Oral Cancer Flashcards
high risk sites for oral cancer
floor of mouth
lateral border of tongue
retromolar regions
soft & hard palate
gingivae
buccal mucosa
oral cavity cancer stats
male 2:1 female
incidence not increasing worldwide (decreasing in men & increasing in women)
linked to reduction in tobacco use
oropharyngeal cancer stats
male 4.8:1 female
rates rapidly rising especially in high income areas (N.America)
linked to rising HPV epidemic
shown to have highest increase for any cancer in scottish cancer registry
risk factors for oral cancer
- smokers who don’t drink - x2 risk
- increases with quantity/duration/frequency of tobacco use
- fewer cigarettes for longer duration is worse than a high no short term - heavy drinkers (3-4 drinks/day) - x2 risk
- never smoked population
- freq more important than duration - smokers & drinkers - x5 risk
- increases with freq & duration of both
- no safe lower limit - betel quid (paan) - x3 risk
- mixture of substances including areca nut with or without tobacco wrapped in betel leaf & placed in mouth - socioeconomic status - x2 risk
- even without other risk factors
- limited education
- SIMD index
other potential risk factors for oral cancer
family history
oral health
sexual activity (increased risk of oropharyngeal cancer)
benefits of stopping smoking & drinking alcohol
demonstrable effects of quitting smoking identified within 1-4yrs after stopping
risk reduced & reached a similar level to those who had never smoked 20yrs after quitting
but risk effects associated with quitting heavy alcohol consumption takes 20yrs to begin to emerge
Improvement in decrease in oral cancer risk achieved quicker by stopping smoking than stopping drinking
Smoking prevention is more important in the short term
potentially malignant lesions
white lesions (leukoplakia) - white patch that cannot be rubbed off and is not any other disease
red lesions (erythroplakia) - red patch that is not any other disease
lichen planus - candida leukoplakia / chronic hyperplastic candidiasis
oral submucous fibrosis
oral cancer in white lesions
incidence 0.2-0.4%
most oral carcinomas in UK arise in initially clinically normal mucosa
most cancer in high incidence areas e.g. india from potentially malignant lesions
worldwide leukoplakia 50-100x more likely to progress to cancer than clinically normal mucosa
erythroplakia
must less frequent than leukoplakia
much higher risk of cancer
greater dysplasia risk (up to 50% already are a carcinoma)
no good follow up studies available
dysplasia
based on cellular atypia and epithelial architectural organisation
categorised as low grade, high grade and carcinoma in situ
histological grading of low grade oral mucosa dysplasia
- easy to identify that tumour originates from squamous epithelium
- architectural change to lower 1/3
- cytological atypia / dysplasia may not be prominent
- shows considerable amount of keratin production
- evidence of stratification
- well formed basal cell layer surrounding tumour islands
- tumour islands are usually well defined and are often continuous with surface epithelium
- invasion pattern with intact large branching rete pegs pushing into underlying CT
- when there is architectural change into middle 1/3 depending on level of cytological atypia will be classified into low or high grade
histological grading of high grade oral mucosa dysplasia
- shows little resemblance to normal squamous epithelium
- architectural change upper 1/3
- usually show considerable atypia
- invade in a non cohesive pattern with fine cords, small islands and single cells infiltrating widely through CT
- mitotic figures are prominent and many may be abnormal
- degree of differentiation is widely used to predict prognosis & shows a significant correlation to survival
carcinoma in situ
theoretical concept
cytologically malignant but not invading
abnormal architecture:
- full thickness (or almost full)
- severe cytological atypia
mitotic abnormalities frequent
histological prognostic factors
pattern of invasion - bulbous rete pegs infiltrating at the same level is considered of a better prognosis than widely infiltrating small islands & single cells
depth of invasion - risk of metastases for tumours >4mm was 4x greater than for a tumour <4mm
perineural invasion - is seen in up to 60% of OSCCs but is more significant when a tumour is seen within a large nerve at a site some distance from the main tumour mass
invasion of vessels - widely thought to be associated with lymph node metastases & a poor prognosis
field cancerisation concept
multiple primaries over time (up to 15-20 in some pts)
concept of field cancerisation is high cancer risk in 5cm radius of original primary which in mouth is most of oral cavity / pharynx
can be synchronous or metachronous lesions i.e. can occur at same time as primary or at later times