Anatomy and Physiology of Teeth: Enamel, Dentin, Pulp, and Periodontal Structures

INTRODUCTION

1. ENAMEL

Anatomy

• Enamel covers the entire crown of the tooth.
• It is the hardest substance in the human body.
• Composed of ~96-97% inorganic material (calcium hydroxyapatite - Ca₁₀(PO₄)₆(OH)₂) and only 2-3% organic material (mainly amelogenin protein) with trace water.
• Average thickness: ~2 mm at the cusp tips.

Microstructure

• Made up of enamel rods (prisms), each ~4-8 μm in diameter, running from the dentinoenamel junction (DEJ) to the outer surface.
• Each rod has a keyhole shape in cross-section - a "head" (crystals parallel to rod axis) and a "tail" (crystals more oblique).
• Rods are tightly interlocked, giving enamel its resistance to masticatory pressures.
• Contour lines of Retzius = striations on rods representing rhythmic growth; the neonatal line marks the prenatal-postnatal transition in deciduous teeth.

Physiology

• Acellular - contains no cells, vessels, or nerves after formation. Cannot regenerate.
• Produced by ameloblasts during tooth development (via Tomes' process) - these cells are lost after eruption.
• Fluoride ions can replace OH⁻ in hydroxyapatite, forming fluorapatite, which is more resistant to acid dissolution - rationale for fluoride in toothpaste.
• Protects underlying dentin and pulp from mechanical and thermal insults.

2. DENTIN

Anatomy

• Forms the bulk of the tooth, extending from the DEJ to the pulp cavity.
• Covered by enamel in the crown and by cementum in the root.
• Yellowish in color; slightly softer than enamel but harder than bone.

Microstructure

• Contains dentinal tubules (dental canaliculi) - microscopic channels running radially from the pulp to the DEJ, giving dentin its characteristic radial striping.
• Each tubule contains an odontoblastic process (Tomes' fiber) - a cytoplasmic extension of odontoblast cells lining the pulp.
• Ground substance: organic matrix (collagen fibrils) + calcium salts (hydroxyapatite).
• No blood vessels within dentin itself.

Types of Dentin

Physiology

• Odontoblasts (lining the pulp surface) continuously synthesize new predentin even after eruption, depositing new dentin inward throughout life.
• Sensitivity - unmyelinated type C nerve fibers extend into the dentinal tubules; stimuli (cold, heat, osmotic) transmitted via hydrodynamic movement of dentinal fluid (Brannstrom's hydrodynamic theory).

3. DENTAL PULP

Anatomy

• Soft connective tissue filling the pulp cavity, which includes:
  • Pulp chamber (in the crown)
  • Root canal (in the root)
  • Apical foramen (opening at root tip through which nerves and vessels enter)

Histology/Microstructure

• Loose connective tissue, well vascularized.
• Odontoblasts arranged in a palisade (outer layer) - specialized cells that form dentin.
• Inner layers: cell-rich zone (fibroblasts, defense cells) and cell-free zone (Weil's zone).
• Nerves: both myelinated (A-delta fibers - sharp pain) and unmyelinated (C fibers - dull, poorly localized pain). Pain of pulpitis is often poorly localized due to predominance of C fibers.
• Blood supply: enters via apical foramen (branches of superior and inferior alveolar arteries).

Physiology

• Dentinogenic function: odontoblasts produce dentin throughout life.
• Nutritive function: maintains vitality of dentin.
• Sensory function: pain transmission via nerve fibers in dentinal tubules.
• Defensive function: immune cells (macrophages, lymphocytes) protect against microbial invasion; tertiary dentin formation in response to injury.
• Inflammatory response: pulpitis (inflammation) occurs due to caries. Because pulp is enclosed in a rigid chamber, inflammation causes pressure buildup → severe pain.

