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LONG ESSAY QUESTIONS

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Q.1 Aetio-Pathogenesis of Acute Osteomyelitis of the Mandible and Clinical Features

Definition

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Etiology (Causative Factors)

• Staphylococcus aureus - most common organism
• Streptococci (viridans group)
• Gram-negative anaerobes: Bacteroides, Fusobacterium, Prevotella
• Mixed flora (polymicrobial) is common in odontogenic osteomyelitis

1. Odontogenic route - most common in mandible
   • Periapical abscess, periodontal disease, pericoronal abscess (especially around lower third molar), infected cysts, post-extraction infection
2. Hematogenous spread - more in children; bacteria spread via bloodstream
3. Direct extension - from adjacent soft tissue infections (e.g., Ludwig's angina)
4. Traumatic - compound fractures, post-surgical contamination
5. Iatrogenic - following tooth extractions, jaw surgeries

• Diabetes mellitus (most important systemic predisposing factor)
• Immunosuppression (HIV, chemotherapy, steroids)
• Malnutrition and anemia
• Osteoporosis
• Radiation-induced bone damage (osteoradionecrosis)
• Bisphosphonate therapy (BRONJ/MRONJ)
• Sickle cell disease
• Paget's disease of bone

• Mandible has a dense cortical bone with limited collateral blood supply
• Maxilla has a rich, multicompartment blood supply from multiple vessels
• Mandibular cancellous bone has fewer vascular channels

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Pathogenesis

• Acute inflammatory exudate (PMN leucocytes) accumulates in the medullary spaces
• Vascular congestion and edema occur
• Intramedullary pressure rises markedly

• Rising pressure compresses the thin intraosseous blood vessels
• Blood supply is cut off - ischemia and infarction of bone follow
• Periosteal vessels are also compromised when pus lifts the periosteum

• Avascular bone segments die = SEQUESTRUM formation (dead bone piece)
• Surrounding living bone attempts to wall off the dead bone by new bone formation = INVOLUCRUM
• Pus finds a path through the cortex and periosteum to reach soft tissues

• Pus tracks through Haversian canals and Volkmann's canals
• Subperiosteal abscess forms
• May penetrate skin/mucosa to form a SINUS (chronic stage)

• Granulation tissue and new bone (involucrum) try to contain infection
• If host defenses fail, chronic osteomyelitis develops

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Clinical Features

• High-grade fever (38-40°C), chills, rigors
• Malaise, fatigue, anorexia
• Elevated ESR, leucocytosis (TLC >11,000/mm³)
• Elevated CRP

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Radiological Features

• Early stage: No radiological changes (bone loss is visible only after 30-50% mineral content is lost)
• Later: "Moth-eaten" or "mottled" radiolucency
• Sequestrum appears as a radio-opaque fragment surrounded by radiolucency
• Involucrum appears as a zone of new bone formation

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Complications

• Sequestrum and sinus tract formation
• Pathological fracture
• Ankylosis of TMJ
• Spread to adjacent spaces (Ludwig's angina, cavernous sinus thrombosis)
• Chronic osteomyelitis

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Q.2 Definition of Carcinoma, TNM Classification of Oral Cavity Carcinoma, and SCC of Buccal Mucosa

Definition of Carcinoma

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TNM Classification of Oral Cavity Carcinoma

T - Primary Tumor

Note: Depth of Invasion (DOI) is a key addition in AJCC 8th edition - it is NOT the same as tumor thickness. DOI is measured from the basement membrane level of the nearest normal mucosa.

N - Regional Lymph Nodes

M - Distant Metastasis

Overall Stage Grouping

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Squamous Cell Carcinoma of Buccal Mucosa

• Most common site of oral cancer in India (due to tobacco/areca nut chewing habits)
• Predominantly affects males over 40 years
• Strongly associated with tobacco chewing, gutka, paan (betel quid) use

• Tobacco (smokeless) - most important in India
• Areca nut (betel nut) - independent carcinogen
• Paan with tobacco (betel quid with tobacco)
• Alcohol (potentiating factor)
• Oral submucous fibrosis (OSMF) - most important premalignant condition precursor in India
• Leukoplakia of buccal mucosa
• HPV (Human Papillomavirus) - less important for buccal mucosa compared to oropharynx
• Chronic trauma from sharp teeth or ill-fitting dentures

