Submitted to:--Dr.

Geeta Kalra
(H.O.D of department of oral
and maxillofacial surgery)
Osteomyelitis Of Jaws Presented By: Anuradha
B.D.S final year
 INDEX
• WHAT IS OSTEOMYELITIS.
• FACTORS PREDISPOSING TO OSTEOMYELITIS.
• PATHOGENESIS OF OSTEOMYELITIS.
• TYPES OF OSTEOMYELITIS.

❑ PATHOGENESIS
❑ CLINICAL FEATURES
❑ HISTOLOGY
❑ RADIOLOGY
❑ MANAGEMENT
 OSTEOMYELITIS
INTRODUCTION
❖ OSTEOMYELITIS is an acute & chronic
inflammatory process in the medullary spaces
or cortical surfaces of bone that extends away
from the initial site of involvement.

❖ Osteomyelitis of the jaws is basically

a infection and inflammation of the bone
marrow , sometimes abbreviated to OM that
occurs in jaws.
 Factors predisposing to
osteomyelitis.
❑ LOCAL FACTORS ❑SYSTEMIC FACTORS
1. TRAUMA. 1. IMMUNE DEFICIENCY STATES.
2. RADIATION INJURY. 2. IMMUNOSUPPRESSION.
3. PAGET'S DISEASE. 3. DIABETES MELLITUS.
4. OSTEOPOROSIS. 4. MALNUTRITION.
5. MAJOR VESSEL DISEASE. 5. EXTREMES OF AGE.
PATHOGENESIS OF
OSTEOMYELITIS
1. Inflammatory process of entire bone
including cortex & periosteum , not just
confined to endosteum.

2. Inflammatory condition beginning in

medullary cavity & havarsian system &
extending to involve periosteum of affected
area.

3. Local factors decreases the vitality of bone.

4. Systemic conditions comprises the defense

system of the host.
 TYPES OF OSTEOMYELITIS
• SUPPURATIVE OSTEOMYELITIS.

• FOCAL SCLEROSING OSTEOMYELITIS.

• DIFFUSE SCLEROSING OSTEOMYELITIS.

• PROLIFERATIVE PERIOSTITIS.
SUPPURATIVE OSTEOMYELITIS
• Source of infection- Usually adjacent focus of
infection associated with teeth or with local trauma.
• It is a polymicrobial infection, predominating
anaerobes such as Bacteriods , porphyromonas or
provetella.
• Staphylococci may be cause when an open fracture
is involved.
• Mandible is more prone than maxilla as vascular
supply is readily compromised.

Cropped panoramic
radiograph of suppurative
osteomyelitis at the right
side of mandible.
 ACUTE SUPPURATIVE OSTEOMYELITIS
• Stages how acute suppurative osteomyelitis
occurs…
1. Organisms entry into the jaw, mostly mandible, compromising
the vascular supply.
2. Medullary infection spreads through marrow spaces.
3. Thrombosis in vessels leading to extensive necrosis of bone.
4. Lacunae empty of osteocytes but filled with pus, proliferate in
the dead tissue.
5. Suppurative inflammation extend through the cortical bone to
involve the periosteum.
6. Stripping of periosteum comprises blood supply to cortical plate,
predispose to further bone necrosis.
7. Sequestrum is formed bathed in pus, separated from
surrounding vital bone.
 CLINICAL FEATURES
❑EARLY:
o Severe throbbing , deep-seated pain
o Swelling due to inflammatory edema.
o Gingiva appears red , swollen & tender.

❑LATE:
• Distension of periosteum with pus.

❑FINAL:
o Subperiosteal bone formation cause
swelling to become firm.
 RADIOGRAPHIC FEATURES
• May be normal in early stages of disease.
• Do not appear until after at least 10 days.

Radiograph may demonstrate

ill-defined radiolucency.

After sufficient bone

resorption irregular, moteaten
areas of radiolucency may
appear.
 MANAGEMENT
ESSENTIAL MEASURES ADJUNCTIVE TREATMENT
• Bacterial sampling & • Sequestrectomy.
culture. • Decortication (if necessary)
• Emperical antibiotic • Hyperbaric oxygen.
treatment.
• Resection & reconstruction
• Drainage. for extensive bone
• Analgesics. destruction.
• Specific antibiotics based
on culture & sensitivity.
• Debridement.
• Remove source of
infection , if possible,
CHRONIC SUPPURATIVE OSTEOMYELITIS
• Inadequate treatment of acute osteomyelitis
• Periodontal diseases
• Pulpal infections
• Extraction wounds
• Infected fractures

✓Spread of Chronic Suppurative osteomyelitis.

