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🦷 ORAL PATHOLOGY - BONE PATHOLOGY

Complete Notes for 3rd Year BDS

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CLASSIFICATION OF BONE DISEASES IN ORAL PATHOLOGY

BONE PATHOLOGY
├── A. Inflammatory Diseases of Bone
│   ├── Osteitis (Dry Socket / Alveolar Osteitis)
│   ├── Acute Suppurative Osteomyelitis
│   ├── Chronic Osteomyelitis
│   │   ├── Focal Sclerosing Osteomyelitis
│   │   └── Diffuse Sclerosing Osteomyelitis
│   ├── Osteoradionecrosis
│   └── Medication-Related Osteonecrosis (MRONJ)
├── B. Benign Fibro-Osseous Lesions (BFOLs)
│   ├── Fibrous Dysplasia (Monostotic / Polystotic)
│   ├── Ossifying Fibroma
│   └── Cemento-Osseous Dysplasias
│       ├── Periapical COD
│       ├── Focal COD
│       └── Florid COD
├── C. Giant Cell Lesions of the Jaw
│   ├── Central Giant Cell Granuloma (CGCG)
│   ├── Giant Cell Tumor
│   ├── Cherubism
│   └── Hyperparathyroidism (Brown Tumor)
└── D. Metabolic / Systemic Bone Disease
    └── Paget's Disease of Bone

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PART A: INFLAMMATORY DISEASES OF BONE

1. OSTEITIS (DRY SOCKET / ALVEOLAR OSTEITIS)

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2. OSTEOMYELITIS OF THE JAWS

Definition

Etiology

• Primary cause: Odontogenic infections and jaw fractures
• In Africa: Acute necrotizing gingivitis (NOMA) is an important cause
• Organisms: Polymicrobial (oral flora); Staphylococcus aureus is most common overall

Predisposing Factors

1. Chronic systemic diseases, immunocompromised states
2. Decreased vascularity of bone
3. Tobacco use, alcohol abuse, IV drug use
4. Diabetes mellitus
5. Exanthematous fever, malaria
6. Sickle cell anemia
7. Malnutrition
8. Malignancy
9. Collagen vascular disease
10. AIDS / HIV
11. Radiation (osteoradionecrosis)
12. Osteopetrosis, Paget's disease, end-stage cemento-osseous dysplasia (hypovascular bone)

Routes of Infection

1. Hematogenous spread (more common in children)
2. Extension from a contiguous site (most common in the jaws - from dental infection)
3. Direct implantation - after compound fractures or surgical procedures

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A. ACUTE SUPPURATIVE OSTEOMYELITIS

• Systemic: fever, malaise, chills, leukocytosis
• Local: throbbing pain, swelling, trismus, loose teeth, pus discharge
• Numbness of lip (Vincent's symptom) due to involvement of inferior alveolar nerve
• Mandible > maxilla (due to denser cortical bone and poorer blood supply)

• Acute phase: bacteria proliferate + neutrophilic infiltrate
• Necrosis of bone cells and marrow within first 48 hours
• Bacteria + inflammation spread through Haversian systems to periosteum
• In children: periosteum loosely attached → subperiosteal abscess
• Lifting of periosteum → further ischemia → more necrosis
• Rupture of periosteum → soft tissue abscess → draining sinus

• Early: no radiographic changes (bone loss not visible until 30-50% mineral loss)
• Later: ill-defined lytic areas with moth-eaten appearance

• Antibiotics (penicillin, clindamycin, cephalexin, cefotaxime)
• Surgical drainage if abscess present
• Extraction of offending tooth

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B. CHRONIC OSTEOMYELITIS

• Marrow fibrosis
• Sequestrum with empty lacunae
• Inflammatory infiltrate of lymphocytes and plasma cells (not neutrophils)
• Periosteal new bone formation (involucrum)

• Ill-defined radiolucency with areas of sclerosis
• Sequestrum appears as a dense radiopaque fragment surrounded by lucency
• Periosteal reaction (onion-skin appearance in some cases)