4. PERIODONTAL STRUCTURES (PERIODONTIUM)

A. Cementum

• Covers the dentin of the root.
• Resembles woven bone but is avascular.
• Produced by cementoblasts.
• Thickest near the root apex.
• Contains cementocytes in lacunae (near the surface) with processes in canaliculi.
• Collagen fibers (Sharpey fibers) from the PDL are anchored into cementum, binding the tooth to the socket.
• Meets enamel at the cementoenamel junction (CEJ) or neck of the tooth.

B. Periodontal Ligament (PDL)

• Dense fibrous connective tissue between cementum and alveolar bone.
• Thickness: 150-350 μm (decreases with age).
• Contains Sharpey fibers (principal collagen fiber bundles) - anchored into cementum and alveolar bone.

• Supportive: suspends tooth in socket; permits slight mobility.
• Sensory: highly innervated - proprioceptive sensations guide chewing force.
• Nutritive: blood vessels supply cementum and alveolar bone.
• Formative/Remodeling: contains cementoblasts, osteoblasts, fibroblasts.
• Eruptive: plays a role in tooth eruption and positional maintenance.

C. Alveolar Bone

• The bone of the jaw that forms the tooth sockets (alveoli).
• Has two layers: cortical plate (outer) + cancellous bone (inner) + alveolar bone proper (lamina dura - socket wall).
• Unlike typical lamellar bone, alveolar bone proper has osteoblasts and osteocytes engaged in continuous remodeling.
• Dependent on tooth presence - resorbs after tooth extraction.

D. Gingiva

• Oral mucosa covering alveolar bone and tooth necks.
• Junctional epithelium: specialized epithelium attaching to enamel/cementum at the CEJ via hemidesmosomes and a thick basal lamina.
• Gingival sulcus: shallow groove between tooth surface and gingival margin (normal depth 1-3 mm).
• Deepening of sulcus → periodontal pockets → bacterial colonization → periodontitis.

SUMMARY TABLE

1. Enamel = hardest, acellular, cannot regenerate - ameloblasts lost after eruption.
2. Dentin sensitivity = hydrodynamic theory (Brannstrom).
3. Pulp pain = poorly localized (C fibers predominate).
4. PDL = 5 principal fiber groups; oblique group is the most numerous.
5. Periodontitis = deepened sulcus → bacterial pockets → bone loss.

Jaw Tumours - 10 Marks

INTRODUCTION & CLASSIFICATION

Classification Overview

JAW TUMOURS
├── ODONTOGENIC
│   ├── Cysts (inflammatory & developmental)
│   └── Tumours (benign & malignant)
└── NON-ODONTOGENIC
    ├── Bone tumours (osteoma, osteosarcoma)
    ├── Fibro-osseous lesions
    └── Metastatic tumours

A. ODONTOGENIC CYSTS

TABLE: Classification of Odontogenic Cysts

1. Radicular (Periapical) Cyst

• Most common jaw cyst.
• Arises from chronic pulpitis (usually due to caries) → pulp necrosis → inflammation exits at apex → granulation tissue → epithelialization → cyst.
• Lined by non-keratinized stratified squamous epithelium.
• X-ray: Periapical radiolucency.
• Treatment: Root canal treatment or tooth extraction + curettage.

2. Dentigerous Cyst

• Most common developmental odontogenic cyst; commonest jaw cyst in children.
• Surrounds the crown of an unerupted tooth (most often mandibular 3rd molar or maxillary canine).
• Cyst wall attaches at the cementoenamel junction.
• X-ray: Unilocular radiolucency around crown of unerupted tooth. Follicular space >4mm is diagnostic.
• Treatment: Marsupialization or enucleation with bone grafting for large lesions.

3. Odontogenic Keratocyst (OKC)

• Now termed keratocystic odontogenic tumour by WHO.
• Characteristic parakeratinized stratified squamous epithelium lining.
• Locally aggressive - high recurrence (up to 60%) if inadequately removed.
• Multiple OKCs → suspect Gorlin syndrome (Nevoid Basal Cell Carcinoma Syndrome - PTCH gene mutation).
• X-ray: Multilocular or unilocular radiolucency, often in mandibular ramus.
• Treatment: Excision; careful margins needed due to high recurrence.