• Oral submucous fibrosis (OSMF)
• Erythroplakia (highest malignant potential - ~50%)
• Leukoplakia (speckled type has highest transformation rate)
• Oral lichen planus (erosive type)

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• Ulceroproliferative lesion most common (raised, everted edges with central ulceration)
• Also can be verrucous, papillary, or flat infiltrative type

• Keratin pearls (epithelial pearls/cell nests) prominent
• Cells resemble normal squamous cells
• Minimal nuclear pleomorphism
• Rare mitotic figures

• Fewer keratin pearls
• More nuclear pleomorphism and hyperchromatism
• Moderate mitotic activity
• Intercellular bridges present

• No keratin pearls
• Marked nuclear pleomorphism, anaplasia
• Numerous mitotic figures (atypical mitoses)
• Minimal resemblance to squamous cells

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• A persistent non-healing ulcer or white/red patch on buccal mucosa
• Initially painless (pain is a late feature)
• Located along the occlusal line (where mucosa is most exposed to tobacco)

• Ulceroproliferative mass on buccal mucosa with indurated (hard), raised, everted edges
• Central necrosis with foul smell
• Pain, burning sensation, dysphagia
• Restricted mouth opening (trismus) - indicates pterygoid muscle invasion
• Reduced mouth opening due to OSMF background
• Fixity to underlying tissues
• Bleeding on touch

• Submandibular and upper deep cervical nodes are first echelon nodes
• Nodes become firm, enlarged, and eventually fixed

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• Local: Skin of cheek, gingiva, retromolar trigone, floor of mouth
• Lymphatic: Submandibular and upper jugular chain nodes
• Distant (rare): Lung, liver

• 5-year survival rate: ~50-60% for Stage I/II; drops significantly for Stage III/IV
• Buccal SCC has poorer prognosis than lip cancer
• Verrucous carcinoma (low-grade variant) has best prognosis

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SHORT NOTES (5 marks each)

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Q.3 Wegener's Granulomatosis (Now called Granulomatosis with Polyangiitis - GPA)

1. Upper respiratory tract involvement (sinusitis, epistaxis, saddle-nose deformity)
2. Lower respiratory tract (pulmonary nodules, cavities, hemoptysis)
3. Renal involvement (glomerulonephritis, hematuria, renal failure)

• "Strawberry gingivitis" - pathognomonic oral finding: red, hyperplastic, granular gingivitis resembling the surface of a strawberry; seen on attached gingiva
• Oral ulcers (painful, irregular)
• Palatal perforation (necrotic granulomas destroy palate)
• Jaw pain, loosening of teeth
• Delayed healing of extraction sockets
• Saddle-nose deformity (due to nasal septal destruction)
• Nasal bleeding and purulent nasal discharge

• Necrotizing granulomas (giant cell granulomas with central necrosis)
• Vasculitis of small vessels
• PMN infiltrate and fibrinoid necrosis

• c-ANCA (anti-PR3) positive - key diagnostic marker
• Elevated ESR, CRP
• Biopsy of affected tissue showing necrotizing granulomatous vasculitis
• Chest X-ray/CT: nodules and cavities
• Urinalysis: red cell casts (renal involvement)

1. Nasal/oral inflammation (oral ulcers or bloody nasal discharge)
2. Abnormal chest X-ray (nodules, cavities, infiltrates)
3. Urinary sediment (microhematuria)
4. Granulomatous inflammation on biopsy

• Induction: Cyclophosphamide + corticosteroids (prednisolone)
• Maintenance: Methotrexate or azathioprine
• Rituximab (anti-CD20) for refractory cases
• TMP-SMX for limited disease

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Q.4 Dry Socket (Alveolar Osteitis)

• Traumatic or difficult extraction (most important)
• Inadequate blood supply to socket
• Dense cortical bone with limited vascularity (mandibular third molar area)
• Excessive irrigation of socket post-extraction
• Oral contraceptive pills (estrogen increases fibrinolysis)
• Smoking (vasoconstriction, reduces blood supply; also dislodges clot by suction)

• Diabetes mellitus
• Immunocompromised states
• Bisphosphonate therapy

1. Fibrinolytic theory (Birn, 1973): Trauma causes release of tissue plasminogen activators (tPA) from alveolar bone cells and surrounding tissue. These activate plasminogen to plasmin, which lyses the blood clot (fibrinolysis). Bacteria and pyrogen contamination further promote fibrinolysis.
2. Bacterial contamination theory: Anaerobic bacteria (Treponema denticola, Bacteroides) release fibrinolytic enzymes that break down the clot.

