primarily by streptococci (alpha hemolytic)
•Oral anaerobes particularly Bacteriodes fragilis, Bacteriodes
melanogenicus and Fusobacterium, peptostreptococcus.
•Staphylococcus aureus.
• Capable of adhering to bone, tend to develop resistance to
antimicrobial therapy
• Capability to survive intracellularly
•In addition Mycobacterium tuberculosis, Treponema palladium
and Actinomyces israelli produce certain specific forms of
osteomyelitis.
• Findings suggestive of pure anaerobic or mixed
aerobic/anaerobic infections

• Mandible is affected more because of the dense, poorly-
vascularised cortical plates and the single blood supply from
the inferior alveolar neurovascular bundle.
• The extensive blood supply of the maxilla makes it less prone
to ostemyelitis when compared to the mandible.
• The thin cortical plates and the porosity of the medullary
portion preclude infections from becoming contained in the
bone and facilitate spread of edema and purulent discharge
into adjacent tissues.
Dentomaxillofacial Radiology
(2005) 34, 86-90

• May involve maxilla or mandible
• Common in infants
• In maxilla it is fairly well localized, where as in mandible it
tends to be more diffuse and wide spread.
• Staph. Aureus or Pyogenes is most commonly found, but
spirochetes or gram –ve bacteria may also be present.
Clinical Features:
• Severe pain, malaise and fever.
• Regional lymphadenopathy.
• Elevated WBC count.
• Teeth involved may become loose and sore.
• Paresthesia or anesthesia of lip.
• Trismus may be present.

1. Primary – resulting from relatively less virulent
organisms.
2. Secondary – occurring after acute phase when
treatment did not succeed in eliminating the
infection.

Clinical Features:
• The arbitrary time limit to differentiate chronic from acute
osteomyelitis is one month.
• Dull aching pain and minimal tenderness.
• Non healing bony and overlying soft tissue wounds with
induration of soft tissues.
• Intra oral or extra oral draining fistulae.
• Thickened or wooden character of bone.
• pathological fractures.
• Sterile abscesses (Brodies abscess) common in long bone,
rare in jaws.
• Loose and sensitive teeth.
• Paresthesia or anesthesia is common.

• Enlargement of bone due to
subperiosteal new bone
deposition.
• Radiopaque sequestra (arrow)
surrounded by the radiolucent
suppuration.
• Worm-eaten appearance of
the body of the mandible.
Radiopaque sequestra
surrounded by the radiolucent
suppuration and a radiopaque
involucrum.

Rare type seen in infants maxilla
• May be caused due to
perinatal,trauma, or due to
contaminated nipples or finger in
mouth, it is also believed to occur
by hematogenous route
(streptococcus).
• May have sudden onset with high
fever, rapid pulse, vomiting,
delirium, and prostration.

i. Chronic Focal Sclerosing Osteomyelitis
ii. Chronic Diffuse Sclerosing Osteomyelitis
2 ) Chronic Focal Sclerosing Osteomyelitis

• Usually due to high tissue
resistance or low grade
infection.
• Mandibular 1st
molar is most
common.
• Radiograph shows well-
circumscribed radio opaque
mass of sclerotic bone
surrounding and extending
below one or both roots.
• Should differentiate from
benign cementoblastoma.

• Proliferative reaction of bone to a
low grade infection.
• Older age group, especially in the
edentulous mandible.
• More in blacks, especially females.
• On occasion there may be acute
exacerbation and mild suppuration.
• Radiologically mimics pagets
disease ‘cotton wool’ appearance.
• mosaic pattern’, indicating
repeated periods of resorption and
repair.
• Trebaculae are bordered by active
layer of osteoblasts and
inflammatory infiltrate.

• Described by Carl Garre in 1893.
• Focal gross thickening of
periosteum of bone, with
peripheral reactive bone
formation.
• Almost always in children or
young adults.
• Mandible is commonly involved.
• Radiograph-- duplication of
cortical layer.
• ‘onion skin’ appearance.

• Term was common in pre antibiotic era.
• After many years of chronic phase the original
cortex is lost, there is much subperiosteal new
bone and even hypercementosis of involved teeth
resembles pagets disease.
• There is recurrent flares of infection.

In radiograph
• blurring of corticomedullary bone border,
• obliteration of marrow spaces and
• poor remodeling of the external contour of the bone.
Here one should wait until the infected bone has
completely separated and ward off by granulation
tissue and then remove, in order to avoid the risk of
infecting adjacent sclerotic bone and starting a fresh
cycle.