B. ODONTOGENIC TUMOURS

TABLE: WHO Classification of Odontogenic Tumours (Key Ones)

1. AMELOBLASTOMA (Most Important - Most Common Odontogenic Tumour)

• Benign but locally aggressive neoplasm arising from odontogenic epithelium (remnants of enamel organ / dental lamina).
• Does not show ectomesenchymal differentiation.

1. Conventional (Solid/Multicystic) - most common
2. Unicystic - less aggressive; 10-20% recurrence
3. Peripheral (Extraosseous) - on gingiva, low recurrence
4. Metastasizing - rare, malignant behavior

• Usually >20 years of age.
• 85% in mandible - most commonly molar/ramus region.
• Slow, painless expansion of jaw.
• MAPK pathway mutation (BRAF V600E) in ~90% of lesions.

• Multilocular "soap bubble" or "honeycomb" radiolucency.
• Root resorption + cortical bone expansion.
• Well-demarcated.

• Follicular pattern: Islands of epithelium; peripheral columnar cells with reversed nuclear polarization + central stellate reticulum-like cells resembling enamel organ.
• Plexiform pattern: Epithelial strands in anastomosing network.
• Other subtypes: acanthomatous, granular cell, desmoplastic, basal cell.
• Classic description: "Piano key" appearance of columnar cells.

• Wide surgical resection with 1 cm margin beyond radiographic extent.
• Recurrent cases with confirmed BRAF mutation: BRAF-targeted therapy (e.g., dabrafenib).
• Prognosis: Good with surveillance; high recurrence if marginally excised.

2. ODONTOMA (Most Common Odontogenic Tumour Overall)

• Arises from both epithelium and mesenchyme; likely a hamartoma not true neoplasm.
• Contains enamel, dentin, cementum, and pulp in disorganized (complex) or recognizable tooth-like structures (compound).

• X-ray: Radiopaque mass.
• Treatment: Simple enucleation; low recurrence; excellent prognosis.

3. ODONTOGENIC MYXOMA

• Arises from odontogenic mesenchyme (dental papilla/follicle).
• Slow-growing, locally invasive, no capsule.
• X-ray: Multilocular radiolucency with "tennis racket" or "soap bubble" pattern.
• Histology: Stellate cells in loose myxoid stroma.
• Treatment: Resection; 25% recurrence.

4. ADENOMATOID ODONTOGENIC TUMOUR (AOT)

• Called "2/3 tumour": 2/3 in females, 2/3 in maxilla, 2/3 associated with impacted canine.
• Well-encapsulated; low recurrence.
• Histology: Duct-like structures + calcifications.
• Treatment: Simple enucleation.

5. CALCIFYING EPITHELIAL ODONTOGENIC TUMOUR (CEOT/Pindborg Tumour)

• Rare; locally invasive.
• Histology: Polyhedral epithelial cells + amyloid deposits + Liesegang ring calcifications ("driven snow" appearance on X-ray).

C. NON-ODONTOGENIC TUMOURS OF THE JAW

SUMMARY TABLE FOR RAPID REVISION

KEY EXAM POINTS

1. Most common jaw cyst = Radicular (periapical) cyst.
2. Most common odontogenic tumour = Odontoma (hamartoma).
3. Most clinically significant odontogenic tumour = Ameloblastoma.
4. Ameloblastoma histology = Reversed nuclear polarization + stellate reticulum = "piano keys."
5. OKC + multiple cysts = Gorlin syndrome (PTCH gene mutation).
6. AOT mnemonic = "2/3 rule" (2/3 female, 2/3 maxilla, 2/3 canine).
7. Burkitt's lymphoma in jaw = EBV, "floating teeth" on X-ray, in children.
8. BRAF V600E mutation in ameloblastoma = target for recurrent disease therapy.

