Premalignancy & Oral Cancer Flashcards
Hyperplasia
increased number of cells
Hyperkeratosis
Thickening of stratum corneum
Orthokeratosis
Hyperkeratosis without parakeratosis (No nuclei)
Parakeratosis
Flattened keratinocyte nuclei within stratum corneum
Hypogranulosis
- Decreased thickness of granular layer
Acanthosis
Thickened squamous cell layer
Epidermal atrophy
Decreased thickness of epidermis
Dyskeratosis
- Abnormally or prematurely keratinized keratinocytes
- identified by prominent eosinophilic (red stain) cytoplasm
Apoptosis
Programmed cell death
Produces colloid bodies
Pleomorphism
variability in size, shape and staining of cells and/or their nuclei
Leukoplakia
- White lesion
- can’t rub off
- no etiology
- no source or diagnosis
- Clinical term ONLY
- no diagnostic meaning
- malignant transformation: 0.7-2%
- most common “risk” lesion
Frictional Hyperkeratosis
- aka Hyperkeratosis without dysplasia
- frictional keratosis (clinical Term)
- associated w/Trauma
- chronic rubbing or friction against oral mucosa
Frictional Keratosis: Location
- Lips
- lateral tongue
- Buccal Mucosa
Frictional Hyperkeratosis: Histology
- Macrophages and epithelial cells→ IL-8→keratinocyte-derived chemokine (KC)=mediates proliferation
Frictional Hyperkeratosis Treatment
- remove irritant
- patient returns in 2-3 weeks (Cell turnover time)
- Biopsy
- if lesion has not regressed
Dysplasia
- Lack of proper maturation
- indicator of premalignancy if in epithelium
- increased risk to become SCC
- Keratinocytes cannot form regular layers and produce normal keratin
Precursor Squamous Lesions
- increased likelihood→SCC
- Adults (50 y.o.)
- strong association w/smoking and alcohol abuse
Precursor Squamous Lesions: Risk Factors
- Tobacco & alcohol
- strong association w/SCC
- Sunlight
- Malnutrition
- Immunocompromising diseases
- HPV
- Unknown (15%)
Precursor Squamous Lesions: Clinical Manifestations
- Various presentation
- Discrete to diffuse
- Lekoplkia to erythroplakia
- Leukoplakic
- less likely to be premalignant
- color due to thickness of dysplasia
- thinner=red
- thicker=white
- color due to thickness of dysplasia
- less likely to be premalignant
- Erythroplakia
- 90% carcinoma insitu or superficially invasive SCC
- Leukoplakic
-
Be highly suspicious of lesions in floor of mouth and ventral tongue
- Biopsy w/resection and clean margins
Dysplastic Lesions
- increased risk to become SCC
Dysplasia: Architectural changes include:
- Increased:
- Cells and mitotic cells in basal layer
- Keratin pearl formation
- Decreased Polarity
-
Parakeratosis
- Cellular pleomorphism
Dysplasia: Cytology features
- increased:
- nuclear size
- nucleus:cytoplasm ratio
- Nuclear pleomorphism
- Nuclear hyperchromasia
- Dyskeratosis
Mild Dysplasia
- Increase crowding of mitotic cells in basal layer
- Dysplasia-lower ⅓ of epithelium
Mild Dysplasia: Management
Depends on location
- High risk area or patient: Complete excision
- low risk area or patient: watch and observe for 3 months
- if lesion does not regress→ excise