• Onset: 2-4 days after extraction (hallmark timing)
• Severe, throbbing, radiating pain - does NOT respond to routine analgesics (NSAIDs/paracetamol)
• Pain radiates to ear, temple, eye
• Socket appears empty - bone walls visible, no clot
• Grey-white necrotic material may line socket
• Foul odor (halitosis) - characteristic feature
• Minimal swelling (unlike abscess)
• No pus (unlike osteomyelitis)
• Tender on palpation of socket
• Mild regional lymphadenopathy

1. Gentle irrigation of socket with warm saline
2. Curettage is avoided (it may damage the socket walls further)
3. Alvogyl packing (eugenol + butamben + iodoform gauze) - the standard treatment; provides immediate pain relief
4. Zinc oxide eugenol (ZOE) dressing
5. Local anesthetic block for immediate relief
6. Analgesics: NSAIDs, opioids if needed
7. Antibiotics: only if systemic signs present

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Q.5 Bite Mark

• Bite marks are used as forensic evidence in criminal cases (assault, rape, child abuse, homicide)
• The dental arch and individual tooth characteristics of a suspect can be matched to a bite mark on a victim (or vice versa)
• Dentists are often called as expert witnesses

1. On human skin: Most commonly seen in cases of assault, sexual violence, child abuse
2. On foodstuffs: Cheese, chocolate, apple, butter - preserve impressions well
3. On other materials: Leather, rubber, pencils

• Appear as two opposing U-shaped (or elliptical) arches of tooth marks
• Individual marks within the arch correspond to individual teeth
• Central area shows sucking/tongue pressure ecchymosis
• May show abrasion, laceration, contusion, or avulsion

• Fresh bite marks change over time due to skin elasticity
• Bite marks must be documented IMMEDIATELY

1. Photography - most important; scale ruler must be included (ABFO No. 2 scale), both with and without scale, various angles, UV photography
2. Swabbing - for salivary DNA; wet and dry swab technique (double swab method)
3. Impressions - polyvinyl siloxane (PVS) impression material for 3D marks
4. Overlay tracings - transparent overlays from suspect's dental models

• Suspect's dental casts are made
• Overlaid on bite mark photographs at 1:1 scale
• Computer-assisted superimposition techniques
• DNA from saliva swab confirms suspect identity

• Can establish that dental contact occurred
• Can narrow down or identify a suspect
• May be the only physical evidence linking suspect to victim

• Accepted as evidence in courts of law
• Dentist can be subpoenaed as expert witness
• Child abuse is most common scenario where bite marks are documented

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Q.6 Fordyce Granules (Fordyce Spots)

• Found in 70-80% of adults
• Rare in children; increase in number with puberty (hormonal influence)
• Slightly more common in males

• During embryonic development, sebaceous glands that normally migrate with hair follicles get "stranded" in the oral mucosa
• Hormonal activation at puberty causes them to become visible

• Buccal mucosa (most common) - along the occlusal line bilaterally
• Vermilion border of lips (especially upper lip)
• Retromolar region
• Labial mucosa

• Small (1-3 mm), yellowish-white, slightly raised papules/spots
• Clusters or linear arrangement along buccal mucosa
• Asymptomatic - patient may notice them incidentally
• No tenderness, no ulceration, no change with time
• Increase in number after puberty
• May become more prominent with stretching of mucosa

• Well-formed sebaceous gland lobules in the lamina propria
• No hair follicle associated (key histological feature)
• Central sebaceous duct opens directly onto mucosal surface
• Filled with sebum (lipid-laden cells)
• Overlying epithelium normal