1. Pathologic fracture
2. Secondary (reactive) amyloidosis
3. Endocarditis
4. Sepsis
5. Squamous cell carcinoma in draining sinus tracts
6. Sarcoma in infected bone

• Long-term antibiotics
• Sequestrectomy + saucerization
• Decortication
• Hyperbaric oxygen (for refractory cases, osteoradionecrosis)
• Resection + reconstruction for persistent cases

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C. FOCAL SCLEROSING OSTEOMYELITIS (Condensing Osteitis)

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D. DIFFUSE SCLEROSING OSTEOMYELITIS

• Ill-defined, controversial diagnosis
• Characterized by: pain, inflammation, gnathic periosteal hyperplasia, sclerosis, and lucency
• Can be confused with florid cemento-osseous dysplasia or Paget's disease
• Treatment: antibiotics, NSAIDs, bisphosphonates; surgery in refractory cases

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E. OSTEORADIONECROSIS (ORN)

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F. MEDICATION-RELATED OSTEONECROSIS OF THE JAW (MRONJ)

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PART B: BENIGN FIBRO-OSSEOUS LESIONS (BFOLs)

Key concept: BFOLs share the same histopathology - cellular fibrous connective tissue with woven bone/osteoid/cementoid material. Radiographic correlation is critical to differentiate them.

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1. FIBROUS DYSPLASIA

Definition

Pathogenesis (Robbins)

• Somatic gain-of-function mutations in GNAS1 gene (encodes Gs-protein alpha subunit)
• Same gene mutated in pituitary adenomas
• Constitutively active Gs-protein → ↑ cAMP → cellular proliferation + disrupted osteoblast differentiation
• Phenotype depends on stage of embryogenesis when mutation is acquired

Forms

Clinical Features (Jaw specific)

• Presents in childhood and adolescence (slow progressive bone enlargement)
• Usually stops enlarging at growth plate closure / puberty
• Painless bony expansion of jaw
• Maxilla > mandible for craniofacial FD
• "Ground glass" appearance on X-ray is characteristic
• Can cause facial asymmetry, malocclusion, eye problems

Radiology

• "Ground glass" or "orange peel" or "smoky/hazy" appearance (most characteristic)
• Ill-defined borders - blends with surrounding bone ("flows into" adjacent bone)
• No cortical expansion initially; bowing and thinning in advanced disease
• No periosteal reaction

Histology (Morphology - Robbins)

• Intramedullary lytic lesions with cortical thinning
• Tan-white and gritty on gross examination
• Curvilinear (C-shaped / Chinese letter shaped) trabeculae of woven bone
• WITHOUT a rim of osteoblasts (no osteoblastic rimming - key feature!)
• Surrounded by moderately cellular fibroblastic proliferation
• Cystic degeneration, hemorrhage, foamy macrophages may be seen
• Variant patterns: pagetoid (thick interconnected trabeculae) and hypercellular pattern

Treatment

• Monostotic: often no treatment; observation
• Symptomatic: curettage (recurrence is common), contouring surgery
• Bisphosphonates for pain reduction
• Surgery timed after puberty (when growth stabilizes)
• Rare complication: malignant transformation (sarcoma), especially with radiation history, McCune-Albright, or Mazabraud syndrome

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2. OSSIFYING FIBROMA

Key Exam Comparison:

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3. CEMENTO-OSSEOUS DYSPLASIAS (COD)

Three Types:

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PART C: GIANT CELL LESIONS OF THE JAW

1. CENTRAL GIANT CELL GRANULOMA (CGCG)

Definition

Etiology and Pathogenesis

• Previously called "giant cell reparative granuloma" (thought to be reparative)
• Now considered a benign neoplasm due to unpredictable aggressive behavior and relationship to giant cell tumor of long bones
• Primary neoplastic cells are the fibroblasts/stromal cells; giant cells are reactive

Clinical Features

• Predominantly children and young adults
• Mandible > maxilla (ratio 2:1); anterior region most common
• Crosses the midline (characteristic feature)
• Painless slow expansion (non-aggressive type)
• Can be locally aggressive: pain, rapid growth, root resorption, cortical perforation

Two Behavioral Types:

Radiology

• Multilocular or unilocular radiolucency (soap-bubble or honeycomb appearance)
• Ill-defined or well-defined borders
• Root resorption and displacement of teeth

Histology

• Vascularized fibrous stroma with fibroblasts and hemosiderin deposits
• Multinucleated osteoclast-type giant cells (variable distribution - clustered near hemorrhagic areas)
• Foci of hemorrhage, hemosiderin pigment
• Woven bone formation at periphery

Differential Diagnosis

Treatment

• Non-aggressive: Curettage (treatment of choice)
• Aggressive: Resection may be needed
• Medical alternatives: intralesional corticosteroids, calcitonin, interferon-alpha (for aggressive cases)
• Recurrence rate: ~15-20% (higher in aggressive type)

Important: Always rule out hyperparathyroidism before diagnosing CGCG (Brown tumor is histologically identical!) - check serum calcium, PTH levels.

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2. GIANT CELL TUMOR (GCT) OF THE JAW

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3. CHERUBISM

Definition

Pathogenesis

• Mutation in SH3BP2 gene on chromosome 4
• Encodes a protein that activates osteoclasts → disrupted jaw morphogenesis
• Some consider it a genetically determined chronic noninfectious inflammatory disorder

Clinical Features

• Presents in early childhood (2-5 years)
• Bilateral symmetric enlargement of both jaws (most characteristic feature)
• Cheek puffing → cherub-like appearance (hence the name)
• Upward rotation of eyes → "eyes raised to heaven" appearance (due to orbital floor involvement)
• All four quadrants involved
• Missing, displaced, unerupted teeth

Radiology

• Bilateral multilocular radiolucencies of mandible and maxilla
• Giant cells + fibrous stroma (same as CGCG histologically)

Histology

• Vascularized fibrous stroma with multinucleated giant cells
• Eosinophilic perivascular cuffing of collagen surrounding capillaries (distinctive feature!)
• Mature lesions: large amounts of fibrous tissue, fewer giant cells

Prognosis and Treatment

• Self-limiting - lesions regress after puberty (usually by late teens)
• Generally good prognosis, especially if limited to mandible
• Surgical recontouring may be done after regression (for cosmetic reasons)
• No aggressive resection needed

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4. BROWN TUMOR (Hyperparathyroidism)

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PART D: METABOLIC BONE DISEASE

PAGET'S DISEASE OF BONE (Osteitis Deformans)

Definition

Epidemiology

• Age: >55 years (usually over 60)
• More prevalent in males (M:F ratio 2:1)
• Geographic distribution: UK, Germany, France, Australia; rare in Asia and Africa
• Accounts for only 0.05% of oral-maxillofacial pathologies

Pathogenesis (Three Phases)

1. Osteolytic phase: Aggressive osteoclastic bone resorption (osteoclasts are large, with many nuclei)
2. Mixed phase: Osteoclastic resorption + osteoblastic formation occurring simultaneously
3. Osteosclerotic phase: Predominantly osteoblastic formation; bone becomes hard, enlarged, brittle

Clinical Features - Systemic

• Often asymptomatic (found incidentally on X-ray or ↑ ALP)
• Bone pain and headaches (skull involvement)
• Bowing of tibia (saber shin)
• Pathologic fractures
• Hearing loss (compression of CN VIII)
• "Leonine facies" (lion-like face with skull involvement)
• Increased cardiac output (hypervascular bone acts as AV shunting) → high-output cardiac failure

Clinical Features - Jaw Specific

• Jaw enlargement (both jaws but maxilla > mandible)
• Teeth become widely spaced (spacing increases)
• Progressive ill-fitting dentures (classic complaint!)
• Hypercementosis (cementum apposition on roots) → ankylosis
• Difficulty/inability to extract teeth due to ankylosis

Radiology

• "Cotton wool" appearance (most characteristic) - alternating radiolucent and radiopaque areas
• Hypercementosis on roots
• Loss of lamina dura
• "Mosaic pattern" on histology (pathognomonic)

Histology (Pathognomonic)