Syphilitic osteomyelitis of the
palate. The gummatous destruction
has produced a palatal perforation.
Radiograph :The perforation which
is the site of gumma of the hard
palate produces a radiolucency
which may be mistaken for a
median palatine cyst.

•Usually hematogenous spread when blood borne bacilli lodge in cancellous
bone.
•May also spread to bone by direct inoculation of bacilli into oral mucosa
due to an ulcer or via a tooth socket.
•The typical reddened abscess with no raise in local temperature occur i.e.
‘cold abscess’.
•The lesion is located centrally.
•The patient present only with swelling and no draining sinus, mimics
parotid swelling this is called ‘lumpy jaw’
•"worm eaten“appearance
•Spiral CT showing osteolytic lesions of the mandible with bony
fragmentation and surrounding soft tissue abscess with right submandibular
lymphadenopathy.

Drugs Regime
Intensive
Treatment
Isoniazid
Rifampicin
Ethambutol
Pyrizinami
de
300mg/day-4 months
15mg/kg body wt-4 months
25mg/kg-2months
later15mg/kg
5-15g/day-4 months
Continuati-
on phase
Isoniazid
Rifampicin
Ciprofoxac
in
300mg/day-4 months
15mg/kg body wt-4 months

Panoramic radiograph showing
ill-defined lytic area extending
posterioinferiorly from primary
right first molar to permanent
right first molar.
FNAC showing
granulomatous areas with
characteristic Langhans’
giant cells and epitheloid
cells surrounded by
lymphocytes and plasma
cells.

• A. Israeli.
• Jaws are involved in cervicofacial type, especially
mandible.
• Clinically soft or firm tissue masses on the skin,
which are purplish, dark red, oily with small zones
of fluctuations.
• Spontaneous drainage of serous fluid containing
yellowish granular material called ‘sulphur
granules’ which represent colonies of bacteria.

• Radiographicaly mandible is thickened and
‘honey combed’ by narrow tracts in
granulation tissue.
• Penicillin is the drug of choice
• Treatment: Penicillin G,10-20 million
units/day IV for 4-6 weeks, followed by
Penicillin V, 1g 4 times/day for 6-12
months.
• OR
• Ampicillin 50mg/kg/day IV for 4-6 weeks,
then Amoxicillin 500mg 3 times/day for 6-
12 months.
• Allergic to penicillin----- Doxycycline
100mg BD/day for 6 months.

Differential diagnosis
Osteogenic sarcoma
• Permeative lesion borders,
• stippled bone pattern,
• destruction of Cortical
outlines,
• perpendicular spiculations
of periosteal new bone,
• destruction of lamina dura,
• and widening of the entire
periodontal ligament space

Fibrous dysplasia
• Superior displacement of
the mandibular canal and
• In the absence of these
findings,
• displacement of the sinus
cortex,
• alteration of the lamina
dura to the abnormal bone
pattern, and
• narrowing of the
periodontal ligament space

Histopathology :
• Blood and aspirate culture.
• FNAC (infants.)
• Samples for culture should be taken from infected
cavity wall, sequestrum, granulation tissue,
involucrum and sinus tract (misleading).
• Organism can be identified and tested for antibiotic
sensitivity.
• In acute form there will be elevated PMN cells.
• But in chronic form some times may be culture –ve
and show only plasma cells and lymphocytes.
• Distinctive histology may be seen in M.Tuberculosis
infection, like caseation and granulomatous lesion.

Blood Tests:
• In acute presentations there is raised white cell
count (PMNs), C- reactive protein and ESR.
The Erythrocyte Sedimentation Rate (ESR): When
inflammation is present in the body, proteins are
produced by the liver and the immune system .
increased presence of these proteins will cause red
blood cells to stick together in solution
,sedimentation rate is increased. many possible
causes of an elevated sedimentation rate, this
blood test is done with other tests to confirm a
diagnosis such as a chronic osteomyelitis.

C-reactive protein (CRP): “acute-phase protein” synthesized
by the liver. as an early defense system against infection.
It is a protein found in the blood, the levels of which rise
in response to inflammation due to trauma, infection or
serious illnesses.
In chronic phase there will be modestly raise in CRP, but
ESR is often very high.