• Lipoma (deeper, single, larger)
• Mucocele (fluctuant, single)
• Candidiasis (white, can be wiped off)
• Milia (on skin, not mucosa)
• Ectopic lymphoid tissue (slightly larger, at soft palate/floor of mouth)

• No treatment required - reassure the patient that it is a normal variant
• If cosmetically bothersome (on lips), options: electrodesiccation, CO₂ laser, micro-punch technique

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Q.7 Ranula

1. Simple (Oral) Ranula: Confined within the floor of the mouth, above mylohyoid muscle
2. Plunging (Cervical) Ranula: Mucous extravasation extends through or around the mylohyoid muscle into the neck - presents as a neck swelling

• Obstruction of sublingual salivary gland duct (Wharton's duct or ducts of Rivinus) due to:
  • Ductal stone (sialolithiasis)
  • Trauma or injury to the gland/duct
  • Mucous plug
  • Congenital ductal narrowing
• True retention cyst (epithelial lining) OR pseudocyst (no epithelial lining - mucous extravasation)

• Obstruction or rupture of the sublingual duct
• Mucous accumulates in the floor of mouth connective tissue
• In plunging type: mucous dissects through mylohyoid muscle weakness/hiatus → enters submandibular or submental space

• Soft, fluctuant, translucent ("frog belly") swelling in the floor of mouth
• Usually unilateral
• Bluish tinge due to thin overlying mucosa and accumulated mucin
• Slow-growing, painless (unless infected)
• Moves the tongue superiorly/laterally
• Transilluminates (positive)
• No tenderness unless secondarily infected

• Neck swelling (submandibular/submental region)
• Soft, compressible, non-tender
• Floor of mouth component may or may not be prominent
• "Hourglass" configuration on MRI when both oral and cervical components present
• No overlying skin changes

• Ultrasound: anechoic (fluid-filled) cystic lesion
• CT/MRI: for plunging ranula to determine extent and relationship to mylohyoid

• Pseudocyst: No epithelial lining; wall composed of compressed connective tissue
• Filled with mucin and inflammatory cells
• Surrounding sublingual gland acini often identified

1. Simple Ranula: Marsupialization (de-roofing) - most preferred conservative surgical procedure; creates a permanent opening so mucin drains freely
2. Excision of sublingual gland - definitive treatment; prevents recurrence
3. Sclerotherapy - OK-432 (picibanil) injection - less invasive alternative
4. Plunging Ranula: Excision of the sublingual gland via intraoral approach + drainage of cervical component

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Q.8 Dentine Dysplasia

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Type I - Dentine Dysplasia (Radicular Type)

• Both primary and permanent dentitions affected
• Teeth appear clinically normal (color, shape of crown is normal)
• Teeth are mobile due to short, blunt, conical roots
• Teeth may exfoliate prematurely
• High susceptibility to periapical pathology without apparent cause

• Obliterated pulp chambers - no visible pulp chamber
• Roots are very short, blunt, conical - "thistle-tube" shape
• Multiple periapical radiolucencies may be present even in non-carious teeth
• "Crescent-shaped" pulp remnants near CEJ (chevron pattern) occasionally seen

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Type II - Dentine Dysplasia (Coronal Type)

• Primary teeth: amber/brownish-blue translucent discoloration (similar to dentinogenesis imperfecta)
• Permanent teeth: appear clinically normal in color

• Primary teeth: obliterated pulp chambers, short roots
• Permanent teeth: large "thistle-tube" shaped pulp (flame-shaped, large pulp chambers extending into roots)
• Pulp stones within pulp chambers of permanent teeth
• "Thistle-tube" appearance of pulp in permanent teeth is characteristic

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Comparison Table:

• Abnormal dentine with irregular dentinal tubules
• Islands of interglobular dentine
• Pulp tissue obliterated by tubular or atubular dentine

• Dentinogenesis Imperfecta (DI): In DI, all teeth show amber discoloration and bulbous crowns; cervical constriction is present; in Dentine Dysplasia Type I, the crown is normal

• Stainless steel crowns for primary teeth
• Overdentures or removable prostheses once teeth are lost
• Dental implants may be challenging due to bone quality