• Mosaic pattern - lamellar bone trabeculae with irregular cement lines forming a "mosaic" or "jigsaw puzzle" pattern
• Osteoblastic-osteoclastic activity (mixed phase)
• Cemento-osseous trabeculae with multiple compartments
• Osteomyelitis can complicate (35% of jaw cases)

Lab Findings

• ↑ Serum Alkaline Phosphatase (ALP) - most significant marker of disease activity
• Normal serum calcium (usually)
• ↑ Urinary hydroxyproline (marker of bone collagen breakdown)

Complications

1. Pathologic fracture
2. Secondary osteomyelitis (especially of jaws)
3. Malignant transformation to osteosarcoma (in ~1% - but sarcoma prognosis very poor)
4. High-output cardiac failure
5. Hearing loss
6. Neurological compression

Treatment

• Bisphosphonates (alendronate, pamidronate, zoledronic acid) - main treatment; inhibit osteoclasts
• Calcitonin (older agent; less effective)
• Analgesics for pain
• Dental considerations: avoid extractions if possible (risk of osteomyelitis); pre-treat with antibiotics

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QUICK COMPARISON TABLE: Giant Cell Lesions

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QUICK COMPARISON TABLE: BFOLs

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HIGH-YIELD EXAM POINTS

1. Sequestrum = dead bone; Involucrum = new bone shell around sequestrum
2. Fibrous dysplasia = GNAS1 mutation; curvilinear bone trabeculae WITHOUT osteoblastic rimming; "ground glass" X-ray
3. Ossifying fibroma = WELL-DEFINED borders; osteoblastic rimming PRESENT; enucleates cleanly
4. CGCG = anterior mandible, crosses midline, multinucleated giant cells + fibrous stroma; ALWAYS rule out hyperparathyroidism
5. Cherubism = SH3BP2 gene; bilateral; self-limiting; eosinophilic perivascular cuffing on histology
6. Paget's disease = "cotton wool" X-ray; mosaic pattern histology; ↑ ALP; hypercementosis; ill-fitting dentures
7. Brown tumor = histologically identical to CGCG; treat the systemic disease (hyperparathyroidism)
8. MRONJ = bisphosphonates most commonly implicated; mandible > maxilla; prevent with dental clearance before starting drug
9. Florid COD = risk of secondary osteomyelitis if traumatized/exposed; no treatment otherwise
10. McCune-Albright = polyostotic FD + café-au-lait spots + precocious puberty (all three together)

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• 6 inflammatory conditions (osteitis through MRONJ) with full clinical + histological details
• 3 BFOLs (fibrous dysplasia, ossifying fibroma, COD) with the critical comparison table
• 4 giant cell lesions with distinguishing histological features
• Paget's disease with jaw-specific features
• Comparison tables and high-yield exam points throughout

• Upload your past year question paper (photo, PDF, or just type out the questions)
• I'll answer each one in structured bullet-point format following Shafer's and Neville's content

• The library I have access to does include Robbins Pathology and several other medical references - Shafer's and Neville's specifically aren't in it, but I know their content well and will answer faithfully to their frameworks (definitions, classifications, histological descriptions, and clinical emphasis that these books use)
• For any question where Shafer's and Neville's differ in classification or terminology, I'll flag both

1. Write about fibrous dysplasia 2. Classify osteomyelitis and describe chronic osteomyelitis 3. Short note on Paget's disease

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📋 SUMMARY OF ALL 12 ANSWERS

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• Q5, Q6, Q7, and Q10 are all variations of the same question (Ameloblastoma) - the single answer above covers all four
• Q8 and Q9 are also the same (AOT) - one answer covers both
• Always write the classification first before describing the specific lesion - examiners give marks for it

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📋 SUMMARY - Q13 to Q25

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• Q15 and Q24 are the same answer (Herpes) - use one answer for both
• Q16 and Q21 are the same (Dental caries) - same answer
• Q17 and Q20 are the same (OLP) - same answer
• Q19 and Q23 have slight differences: Q19 asks for pemphigus specifically; Q23 asks for vesiculobullous classification first, then PV - start Q23 with the full vesiculobullous classification table before going into PV