Pathogenesis, Diagnosis and Treatment of Jaw Tumours - 10 Marks

I. PATHOGENESIS

A. Odontogenic Remnants - The Core Concept

B. Pathogenesis of Specific Tumours

1. Radicular (Periapical) Cyst

Dental caries → Pulpitis → Pulp necrosis
       ↓
Bacteria/toxins exit apical foramen
       ↓
Periapical inflammation → Periapical granuloma
       ↓
Stimulation of Rests of Malassez (epithelial cell rests in PDL)
       ↓
Epithelial proliferation + Cystic degeneration
       ↓
Radicular cyst formation

• Epithelium proliferates under influence of inflammatory cytokines (IL-1, IL-6, TNF-α, EGF).
• Central liquefaction due to accumulation of cellular debris, cholesterol crystals, and increased osmotic pressure → cyst expansion.

2. Dentigerous Cyst

• Arises from accumulation of fluid between the crown of an unerupted tooth and the reduced enamel epithelium.
• The enlarged follicular space >4mm from crown surface confirms cyst formation.
• Risk: Can transform into ameloblastoma or rarely squamous cell carcinoma if left untreated.

3. Odontogenic Keratocyst (OKC)

• Arises from dental lamina rests or from basal cells of overlying oral epithelium.
• Has intrinsic growth potential - proliferates independently (not merely from fluid pressure like other cysts).
• Associated with PTCH1 (Patched) gene mutation - a tumour suppressor gene in the Hedgehog signalling pathway.
• Multiple OKCs = Gorlin-Goltz Syndrome (PTCH germline mutation + basal cell naevi + calcification of falx cerebri).
• High recurrence (up to 60%) because daughter cysts ("satellite cysts") remain in bone after incomplete removal.

4. Ameloblastoma

• Arises from:
  • Remnants of dental lamina
  • Reduced enamel epithelium
  • Lining of dentigerous cysts
  • Basal cells of oral mucosa
• Molecular pathogenesis: Mutations in the MAPK signalling pathway found in ~90% of all lesions:
  • BRAF V600E mutation - most common
  • Less common: RAS mutations (NRAS, KRAS), FGFR2 mutations, SMO mutations
  • These mutations → uncontrolled cell proliferation + local bone invasion
• Growth mechanism: Invades medullary (cancellous) bone trabeculae - extends histologically beyond the radiographic margin, explaining high recurrence.
• Tumour does not show ectomesenchymal differentiation (distinguishes it from ameloblastic fibroma).

5. Odontogenic Myxoma

• Arises from odontogenic ectomesenchyme (dental papilla or follicular mesenchyme).
• Stellate cells embedded in loose myxoid stroma (rich in glycosaminoglycans).
• No true capsule → locally invasive growth.

6. Non-Odontogenic Mechanisms

• Fibrous dysplasia: GNAS gene mutation (Gs-alpha protein) → abnormal osteoblast differentiation → replacement of normal bone by fibrous tissue + disorganized woven bone.
• Central Giant Cell Granuloma: Reactive/neoplastic; osteoclast-like giant cells driven by RANKL signalling; aggressive form shows SH3BP2 or RAS mutations.
• Osteosarcoma of jaw: Radiation exposure, Paget's disease, fibrous dysplasia malignant transformation, or de novo.

II. DIAGNOSIS

Step 1 - Clinical Assessment

• Age, gender (AOT: young females; ameloblastoma: >20 years)
• Duration and rate of growth
• Pain (usually absent in benign tumours; present in infections/malignancy)
• Loosening of teeth, paraesthesia (numbness = aggressive/malignant behaviour)
• Family history (Gorlin syndrome)

• Site, size, shape of swelling
• Consistency: bony hard (osteoma), rubbery (myxoma), soft (cyst)
• Expansion: buccal/lingual cortical plate
• Egg-shell crackling (beaten copper appearance)
• Tooth mobility, sensibility testing
• Regional lymphadenopathy (malignancy)
• Skin: basal cell naevi (Gorlin syndrome)