• Nearly 30-60 % of mineral loss is required for
significant radiographic changes.
• The full extent of bone destruction cannot be
determined radiographicaly until 3 weeks after
initiation of osteomyelitic process.
• Radiographic process lag behind the actual
clinical situation.

•Takes 3 weeks to develop.
•So in acute osteomyelitis there is no much changes seen in
plain x-rays, except for some times the individual trabaculae
become fuzzy and indistinct.
•Well established osteomyelitis can be identified in radiographs
by criteria given by Worth in 1969:

• Scattered areas of bone destruction,
separated by variable distances. The
appearance is one of increased
radiolucency, which may be uniform
or patchy.
• “moth–eaten” appearance, because of
enlargement of medullary spaces and
widening of Volkmann's canals.
• Bone destruction of varied extent in
which there are ‘sequestra’ with a
trabecular pattern and marrow spaces.
• A sheath of new bone, ‘involucrum’,
is often found separated from
sequestra by a zone of radiolucency.

• Can identify collection of
fluid (pus) in the soft
tissues and adjacent to
bones can also be used
for ultrasound guided
aspiration.
• Scintigraphy using 99m
Tc methylene
diphosphonate can be
done.
• PET scan can be done
using radioisotopes like
gallium or indium-
labeled white cells which
is less sensitive but more
specific.

• useful in determining the presence of reactive bone,
thus it is helpful in the diagnosis of bone diseases.
• (Tc99m) labeled diphosphonates are given
intravenously--- accumulates in areas of increased
osteoblasts activity (reactive new bone formation and
increased blood flow).
The images obtained are
• immediate (flow),
• 15 minute (blood pooling), and
• 4 hour (bone imaging)
• osteomyelitis results in intense uptake in all 3 phases.
for acute osteomyelitis --almost 95% and findings
generally are positive in 2-3 days of infection
Three-phase bone scanThree-phase bone scan

In--uses white blood cells labeled with radioactive
indium as the tracer.
• used for the diagnosis of osteomyelitis at sites of
fracture nonunion.
• Scintigraphy cannot distinguish between reactive
bone associated with osteomyelitis and that seen in
conditions as fibrous dysplasia.
• Here the patient’s own W.B.C are labeled in vitro
and reinjected. Imaging is performed 8 to 24hrs after
the injection, during which time. It is the most
sensitive test and specific test for infections.

• Gallium citrate scanning an analog of calcium and
iron and attaches to transferrin to accumulate at
sites of inflammation.
• Dual tracer scans --examinations combine an
inflammation imaging tracer (indium or gallium)
with an "anatomic" tracer (either technetium bone
scan or technetium sulfur colloid marrow scan),
with images being collected either sequentially or
simultaneously.

• Magnetic resonance imaging (MRI) is able to
depict the bone marrow inflammation itself.
Therefore, it has been described to be of value in
defining the extent of the inflammatory process and
in distinguishing OM from cellulitis.
• CT scan: accurate for detecting cortical destruction,
intraosseous gas, periosteal reaction, and soft tissue
extension.

• (A) Defect in the trabecular bone
(arrow).
• (B) Osteosclerosis (arrow) and
thickening of cortical bone
(arrowhead).
• (C) Defect in the cortical bone
(white arrow), periosteal reaction
(white arrowhead) and
osteosclerosis (black arrow).
• (D) Sequestrum (arrow) and
thickening of the cortical bone
(arrowhead).
• (E) Periosteal reaction
(arrowhead) and defects of the
cortical bone (arrows).
• (F) Change in the bone width
(between arrows)Dentomaxillofacial Radiology (2005)
34, 86-90

• Image hard tissues in the maxillofacial region.
• capable of providing images of <0.5mm resolution that
are of high diagnostic quality, with shorter scanning
times (10–70 s).
• and considerably lower doses of radiation than
conventional CT.
• Three-dimensional volumetric surface reconstructions
showing the topography of the osteomyelitic defect
used to plan the resection.
preoperatively planned resection borders (dotted lines)
were calculated by reference to the extent of the lesion
measured from axial and cross-sectional images.

A. Conservative
B. Surgical

• Supportive therapy- e.g. nutrition.
• Blood transfusion- if anemic.
• Control of pain- using analgesics and sedatives.
• Antimicrobial agents.
CONSERVATIVE MANAGEMENTCONSERVATIVE MANAGEMENT::

• Penicillin remains the time- honoured antibiotic
of choice for osteomyelitis.
• Initially gram stain guided empirical therapy is
started usually with penicillin.
• Then after obtaining culture and sensitivity report
specific therapy is started.