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Q.9 Erythema Multiforme

• Herpes Simplex Virus (HSV 1 and 2) - responsible for ~70% recurrent EM (HSV-associated EM/HAEM)
• Mycoplasma pneumoniae

• Sulfonamides, penicillin, NSAIDs, phenytoin, barbiturates

• T-lymphocyte mediated immune reaction
• In HSV-associated EM: viral DNA fragments (HSV pol gene) are carried by CD34+ Langerhans cells to skin/mucosa, triggering an inflammatory cascade
• IFN-γ released → cytotoxic T-cells attack keratinocytes → cell death → bullae and erosions

• Target (iris) lesion - pathognomonic: three concentric zones - central dark area/blister, surrounding pale edematous ring, outer red ring
• Located on dorsum of hands, extensor surfaces of limbs (acral distribution)
• Macular, papular, bullous lesions

• Sudden onset of painful oral erosions and ulcers
• Lower labial mucosa most commonly involved - with hemorrhagic crust formation on lips
• Crusted hemorrhagic lips - hallmark
• Painful ulcers on buccal mucosa, tongue, palate
• Bleeding, oozing erosions
• Dysphagia and difficulty eating
• May have preceding history of HSV labialis (cold sore) 1-3 weeks before

• Ocular: conjunctivitis, corneal scarring
• Genital: painful erosions

• Mild fever, malaise
• Cervical lymphadenopathy

• Subepithelial bullae formation
• Liquefaction degeneration of basal cell layer
• Perivascular lymphocytic infiltration in superficial dermis/lamina propria
• Keratinocyte necrosis (apoptotic cells = Civatte bodies)

• Mild (EM Minor): Supportive - topical corticosteroids, antiseptic mouthwashes, analgesics
• Moderate: Systemic prednisolone (controversial but used)
• Recurrent HAEM: Long-term oral acyclovir (400 mg BD for 6 months) - prevents HSV reactivation and hence EM episodes
• Severe (EM Major/SJS): Hospitalization, IV fluids, ophthalmology consultation

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Q.10 Ehlers-Danlos Syndrome (EDS)

• Defects in Type I, III, or V collagen (COL1A1, COL3A1, COL5A1 genes)
• Or enzymes processing collagen: lysyl hydroxylase (Type VI), tenascin-X

1. Classical EDS (cEDS) - COL5A1/COL5A2 mutations
2. Hypermobile EDS (hEDS) - most common; no gene identified
3. Vascular EDS (vEDS) - COL3A1; most dangerous (risk of arterial rupture)
4. Kyphoscoliotic EDS - lysyl hydroxylase deficiency

• Skin hyperextensibility (stretches more than normal; snaps back)
• Velvet-like, soft, fragile skin
• Easy bruising, poor wound healing
• "Cigarette paper" (fish-mouth) scars after minor wounds - pathognomonic
• Papyraceous scars
• Molluscoid pseudotumors at pressure points

• Hypermobile joints (positive Beighton score)
• Recurrent joint dislocations (shoulder, hip, patella)
• Joint pain, arthralgia
• Pes planus

• Mitral valve prolapse
• Aortic root dilation (especially vascular EDS)
• Hernias, visceral prolapse
• Muscle weakness

• Temporomandibular joint (TMJ) hypermobility and recurrent dislocations
• Difficulty chewing due to TMJ instability
• Increased joint laxity - mouth can be opened excessively wide
• Fragile oral mucosa - tears easily during dental procedures
• Difficult to achieve local anesthesia (LA dissipates rapidly through lax connective tissue - reduced efficacy of injections)
• Gingival fragility and easy bleeding during probing/scaling
• Periodontal problems due to poor collagen quality
• Short lingual frenulum or bifid uvula (rare)
• Delayed wound healing post-extraction
• Increased risk of ecchymosis/bruising post-injections

• Gentle instrumentation to avoid mucosal tearing
• Extra care during LA administration; may need higher doses
• Warn patient of bruising post-injection
• Avoid trauma to TMJ during prolonged procedures
• Coordinate with physician before surgery

• Clinical (Beighton Score for hypermobility)
• Skin biopsy with electron microscopy (collagen fibril abnormalities)
• Genetic testing
• Echocardiography (for vascular complications)