Step 2 - Radiological Investigations

Step 3 - Laboratory / Special Investigations

• Aspiration of cyst: Straw-coloured fluid (dentigerous/radicular cyst); cheesy white material (OKC - keratin); blood (aneurysmal bone cyst/vascular lesion).
• Incisional biopsy: Mandatory before definitive treatment; confirms histological type.
• Fine Needle Aspiration Cytology (FNAC): For associated soft tissue masses.
• Immunohistochemistry (IHC): BRAF V600E staining in ameloblastoma.
• Molecular testing: MAPK/BRAF mutation analysis for recurrent ameloblastoma (guides targeted therapy).
• Blood tests: CBC, LFT, RFT; serum ALP elevated in fibrous dysplasia/Paget's; serum Ca/PO4.

Histopathological Diagnosis (Definitive)

III. TREATMENT

A. Odontogenic Cysts

B. Benign Odontogenic Tumours

1. Ameloblastoma

• Gold standard: En bloc resection with 1 cm margin of normal bone beyond radiographic extent.
• Tumour infiltrates cancellous bone trabeculae - extends beyond what X-ray shows.
• Simple enucleation alone = NOT acceptable (high recurrence ~22% even with en bloc; much higher with curettage alone).
• Mandible: Segmental mandibulectomy ± marginal resection; lingual/buccal cortical plates sacrificed.
• Maxilla: More aggressive surgery due to proximity to vital structures (orbit, skull base).
• Reconstruction: Immediate or delayed reconstruction with:
  • Titanium plates + iliac crest bone graft
  • Free fibula flap (gold standard for large mandibular defects)
• Recurrent ameloblastoma with BRAF V600E mutation: BRAF inhibitor dabrafenib ± MEK inhibitor trametinib.
• Unicystic type: Less aggressive; enucleation with clear margins; 10-20% recurrence.
• Peripheral type: Local excision; very low recurrence.
• Surveillance: Regular clinical + OPG/CT follow-up (recurrence can appear years later).

2. Odontoma

• Simple enucleation - curative; extremely low recurrence; excellent prognosis.

3. Odontogenic Myxoma

• Resection (locally aggressive, no capsule); 25% recurrence; close follow-up.

4. AOT

• Simple enucleation; rarely recurs; excellent prognosis.

5. OKC (Keratocystic Odontogenic Tumour)

• Enucleation + Carnoy's solution (chemical fixation of satellite cysts) + peripheral ostectomy.
• Some surgeons prefer resection for large/recurrent lesions.
• Gorlin syndrome patients: lifelong surveillance.

C. Malignant Odontogenic Tumours / Jaw Malignancies

D. Reconstructive Considerations After Jaw Resection

1. Titanium reconstruction plate - temporary/permanent.
2. Iliac crest bone graft - for small to medium defects.
3. Free fibula flap - gold standard for large mandibular reconstruction.
4. Dental rehabilitation with implants after osseointegration.

SUMMARY

DIAGNOSIS PATHWAY FOR JAW TUMOUR
History + Examination
        ↓
OPG (Panoramic X-ray) - first imaging
        ↓
CT/CBCT for detailed bone assessment
        ↓
Aspiration biopsy (cyst fluid)
        ↓
Incisional biopsy + histopathology (DEFINITIVE)
        ↓
MRI / molecular tests if malignancy suspected
        ↓
Multidisciplinary treatment planning

1. Pathogenesis = odontogenic epithelial remnants (Rests of Malassez, dental lamina rests) + MAPK/BRAF mutations in ameloblastoma + PTCH mutation in OKC.
2. Gold standard diagnosis = incisional biopsy + histopathology.
3. Ameloblastoma treatment = 1 cm en bloc resection + free fibula flap for reconstruction.
4. OKC = most aggressive cyst; Carnoy's solution to destroy satellite cysts; related to Gorlin syndrome.
5. Recurrent ameloblastoma = BRAF inhibitor (dabrafenib).
6. Soap bubble X-ray = Ameloblastoma; Ground glass = Fibrous dysplasia; Sunray = Osteosarcoma.