Regime 1: for hospitalized/medically compromised patient IV is
given:
when improved for 48-72 hrs switch to
OR
 when improved for 48-72 hrs switch to
ANTIBIOTIC TREATMENT:ANTIBIOTIC TREATMENT:
Aqueous penicillin 2million U (IV) + metronidazole 500mg 6hrly
Penicillin V 500mg 4hrly po+ metronidazole 500mg 6hrly orally,Penicillin V 500mg 4hrly po+ metronidazole 500mg 6hrly orally,
for additional 4-6 weeksfor additional 4-6 weeks
Ampicillin /sulbactam 1.5-3g I V 6hrlyAmpicillin /sulbactam 1.5-3g I V 6hrly
Amoxacillin/cluvalinic acid (Augmentin) 875/125 mgAmoxacillin/cluvalinic acid (Augmentin) 875/125 mg
Orally bid for additional 4-6 weeksOrally bid for additional 4-6 weeks

Clindamycin ,Cefoxitin
OR
OR
until no symptoms then switch to
Regime 2: For out patient treatment
Clindamycin 600-900mg 6hrly IV ThenClindamycin 600-900mg 6hrly IV Then
Clindamycin 300-450mg 6hrly orallyClindamycin 300-450mg 6hrly orally
Cefoxitin(Mefoxin) 1g 8hrly IV Or 2g 4hrly IM Or IVCefoxitin(Mefoxin) 1g 8hrly IV Or 2g 4hrly IM Or IV
Cephalexin (keflex) 500mg 6hrly orally, for 2-4 weeksCephalexin (keflex) 500mg 6hrly orally, for 2-4 weeks
Penicillin V 2g + metronidazole 0.5g 8hrlyPenicillin V 2g + metronidazole 0.5g 8hrly
orally for 2-4 weeksorally for 2-4 weeks

• Closed wound irrigation-suction:
Antibiotic in high concentrations placed in direct
contact with bone manually or implantable pump.
Neosporin --- 1% with 0.1% polymyxin B in
equal volume installed on 12 hr cycle.
• Antibiotic-impregnated beads:
After decortication Tobramycin or Gentamycin
contained in acrylic resin bone cement beads left in
place for 10-14 days & then removed
Clindamycin is effective against streptococci &
oral anaerobes can also be used with
methylmethacrylate.
Local antibiotic therapyLocal antibiotic therapy::

• Intra – arterial antibiotic
therapy.
• Local implantation of
antibiotic – saturated
beads.
• HBO therapy.

1. Incision and drainage:
• Incisions made intra orally or extra orally depending
upon location.
• In patients with compromised systemic conditions or
toxemia, surgical interference may be post- poned for
2-3 days.
2. Extraction of loose or offending teeth :
3. Debridement :
• Following incision and drainage thorough debridement
should be done and irrigation with hydrogen peroxide
and saline should be done.

4. Decortication :
• Obwegesser (1960) advocated this method,
which include removal of chronically infected
lateral and inferior cortical plates of bone 1-2
mm beyond the area of involvement, to gain
access to Medullary cavity.

5. Sequestrectomy :
• Sequestra are usually :
a. Cortical
b. Cancellous
c. Cortico-cancellous
• The Seqeustrum for operative purpose can be
classified as :
i. Small and accessible – intra oral approach.
ii. Large and inaccessible – extra oral approach.

6. Saucerization :
• Excision of margins of necrotic bone.
• Permits visualization and removal of formed and
forming sequestra.
• Also smoothen the surface for better soft tissue
adaptation avoiding creation of dead space.

7. Continuous or intermittent indwelling closed
catheter irrigation:
• After sequestrectomy or decortication, 2
polyethylene chain tubes, 3-4 mm in diameter and
6-10 inches long are placed through a separate
incision.
• One tube is attached to a low pressure suction to
allow drainage of pus.
• Another is kept patent to provide irrigation and
local antibiotic administration.
• Daily, first saline irrigation followed by antibiotic
instillation should be performed until – ve culture
are obtained.

8. Trephination or fenestration :
• Bony hole or windows are made adjacent to the
infectious process for tissue ammoniation and
decompression of the medullary compartment.
9. Resection :
• When extensive involvement of bone is seen.
• Can choose various techniques like
hemimandibulectomy, segmental resection etc,
according to the extent of bone to be removed.