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Q.11 Addison's Disease

• Bilateral adrenalectomy
• Metastatic carcinoma (lung, breast)
• Amyloidosis, sarcoidosis
• Waterhouse-Friderichsen syndrome (meningococcal septicemia)
• Hemochromatosis

• Destruction of adrenal cortex → ↓ cortisol production
• ↓ Cortisol → loss of negative feedback on hypothalamus/pituitary
• → ↑ ACTH (and ↑ MSH - melanocyte stimulating hormone) production from pituitary
• ↑ MSH stimulates melanocytes → hyperpigmentation
• ↓ Aldosterone → sodium loss, potassium retention, hypotension

• Oral mucosal hyperpigmentation - most characteristic oral finding
• Brown/black patches/macules on:
  • Buccal mucosa (along occlusal line)
  • Gingiva
  • Tongue (especially borders)
  • Palate
  • Lips
• Pigmentation is multifocal, irregular
• May precede skin pigmentation
• Oral pigmentation occurs because melanin deposition is stimulated by excess ACTH/MSH

• Bronze (tan) skin pigmentation - especially in sun-exposed areas, pressure points, skin creases, knuckles, buccal mucosa
• Weakness, fatigue, lethargy
• Anorexia, nausea, vomiting, weight loss
• Hypotension (postural)
• Salt craving
• Hypoglycemia episodes
• Depression, psychosis

• Serum cortisol: low (morning cortisol <3 μg/dL diagnostic)
• Serum ACTH: elevated (distinguishes primary from secondary)
• ACTH stimulation test (Synacthen test): inadequate cortisol rise
• Electrolytes: ↓ Na+, ↑ K+
• Blood sugar: low
• ACTH antibodies (autoimmune)

• Acute life-threatening emergency triggered by stress, infection, surgery, or steroid withdrawal
• Features: Severe hypotension, vomiting, abdominal pain, shock, altered consciousness
• Management: IV hydrocortisone 100 mg stat + IV normal saline

• Steroid cover before dental treatment (to prevent adrenal crisis under stress)
• Double the morning steroid dose on day of procedure
• Monitor BP throughout procedure
• Avoid GA without endocrinologist consultation
• Have hydrocortisone injection available in clinic (emergency)

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Q.12 Squamous Papilloma

• HPV (Human Papillomavirus) - most important; predominantly HPV Types 6 and 11 (low-risk types)
• HPV 16 and 18 (high-risk types) associated with malignant transformation - rare
• Direct contact/inoculation (kissing, orogenital contact, contaminated instruments)
• May also be reactive (non-viral, traumatic) in some cases

• Most common oral epithelial neoplasm in children and adults
• No strong sex predilection
• Can occur at any age; peak in 3rd-4th decade

• Soft palate and uvula (most common)
• Tongue (lateral borders, ventral)
• Lips
• Gingiva
• Buccal mucosa
• Hard palate

• Exophytic, white, cauliflower-like or wart-like mass
• Pedunculated (on a stalk) or sessile (broad base)
• Multiple finger-like or papillary projections
• Surface: white (keratinized) or pink (non-keratinized)
• Size: usually small (0.5-1.5 cm), rarely larger
• Painless - discovered incidentally
• Soft, non-tender consistency
• Solitary (multiple lesions suggest condyloma acuminatum or verruca vulgaris)
• Slow growing

• Multiple finger-like projections of stratified squamous epithelium
• Each projection has a thin fibrovascular core (connective tissue stalk)
• Surface: may be keratinized or non-keratinized
• Koilocytes (hallmark of HPV infection): squamous cells with pyknotic, raisin-like nuclei surrounded by a clear cytoplasmic halo in the upper spinous layer - perinuclear vacuolization
• Mild epithelial hyperplasia
• Minimal inflammation in connective tissue core
• No dysplasia (benign lesion)

• Primarily clinical and histopathological
• In situ hybridization (ISH) or PCR for HPV typing if needed

• Surgical excision - treatment of choice; complete excision at base
• Laser ablation (CO₂ laser)
• Electrodesiccation/cryotherapy
• Recurrence is uncommon if completely excised at the base

• Benign, excellent prognosis
• Malignant transformation is extremely rare (only with high-risk HPV 16/18)

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