Incidence
- 2-3rd decade
Common site
- 70 – 80% mandible especially 3rd molar and ascending ramus region
Pathology
- Rests of dental lamina
Pathogenesis
- PCTH tumor suppressor mutation
- High epithelial proliferation (Ki67+ve)
- Apoptosis evasion by increased Bcl2
- Over expression of interface proteins:
- MMP 2 and 9
- TGF
- IL-1 and IL-6
Clinical
- Painless
- Slow growing expansile intraosseous mass
- Discovered on routine x-ray
- Grow in anterior – posterior direction. Reach large sizes without gross bony expansion
Clinical subtypes
- Solitary lesion
- Multiple lesions
- Syndrome associated lesion: Gorlin Goltz syndrome
- Therefore do full body check up
Histology
- Cyst wall:
- Fibrous
- Thin and corrugated/ folded
- Contains daughter/satellite cyst
- Epithelial lining:
- Flat basement membrane
- Hyaline/Rushton bodies
- Keratinized squamous epithelium
- Lack rete pegs
- Thin and even thickness, < 10 cells thick
- Lumen:
- Straw colored fluid (keratin)
- Basal cells Ki67 and Bcl2 positive – shows high mitotic figures
Radiology
- Unilocular/multilocular radiolucency, some with impacted teeth
- Well circumscribed radiolucency with radiopaque margins
Biopsy
- Aspirational biopsy:
- Greasy fluid
- Pale in color
- Contains keratotic squames
Differential diagnosis
- Radiologically:
- Histologically:
Management
- Wide surgical excision to avoid recurrence (significant recurrence rates)
- Marsupialization
- Curettage
- Enucleation with application of Carnoy’s solution
Reasons for increased recurrence rate
- Thin fragile lining – difficult to enucleate intact
- Finger like cystic extensions into cancellous bone
- Presence of satellite/daughter cyst in cystic wall/capsule
- Formation of additional keratocysts from other rests of dental lamina
- Inferior standards of surgical treatment
- Possibly a neoplasm
Reasons it can be considered a neoplasm
- High recurrence rate
- Fast growth/aggressive behaviour
- Can invade adjacent tissues
- Possible malignant transformation
- Associated with mutated PTCH suppressor gene
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