10. Immediate and/or delayed reconstruction:
• Is advocated to maintain the continuity of the
fragments.
• To prevent pathological fracture.
• To prevent deformity.
• To provide attachment of soft tissue.

• Short term -100% oxygen inhalation therapy at a pressure
greater than that of sea level. The pressure is usually
about 2.4 absolute atmospheres or ATA.
• Given as adjuncts for chronic Suppurative and chronic
sclerosing osteomyelitis
• 5 days per week 30, 60 or more dive in monophase
chamber inhalation of 100% Humidified O2 under
pressure at 2.4 ATA for 90mins.
• Each dive is 90 minutes in length

1. Enhancement of lysosomal degradation potential of
polymorphoneuclear leucocytes and O2 radicals.
2. Free radicals of O2 radicals are toxic to many
pathogenic anaerobes.
3. Many exotoxins liberated by microorganisms are
rendered inert by exposure to elevated partial pressure
of O2.
4. Tissue hypoxia is intermittently reversed, mimicking
tissue level during wound healing.
5. Positive enhancement of neoangiogenesis, in the
aerobic portion of proliferative phase of wound
healing.

• Decompression sickness
• Elective surgery to prevent clinical radiation
necrosis
• Treatment of osteoradionecrosis
• Non healing diabetic ulcers

• Partial reversal of 3-H tissue
• physical mechanism
• dissolution of oxygen into blood
• 80-100 mm Hg range to 1000-1200 mm Hg
• HBO elevates the PAO2
• irrespective of hemoglobin
• O2 gradients -radiated tissue from 50 to 250 mm Hg-macrophage
activity
• HBO inhibits inflammation through direct bactericidal effects on
anaerobes due to increased production of free radical and toxic products
• HBO enhances phagocytic killing by WBC (Parl 1994)
• Angiogenic and fibroblastic effects- collagen synthesis crucially
depends on the availability of molecular O2 that incorporates into a
peptide chain to form hydroxyl propyl and hydroxyl lysyl residues.

Protocol of hyperbaric oxygen for elective
surgery.
• 20 sessions of hyperbaric oxygen prior to elective surgery,
followed by 10 sessions after surgery
• 100% oxygen at 2.4 atmospheric pressure or ATA for 90
treatment minutes
• single person chambers 120 treatment minutes
• The elective surgery protocol is used in all elective surgery in
radiated tissue, which may range from tooth extraction, to bone
graft reconstruction to vascularized pedicled and free anatomic
transfers
• effects of hyperbaric oxygen are permanent,

Contraindications: by HBO committee of the
Undersea Medical Society (1988) & Marx (1985)
-Pnemothorax
-Optic neuritis
-Acute viral infections
-Acute Seizures
-Uncontrolled high fever.
-Malignancy.
-H/o Ear or thoracic surgery.

Potential Complications: [Gabb & Robbin 1987]
-Rupture of tympanic membrane.
-O2 Toxicity.
-Eustachian tube dysfunction.
-Pnemothorax.
-Arterial gas embolism.
-Middle ear hemorrhage.
-Deafness.
-Equipment malfunction.

Osteoradionecrosis
• >50Gy radiation kills bone cells
• Nonhealing hypoxic wound
• c/f: trismus fetiod odor, >temp,
• Exposed bone –grey or yellow color
• Fistula
• Pathological #
• Treatment: antibiotics, irrigation, debride

• Most serious complication of radiation therapy.
• Probably the first evidence of ORN related to radiotherapy was
reported by Regaud in 1922
• Its pathology was further described by Ewing in 1926, under
the name ‘radiation osteitis’
• Meyer classified ORN as one special type of osteomyelitis.
• Titterington also related ORN to osteomyelitis, providing one
of its first definitions, and used the term ‘osteomyelitis of
irradiated bone’
• Marx defined it as ‘an area greater than 1 cm of exposed bone
in a field of irradiation that had failed to show any evidence of
healing for at least 6 months’. He also clarified that in ORN
there is no intersticial infection, but only superficial
contamination

• An exposure of irradiated bone which fails to heal
with out intervention (Marx 1983)
• It is a chronic nonhealing wound caused by
hypoxia, hypocellularity, and hypovascularity of
irradiated tissue. Marx and Johnson (1987)
• Clinical definition by Van Merkesteyn (1995)
Bone and soft tissue necrosis of 6 months
duration excluding radiation induced periodontal
breakdown

• Before 1960 orthovoltage -ORN ranging from 17%-37%
• megavoltage therapy is bone sparing.
• Incidence ranges from upto 10%. When the level of
radiation is less than 60 Gy.
• By Reuther et al the incidence was found to be 8.2% in
population of 830 individuals investigated for over a
period of 30 years
• Mandible is affected more commonly; because most oral
tumors are peri mandibular. More extensive blood
supply in maxilla
• Incidence thought to be less after hyperfractionated
radiotheryapy at 72-80 Gy or moderately accelerated
fractionized radiotherapy of 64-72 Gy.

