Osteomyelitis

• Dr asmaa s

• (PATHOGENESIS & MANAGEMENT)

•

• WHAT IS OSTEOMYELITIS

• FACTORS PREDISPOSING TO OSTEOMYELITIS

• PATHOGENESIS OF OSTEOMYELITIS

• TYPES OF OSTEOMYELITIS

• PATHOGENESIS
• CLINICAL FEATURES
• HISTOLOGY
• RADIOLOGY
• MANAGEMENT

• I. Suppurative osteomyelitis:

• Acute suppurative osteomyelitis
• Chronic suppurative osteomyelitis

• Nonsuppurative osteomyelitis

• Chronic focal sclerosing osteomyelitis
• Chronic diffuse sclerosing osteomyelitis
• Garre's chronic sclerosing osteomyelitis (proliferative osteomyelitis)


• III. Osteoradionecrosis /Radio osteomyelitis

• OSTEOMYELITIS

• WHAT’S IN THE NAME?

• The word “osteomyelitis” originates from the ancient Greek words osteon (bone) and muelinos (marrow)
• and literally means infection of medullary portion of the bone.

WHAT IS IT?

• It is an acute & chronic inflammatory process in the medullary spaces or cortical surfaces of bone that extends away from the initial site of involvement.

• FACTORS PREDISPOSING TO OSTEOMYELITIS

• LOCAL FACTORS

• (decreased vascularity/vitality of bone)

• Trauma. Radiation injury. Paget’s disease.

• Osteoporosis. Major vessel disease.
• SYSTEMIC FACTORS
(impaired host defense)

• Immune deficiency states.

• Immunosuppression Diabetes mellitus.
• Malnutrition. Extremes of age.

• PATHOGENESIS OF OSTEOMYELITIS

• Inflammatory process of entire bone including cortex & periosteum, not just confined to endosteum

• Inflammatory condition beginning in medullary cavity & havarsian system & extending to involve periosteum of affected area
• Local factors decreases the vitality of bone Systemic conditions comprises the defense system of the host


(IV) PATHOLOGY

• Acute inflammation of marrow tissues

• Spread of exudate along the marrow spaces

• Thrombosis of vessels due to compression

• Necrosis of bone

• Liquefaction of necrotic tissues

• Lifting of periosteum causing further necrosis

• Finally ,Osteoclastic activity >>> SEQUESTRUM

• TYPES OF OSTEOMYELITIS

• SUPPURATIVE OSTEOMYELITIS

• FOCAL SCLEROSING OSTEOMYELITIS

• DIFFUSE SCLEROSING OSTEOMYELITIS

• PROLIFERATIVE PERIOSTITIS

• ONSET OF DISEASE
• 4 WEEKS
Acute suppurative
osteomyelitis
• Chronic suppurative osteomyelitis
• t
• Onset of disease
• Deep bacterial invasion into medullary & cortical bone

• SUPPURATIVE OSTEOMYELITIS

• SUPPURATIVE OSTEOMYELITIS













• Source of infection is usually an 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 a 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

• Organisms entry into the jaw, mostly mandible, compromising the vascular supply
• Medullary infection spreads through marrow spaces

• Thrombosis in vessels leading to extensive necrosis of bone

• Lacunae empty of osteocytes but filled with pus , proliferate in the dead tissue

• Suppurative inflammation extend through the cortical bone to involve the periosteum

Stripping of periosteum comprises blood supply to cortical plate, predispose to
• further bone necrosis

Sequestrum is formed bathed in pus, separated from surrounding vital bone

• ACUTE SUPPURATIVE OSTEOMYELITIS
CLINICAL FEATURES
• EARLY :
• Severe throbbing, deep- seated pain.
• Swelling due to inflammatory
• edema.
• Gingiva appears red, swollen & tender.

• LATE :

• Distension of periosteum with pus.

• FINAL:

• Subperiosteal bone formation cause swelling to become firm.

• HISTOLOGY

• Submitted material for biopsy predominantly consists of necrotic bone & is diagnosed as sequestrum

• Bone shows:

• Loss of osteocytes from
• lacunae.
• Peripheral resorption.
• Bacterial colonization.
• Acute inflammatory infiltrate consisting of polymorphonuclear leukocytes in haversian canals & peripheral bone.
• ACUTE SUPPURATIVE OSTEOMYELITIS

• ACUTE SUPPURATIVE OSTEOMYELITIS

• After sufficient bone resorption irregular, mot- eaten areas of radiolucency may appear.

• 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.

• MANAGEMENT
• ACUTE SUPPURATIVE OSTEOMYELITIS

• ESSENTIAL MEASURES

• Bacterial sampling & culture.
• Emperical antibiotic treatment.
• Drainage.
• Analgesics.
• Specific antibiotics based on culture & sensitivity.
• Debridement.

• Remove source of infection, if possible.

• ADJUNCTIVE TREATMENT

• Sequestrectomy.
• Decortication (if necessary)
• Hyperbaric oxygen.
• Resection & reconstruction for
• extensive bone destruction.

• ACUTE SUPPURATIVE OSTEOMYELITIS

• COMPLICATIONS
• Rare but include:
• Pathological fracture
• Extensive bone destruction.
• Chronic osteomyelitis Inadequate treatment.

• Cellulitis Spread of virulent bacteria.