EPULIS - Definition, Types, Pathogenesis & Management (10 Marks)

DEFINITION

Epulis is defined as any benign, localised swelling or tumour-like growth arising from the gingiva (gum tissue). It is not a single pathological entity but a clinical term covering a group of reactive, inflammatory, or neoplastic lesions originating from the gingiva or periodontal tissues.

TYPES OF EPULIS

DIAGRAM

DETAILED DESCRIPTION OF EACH TYPE

1. FIBROUS EPULIS (Most Common Type)

• Chronic local irritation: dental calculus, rough tooth edges, ill-fitting crowns, orthodontic appliances
• Poor oral hygiene

• Firm, pale pink, sessile or pedunculated nodule on the gingiva
• Usually between teeth (interdental papilla region)
• Painless, slow-growing
• Surface may be ulcerated (from biting)
• Size: few mm to >1 cm
• Does NOT bleed easily

• Dense fibrous connective tissue
• Variable chronic inflammatory cell infiltrate (lymphocytes, plasma cells)
• Covered by stratified squamous epithelium
• May contain calcifications (ossifying variant = Peripheral Ossifying Fibroma)

Chronic irritation (calculus/trauma)
        ↓
Stimulation of gingival fibroblasts
        ↓
Excessive collagen/fibrous tissue production
        ↓
Fibrous epulis

• Remove causative irritant (scaling and root planing)
• Surgical excision down to periosteum + curettage of underlying bone
• Recurrence: 15-20% if cause not removed

2. VASCULAR EPULIS (Pyogenic Granuloma)

• Minor trauma, poor oral hygiene, dental calculus
• Pregnancy - due to elevated oestrogen/progesterone → increased vascular proliferation
• Hormonal medications (OCP)
• BRAF/RAS mutations identified in some cases

• Pregnancy Epulis (Granuloma Gravidarum): Occurs in ~1% of pregnant women; usually in 1st trimester; commonly on anterior maxillary gingiva; may spontaneously regress postpartum.

• Bright red to reddish-purple, soft, smooth or lobulated nodule
• Bleeds easily (even with gentle touch)
• Grows rapidly
• Usually painless
• Most common on anterior maxillary gingiva
• Can reach 1-2 cm size

• Lobular proliferation of capillaries (lobular capillary haemangioma)
• Loose oedematous stroma
• Abundant inflammatory cells
• Ulcerated surface common

Local trauma / Hormonal influence (pregnancy)
        ↓
Inflammatory mediators + VEGF ↑
        ↓
Capillary proliferation + granulation tissue
        ↓
Vascular Epulis / Pyogenic Granuloma

• Oral hygiene improvement + remove irritant
• Surgical excision - most reliable; include base + periosteum
• Alternatives: Laser (Nd:YAG, Er:YAG, pulsed dye), cryosurgery, electrocautery
• In pregnancy: conservative management initially; excise if large, bleeding, or persists postpartum
• Recurrence: ~15% (especially if incomplete excision)

3. GIANT CELL EPULIS (Peripheral Giant Cell Granuloma - PGCG)

• Bluish-red to purple, soft nodule (due to haemosiderin deposits + vascularity)
• Size: 10-20 mm (can be larger)
• Located between or around the teeth - especially anterior mandible/maxilla
• Can cause superficial bone resorption ("cupping" of underlying alveolar bone on X-ray)
• May be associated with dental implants
• Occurs at any age; slight female predilection
• Associated with cherubism (autosomal dominant; SH3BP2 mutation) when multiple

• Multinucleated osteoclast-like giant cells scattered throughout fibrovascular stroma
• Spindle-shaped mesenchymal cells
• Haemosiderin deposits + inflammatory infiltrate
• Resembles giant cell tumour of tendon sheath histologically

Local trauma / tooth extraction / ill-fitting denture
        ↓
RANKL-mediated osteoclast recruitment
        ↓
Multinucleated giant cell proliferation
        ↓
Giant Cell Epulis

• Must be distinguished from Central Giant Cell Granuloma (which is intraosseous) and Brown tumour of hyperparathyroidism (systemic - check PTH, Ca, PO4).