Radiation beam
Field effect
•greater -central beam
•tapers off -outward
•resemble a target
•center -most affected
•Healing -reduced or absent

1. The affected site should have been previously irradiated;
2. There should be absence of recurrent tumour on the
affected site;
3. Mucosal breakdown or failure to heal should occur,
resulting in bone exposure (except in cases of bones that
lie within thick soft tissue integument’s, such as the
pelvis or femur, or rarely in cases of a pathological
fracture of the mandible after irradiation);
4. The overlying bone should be ‘dead’, usually due to a
hypoxic necrosis;
5. Cellulitis, fistulation, or pathologic fracture need not be
present to be considered ORN

• Bone exposure resulting from tumor necrosis where tumor
death results in a loss of soft tissue coverage.
• bone exposure at the site of tumor during or within a
week of radiotherapy
• Bone exposure as a consequence of tumor recurrence.
• In all cases surgical resection was undertaken –tumor
recurrence
• Bone exposure resultant from oral surgical or dental
interventions.
• Extractions sites. Persistent bone necrosis due to denture
irritation
• Bone exposure de novo.
• no obvious source of trauma

Int J Oral Maxillofac Surg. 2003
Jun;32(3):289-95
• Osteoradionecrosis of the jaws as a side effect of
radiotherapy of head and neck tumor patients--a report of a
thirty year retrospective review
• Reuther T, Schuster T, Mende U, Kubler A.
• Retrospective 830 pts
• Incidence 8.2%
• 3 fold higher in Men
• Body of mandible
• Extraction -50%
• Presurgical earlier ORN
• Combined radio and chemo

• Acording to Myers: It is caused due to infection following trauma to jaws
after radiation therapy.
This hypothesis is no longer accepted.
• According to Marx: It is characterised By 3-H.
Radiation
Tissue death due to direct Irreversible cellular
Radiation change dysfuntion
HYPOCELLULARITY Damage to bone vascular
damage
tissue components
Tissue Break down endarteritis and
thrombosis
HYPOXIA, HYPOVASCULARITY
Osteoradionecrosis
Loss of
reparative
function

British Journal of Oral and Maxillofacial Surgery 46 (2008) 653–660
Radiation
generation of ROS
Injured endothelial cells cytokine fibroblasts
Vascular thrombosis atypical myofibroblasts
irreversible DNA Damage
Tissue loss fragile paucicellular cellular fibrosis
replacement
Trauma osteoradionecrosis

• Staging according to MARX:
Stage I: Superificial osteoradionecrosis that resolve with irrigation and
HBO
Stage II: Progressive lesions that Doesn’t heal with Stage I treatment
Stage III: Presence of fistulae, pathological fracture or resorption
Stage III R: Phase of Early reconstruction after 10 weeks of resection.
• Store and Boysen’s classification of mandibular ORN.
Stage Criteria
0 Mucosal defects only
I Radiological evidence of necrotic bone with intact mucosa
II Positive radiographic findings with denuded bone intraorally
III Clinically exposed radionecrotic bone, verified by imaging
techniques, along with skin fistulas and infection
• HEAD & NECK—DOI 10.1002/hed November 2011

Precipitating factors
• Triad
Concept challenged by Gowgiel. Approximately one third of
ORN occur spontaneously.
INFECTION

Microbiology
• Cultures streptococci, Candida spp., and gram
negative organisms.
• When skin is affected S. aureus and S.epidermidis.
• No organisms are found deep in bone.
• Radiation predisposes to actinomycotic infection;
because is favorable environment for microorganism
to flourish due to bone tissue alteration

CLINICAL FEATURES
• Within two years
• Asymptomatic dehiscence of mucosa
• Glabrous skin
• As necrosis progresses site more erythematous
and severe, deep burning pain
• Evidence of exposed bone

