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potentially malignant oral lesions (Oral SCC: carcinoma w squamous…
potentially malignant oral lesions
Oral SCC: carcinoma w squamous differentiation from mucosal epithelium, invaded through BM into CT
WHO 2017: Oral Potentially Malignant Disorders (Clinical), Oral Epithelial Dysplasia (Histological)
Oral potentially malignant disorders: all clinical presentations risk of cancer development in clinically definable precursor lesions or in clinically normal oral mucosa WHO 2017 (erythroplaskia, erythroleukoplaskia, leukoplakia, oral submucous…)
Leukoplakia: white plaques questionable risk excluded other diseases that carry no incr risk cancer
Assessment clinical features: COLOUR incr redness incr risk transformation, ? association w candida
TEXTURE: homogenous (little risk transformation), non homogenous (incr risk)
SITE: FOM incr risk transformation (no keratin)
Erythroplakia: fiery red patch cannot be characterised as any other lesion, older smoking/alc pts
Oral submucous fibrosis: epithelial atrophy w fibrosis of lamina propria & submucosa, trismus. Betel users
Palatal lesions in reverse smokers: smoke w lit end of cigar in mouth
Lichen planus: immune-mediated mucocutaneous disorder w chronic inflam …
Actinic keratosis: PMOD of lip related to UV exposure, incr risk malignant transformation,
Epithelial dysplasia: WHO 2017 (mild, mod, severe), binary grade (low grade, high grade), maturation disrupted
Assessment dysplasia: gold standard, incr dysplasia = incr risk transformation, predictor behaviour high grade lesions but less useful predict outcome in lesions w min/no dysplasia. Pts w severe dysplasia > risk malignant transformation than those w no dysplasia. Less certainty w lower grades dysplasia. Lack association between dysplasia grading & malignant transformation
Management lesions w no or mild dysplasia – photograph, remove aetiological factors, consider removal, reg reviews
Management lesion w mod or severe dysplasia: removal, check aetiological factors, reg reviews
Predict behaviour of lesion? Exam, biopsy to assess dysplasia. What else can we assess? Clinical assessment (smear, brush biopsy), lab (biopsy – molecular techniques…)
Toluidine blue (nuclear changes), cheap & simple, detect occult oral mucosal lesions or demarcate extent, detects oral carcinomas BUT subjective interpretation
Tissue Fluorescence Imaging: autofluorescence after blue excitation light, autofluorescnece altered in abnormal tissues vs w normal tissue, distinguishes healthy mucosa, identifies occult lesional tissue
Brush biopsy: atypical cells, scalpel biopsy follows
DNA ploidy: genetic instability & DNA aberration, genetically stable diploid cells replaced by unstable aneuploid cells, oral SCC aneuploidy cell pop, ploidy status prognostic factor SCC
Loss heterozygosity (LOH): loss genomic material in 1 pair chromosomes, deleted regions contain TSG, LOH at 3p common in oral SCC
Microsatellite Instability (MSI)
P53 expression: mutation in carcinogenesis, detected in histological sections w immune…
Predictors malignant transformation: non-smoking, site, non-homogenous, size, dysplasia grade
Saliva: Oral Fluid NanoSensory Test, proteins & nucleic acid targets