1. Infections in the medullary spaces spread and form

granulation tissue.
2. Granulation tissue forms dense scar to wall off the
infected area.
3. Encircled dead space acts as a reserviour for bacteria &
antibiotics have great difficulty reaching the site.
CLINICAL FEATURES
➢Swelling
➢Pain
➢Sinus formation
➢Purulent discharge
➢Sequestrum formation
➢Tooth loss
➢Pathologic fracture
 RADIOLOGY
• Patchy, ragged & ill defined radiolucency.
• Often contains radiopaque sequestra.

• Sequestra lying close to

the peripheral sclerosis
& lower border.

• New bone formation is

evident below lower
border.
FOCAL SCLEROSING OSTEOMYELITIS
• Also known as “condensing osteitis”.
• Localized areas of one sclerosis.
• Bony reaction to low-grade peri-apical
infection or unusually strong host
defensive response.
• Association with an area of inflammation
is critical.
 CLINICAL FEATURES
1. Children & young adults are affected.
2. In mandible , premolar & molar regions are
affected.
3. Bone sclerosis is associated with non-vital
or pulpitic tooth.
4. No expansion of the jaw.
 RADIOLOGY
▪ Localized but uniform increased radiodensity related to
tooth.
▪ Widened periodontal ligament space or peri-apical area.
▪ Sometimes an adjacent radiolucent inflammatory lesion
may be present.

Increased areas of
radiodensity surrounding
apices of non-vital
mandibular first molar.
 MANAGEMENT
• Elimination of the source of inflammation
by extraction or endodontic treatment.
• If lesion persists and periodontal
membrane remains wide, re-evaluation of
endodontic therapy is considered.
• After resolution of lesion, inflammatory
focus is termed as bone scar.
DIFFUSE SCLEROSING OSTEOMYELITIS

• It is an ill-defined , highly controversial,

evolving area of dental medicine.
• Exact etiology is unknown.
• Chronic intraosseous bacterial infection creates
a smoldering mass of chronically inflamed
granulation tissue.
 CLINICAL FEATURES
1. Arises exclusively in adult-hood with
no sex pre-dominance.
2. Primarily occurs in mandible.
3. No pain.
4. No swelling.
 RADIOLOGY
• Increased radiodensity may be seen surrounding
areas of lesion.

Diffuse area of
increased radiodensity
of RT. Side of mandible
 MANAGEMENT
1. Elimination of originating sources of inflammation
via extraction & endodontic treatment.
2. Sclerotic area remain radiographically.
PROLIFERATIVE PERIOSTITIS
❖Also known as “Periostitis ossificans” & “Garee’s
osteomyelitis”.
❖It represents a periosteal reaction to the presence of
inflammation.
❖Affected periosteum forms several rows of reactive vital
bone that parallel each other & expand surface to altered
bone.
CLINICAL FEATAURES
1. Affected patients are primarily children &
young adults.
2. Incidence is mean age of 13 years.
3. No sex predominance is noted.
4. Most cases arise in the premolar & molar area
of mandible.
5. Hyperplasia is located most commonly along
lower border of mandible.
6. Most cases are uni-focal, multiple quadrants
may be affected.
 RADIOLOGY
• Radiopaque laminations of bone roughly
parallel each other underlying cortical
surface.
• Laminations may vary from 1-12 in
number.
• Radiolucent separations often are present
between new bone & original cortex,
 MANAGEMENT
❖Removal of infection.
❖After infection has resolved, layers of
bone will consolidate in 6-12 months.
SURGICAL MANAGEMENT
Incision and drainage of abscess formation
Extent of surgery

Removal of loosened teeth, foreign bodies/

implants and sequestra
Local curettage and saucerization of the
infected bone
Decortication
Resection and reconstruction
SURGICAL TECHNIQUE FOR SAUCERIZATION
• Access to the bone by creating a mucoperiosteal flap, usually using a gingival crest incision.
• Refection of flap should be as limited as possible to preserve local blood supply.
• Affected teeth (loosened and other dental foci within affected area) are extracted.
• The lateral cortex of the mandible is reduced using burs or rongeurs, until the sufficient bleeding
bone is encountered at all margins , approximately to the level of unattached mucosa, thus
producing a saucer-like defect.
• Local debrided area is thoroughly irrigated with sterile saline solution with or without additional
antibiotic such as neomycin.
• If there is substantial local bleeding due to hyperemia caused by the inflammatory process , a
medicated pack may be placed and serve as local compression device.
• The buccal flap is trimmed and a medicated pack(such as iodoform gauze lightly covered with
antibiotic and local steroid ointment is placed for hemostasis and to maintain the flap in a retracted
position. The pack is placed firmly without pressure and retained by several non-resorbable sutures,
extending over the pack from the lingual to the buccal flap.
• The pack is remained in situ for several days up to 2 weeks or even more in some instances and may
be replaced several times, until the surface of the bed of granulation tissue is epithelialized and the
margins have healed.