• Surgical excision + peripheral ostectomy (curettage of underlying bone)
• Check serum calcium and PTH (to rule out hyperparathyroidism)
• Recurrence: 10-15%

4. EPULIS FISSURATUM (Denture Epulis)

• Firm, fissured, whitish-pink folds of hyperplastic tissue
• Located in the labio-alveolar sulcus (vestibular fold)
• Usually fits around the denture flange like a clamp
• Painless usually; may be tender if ulcerated
• Chronic condition in elderly edentulous patients

• Dense fibrous connective tissue
• Chronic inflammatory infiltrate
• Hyperplastic epithelium; may show pseudoepitheliomatous hyperplasia
• Sometimes called granuloma fissuratum in skin literature

Worn/old/ill-fitting denture
        ↓
Chronic repetitive trauma to sulcus mucosa
        ↓
Reactive fibrous hyperplasia
        ↓
Epulis Fissuratum

• New well-fitting denture - mandatory first step
• Surgical excision of excess tissue (once new denture fabricated)
• Small lesions may resolve with new denture alone
• Biopsy to rule out squamous cell carcinoma (chronic irritation = risk factor)

5. CONGENITAL EPULIS (Granular Cell Tumour of Newborn)

• Present at birth (congenital)
• Smooth, pink, pedunculated nodule on the anterior maxillary or mandibular alveolar ridge
• Female predominance (8:1 female:male)
• Can interfere with feeding/breathing if large
• Regresses spontaneously in many cases

• Large polygonal cells with abundant granular eosinophilic cytoplasm
• Unlike adult granular cell tumour - S-100 negative (differentiates it)

• Exact origin unclear - possibly from primitive mesenchymal cells or undifferentiated neural crest cells of alveolar ridge
• Regresses spontaneously - suggests hormonal influence (oestrogen receptor positive in some)

• Small lesions: observe (may regress spontaneously)
• Large/symptomatic lesions: surgical excision
• Excellent prognosis; no recurrence after excision

COMPARISON TABLE

GENERAL MANAGEMENT PRINCIPLES

STEP 1: History (irritant? pregnancy? denture? newborn?)
STEP 2: Clinical examination + X-ray (OPG/periapical)
STEP 3: Remove causative factor (calculus, ill-fitting denture)
STEP 4: Oral hygiene instruction
STEP 5: Surgical excision (under LA) + histopathological examination
STEP 6: Regular follow-up (watch for recurrence)

• Conventional scalpel excision (most common)
• Electrocautery
• Laser excision (Er:YAG, Nd:YAG, CO₂) - less bleeding, better healing
• Cryosurgery

• Peripheral ameloblastoma
• Squamous cell carcinoma
• Brown tumour of hyperparathyroidism (for giant cell epulis)
• Kaposi sarcoma (in HIV patients)

KEY EXAM POINTS

1. Epulis = clinical term for ANY benign gingival swelling - not a single diagnosis.
2. Most common = Fibrous epulis.
3. Bleeds most = Vascular (pyogenic granuloma); especially in pregnancy.
4. Bluish-red + bone cupping on X-ray = Giant cell epulis → rule out hyperparathyroidism (check PTH, serum Ca).
5. Around denture flange in elderly = Epulis fissuratum → new denture first, then excise.
6. Newborn + maxillary alveolar ridge + female = Congenital epulis (S-100 negative).
7. Always send excised tissue for histopathology - to rule out malignancy.
8. Pregnancy epulis may regress spontaneously postpartum - conservative initially.