Oral Dysplasia and Potentially Malignant Disorders Flashcards
Oral cancer red flags
Non-homogenous
Non-healing
Indurated
Exophytic
>3 week duration
RF for oral cancer
Alcohol
Smoking
HPV
Poor OH
Betel nut/ tobacco
Socio-economic background
Low fruit/ vege
What is OED
Abnormal growth
Only histological diagnosis
Architectural changes of dysplasia
Irregular epithelial stratification
Loss of polarity of basal cells
Drop shaped rete ridges
Increased number of mitotic figures
Abnormally superficial mitoses
Cytological features
Abnormal variation in nuclear size
Abnormal variation in nuclear shape
Abnormal variation in cell size
Abnormal variation in cell shape
Increased nuclear cytoplasmic ratio
Atypical mitotic figures
Increased number and size of nucleoli
Hyperchromasia
Dysplasia grading system
Normal
Low grade
High grade
Cancer
OED molecular markers
Signalling pathways:
EGFR
Cell cycle:
Ki67, p53, pRB
Immortalization: Telomerase
Apoptosis:
p53, p21
Angiogenesis:
VEGF
Basal hyperplasia
Increased basal cell numbers
Architecture (regular stratification, larger basal compartment)
NO CELLULAR ATYPIA
Mild Dysplasia
Architecture changes in lower 3rd
Mild atypia
Pleomorphism
Hyperchromatism
Basal cell hyperplasia
Moderate Dysplasia
Architecture changes into middle 3rd
Moderate atypia
Pleomorphism
Hyperchromatism
Severe Dysplasia
Architecture changes into upper 3rd
Severe atypia
Numerous mitoses
Loss of polarity
Hyperchromatism
Carcinoma-In-Situ
Theoretic concept
Malignant but non-invasive
Abnormal architecture
Pronounced atypia
Management of OED
Mild/ Low grade:
Monitored for at least 5 years
Moderate/ Severe:
Removal of lesion via OMFS
What is OPMD?
Mucosal abnormality with statistically increased risk of developing oral cancer
Types of OPMD?
Leukoplakia
Proliferative Verrucous Leukoplakia
Erythroplakia
Oral submucous fibrosis
OLP
OLTR
Keratosis
Palatal lesions in reverse smokers
Oral Lupus Erythematous
Dyskeratosis Congenita
Oral GvsHD