• Tissue surrounding may be ulcerated from infection
or recurrent tumor.
• Trismus
• Fetid breath
• Elevated temperature
• Exposed bone with a grey to yellow color
• Intraoral and extra oral fistula
• Pathological fracture

Radiographic changes
• Little-evident
• sequestra or involucra occur late
• radiolucent modeling -nonsclerotic
• Nuclear isotope technetium 99 methylene
diphosphonate
• Bony algorithm high resolution CT

Histologically
• look like MICROANATOMIC DESERT
• Reduced vascularity, fibrosis
• Diagnosis of osteoradionecrosis should focus primarily on
ruling out recurrent or metastatic disease. Therefore is
diagnosis of exclusion

Prevention of ORN:
• Through dental Check up
• Through oral prophylaxis
• Extraction of teeth with poor prognosis
• Complete healing of extraction sockets prior to radiation
• Restoration of teeth as required
• Meticulous oral hygiene maintanence
• Correction of any systemic medical disorder
• All invasive and extraction procedures to be avoided for a
period of 3 months post radiation therapy

Post irradiation care
• Dentures should not be used for one year
• Good oral hygiene maintenance
• Fluoride therapy
• Saliva substitute to prevent dry mouth
• Pulpitis- endodontic therapy
• Atraumatic extractions –no flap or linear closure
• Local anesthetic without adrenaline should be used
• Antibiotic should be administered

Management of osteoradionecrosis
• Aim - To control frank infection
• Antibiotics
• Penicllin plus metronidazole or clindamycin
• Supportive therapy with fluids
• Pulsating irrigation device can be used. High pressure
should not be used debris might be forced deeply into
tissues
• Exposed bone can be mechanically debrided and
smoothed with round burs and covered with a pack
saturated with zinc peroxide and neomycin

Conservative management of osteoradionecrosis
J K Wong, R E Wood, Mc Lean
Triple O 1997; 84:16-21
• local irrigation (saline solution, NaHCO3, or
chlorhexidine), systemic antibiotics in acute infectious
episodes, avoidance or irritants and oral hygiene
instruction.
• Simple management refers to the gentle removal of
sequestra in sequestrating lesions
• Had 48% success rates

Treatment of osteonecrotic wounds
• Rule out neoplastic disease
• Stabilize the patient medically especially nutritional
status
• Preoperative hyperbaric oxygen
• Debridement of necrotic mass
• Postoperative hyperbaric oxygen
• Soft tissue vascular flap support
• Bony reconstruction

Ultra sound therapy
• Is non invasive and reportedly promotes neovascularity
and neocellularity of ischemic tissues

Major healing of refractory mandible osteoradionecrosis after
treatment combining pentoxifylline and tocopherol: a phase II trial.
Head Neck. 2005 Feb;27(2):114-23.
Delanian S, Depondt J, Lefaix JL
• Effective in reversing fibronecrotic process
• Eighteen patients
• a daily oral combination of 800 mg of PTX and 1000 IU of
vitamin E for 6 to 24 months
• In addition, the last eight patients who were the worst cases
were given 1600 mg/day clodronate 5 days
• at 6 months, with 84% healing

• Bedwinek et.al T3 AND T4 lesions - more prone
• higher tissue destruction, larger treatment volume. No necrosis
if 50-60Gy used
• Low dosing brachytherapy higher ORN, secondary to decay
profile of a combination of mix of alpha, beta and gamma
particle spin off.

Stage I
30 x (100% O2 for 90 mins at 2.4 ATA)
Examine exposed bone
No surgery cutaneous fistula
No antibiotics
Rinsing only pathologic fracture
resorption of Inferior border
of mandible
Response
no response
10x (100% O2 for
90 mins at 2.4 ATA)
Stage I responder
Stage II
Stage III

Stage II
Surgery maintain inferior border
10x (100% O2 for 90 mins at 2.4 ATA)
Response no response
Stage II responder
Healing with out
exposed bone
stage III
Excision of nonviable bone
Fixation of mandibular segments 10x
(100% O2 for 90 mins at 2.4 ATA)
Reconstruction after
three monthsNo HBO Required

REFERENCES
• Oral and Maxillofacial infections – Topazian
• Burkets Oral Medicine Diagnosis And Treatment
• A text book of Oral Pathology – Shafer
• Oral and maxillofacial surgery by Daniel M Laskin.
• Oral and maxillofacial Pathology(neville)