• Septicemia Immuno-compromised patient.

• CHRONIC SUPPURATIVE OSTEOMYELITIS

• Inadequate treatment of acute osteomyelitis
• Periodontal diseases
• Pulpal infections
• Extraction wounds
• Infected fractures


• Infection in the medulllary spaces spread and form granulation tissue

• Granulation tissue forms dense scar to wall off the infected area

• Encircled dead space acts as a reserviour for bacteria & antibiotics have great difficulty reaching the site

• CHRONIC SUPPURATIVE OSTEOMYELITIS

• CLINICAL FEATURES

• Swelling

• Pain

• Sinus formation Purulent discharge Sequestrum formation Tooth loss

• Pathologic fracture

• CHRONIC SUPPURATIVE OSTEOMYELITIS

• HISTOLOGY

• Inflammed connective tissue filling inter-trabecular areas of bone.
• Scattered sequestra. Pockets of abscess.

• CHRONIC SUPPURATIVE OSTEOMYELITIS

• 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.

• CHRONIC SUPPURATIVE OSTEOMYELITIS

MANAGEMENT

• Difficult to manage medically.
• Surgical intervention is mandatory, depends on spread of process.
• Antibiotics are same as in acute condition but are given through IV in high doses.
• SMALL LESIONS
• Curretage, removal of necrotic bone and decortication are sufficient.

• EXTENSIVE OSTEOMYELITIS

• Decortication combined with transplantation of cancellous bone chips.

• PERSISTANT OSTEOMYELITIS

• Resection of diseased bone followed by immediate reconstruction with an autologous graft is required.
• Weakened jawbones must be immobilized.

• FOCAL SCLEROSING OSTEOMYELITIS

• Also known as “Condensing osteitis”.

• Localized areas of bone sclerosis.

• Bony reaction to low-grade peri-apical infection or unusually strong host defensive response.

• Association with an area of inflammation is critical.

• FOCAL SCLEROSING OSTEOMYELITIS

• CLINICAL FEATURES

• Children & young adults are affected.

• In mandible, premolar & molar regions are affected.

• Bone sclerosis is associated with non-vital or pulpitic tooth.

• No expansion of the jaw.

• HISTOLOGY
• Dense sclerotic bone. Scanty connective tissue. Inflammatory cells.

• FOCAL SCLEROSING OSTEOMYELITIS

• 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 nonvital mandibular first molar

• MANAGEMENT

• Elimination of the source of inflammation by extraction or endodontic treatment.


• If lesion persists and periodontal membrane remains wide, reevaluation of endodontic therapy is considered.

• After resolution of lesion, inflammatory focus is termed as bone scar.

• FOCAL SCLEROSING OSTEOMYELITIS

• 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 inflammed granulation tissue.

• DIFFUSE SCLEROSING OSTEOMYELITIS

• CLINICAL FEATURES

• Arises exclusively in adult-hood with no sex pre-dominance.
• Primarily occurs in mandible. No pain.
• No swelling.

• HISTOLOGY

• Bone sclerosis and remodling. Scanty marrow spaces.
• Necrotic bone separates from vital bone & become surrounded by granulation tissue. Secondary bacterial colonization often is visible.




• RADIOLOGY

Increased radiodensity may be seen surrounding areas of lesion.

• DIFFUSE SCLEROSING OSTEOMYELITIS

• Diffuse area of increased radiodensity of Rt. Side of mandible

• MANAGEMENT

• Elimination of originating sources of inflammation
• via extraction & endodontic treatment.


• Sclerotic area remain radiographically.
• DIFFUSE SCLEROSING OSTEOMYELITIS

• 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 of altered bone.

PATHOGENESIS

• The spread of low-grade, chronic apical inflammation through cortical bone

Periosteal reaction occurs

Stimulates proliferative reaction of periosteum

• PROLIFERATIVE PERIOSTITIS

• CLINICAL FEATURES

• Affected patients are primarily children & young adults.
• Incidence is mean age of 13 years. No sex predominance is noted.
• Most cases arise in the premolar & molar area of mandible.

• Hyperplasia is located most commonly along lower border of mandible.

• Most cases are uni-focal, multiple quadrants may be affected.

• PROLIFERATIVE PERIOSTITIS

• HISTOLOGY

• Parallel rows of highly cellular
• & reactive woven bone .

• Trabeculae are frequently oriented perpendicular to surface.

• Trabeculae sometimes form an interconnecting meshwork of bone.

• Between trabeculae, uninflammed fibrous tissue is evident.

• PROLIFERATIVE PERIOSTITIS

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.

• PROLIFERATIVE PERIOSTITIS

• MANAGEMENT

• Removal of infection.

• After infection has resolved, layers of bone will consolidate in 6-12 months .

• QUESTIONS
• WHY IS MANDIBLE MORE PRONE TO OSTEOMYELITIS THAN MAXILLA?


• WHY RADIOGRAPHIC FEATURES IN ACUTE SUPPURATIVE OSTEOMYELITIS APPEAR AFTER 10- 14 DAYS OF DISEASE?

• REFRENCES:

• J.V. SOAMS 4TH EDITION.
• NEVILLE & DAM 3RD EDITION.
• R.A. CAWSON 8TH EDITION.
• GOOGLE FOR IMAGES.