Dysplasia Flashcards
2 distinct disease patterns for oral cancer
Oral cavity cancer (OCC)
Oroparyngeal cancer (OPC)
Oral cavity cancer
Male to female - 2:1
2.5 per 100 000 population
Incidence not increasing worldwide but decrease in man and increase in women (linked to reduction in tobacco use)
Commonest sites for oral cancer
FOM*
Lateral border of tongue*
Soft* and hard palate
gingivae
Retromolar area*
Buccal mucosa
*- mainly in drinkers and smokers (SSC)
Oro phyrangeal
1.4 per 100 000 population
Male to female -4.8 : 1
Linked to HPV epidemic (especially in high income area)
In Scotland -highest increase of OC for any cancer (85%)
Risk factors for oral cavity cancer
Smokers who don’t drink- 2x risk(increase with quantity, duration, frequency of tobacco use; fewer cigarettes for longer times worse than high numbers in short time)
Smokers who drink x5 (increase with frequency and duration of smoking and alcohol consumption, no safe lower limit)
Drinkers- x2 (3-4 drinks/day; frequency more important than duration)
Betel quid- X3
Socioeconomic status- X2 (even without other risk factors; low education)
Uncertain risk factors
Family history - 1st degree relative with H&N cancer is important
Oral health- poor OH can be associated with increased cancer risk- small effect though
Sexual activity - more partners (if 4+ oral sex partners, if 6+ sexual partners in life, early age of sexual activity - risk of OPC)
Benefits of stopping smoking and alcohol
Benefits showed after 4 years of stopping smoking-
risk will reduce and reach the similar level of the one that never smoked after 20 years of stopping
Stopping heavy alcohol- after 20 years, risk becomes smaller
Potentially malignant leasions
“Premalignant means”
En route to become cancer
Much more likely to become cancer
White leasions
Red lesions
LP
Oral submucous fibrosis
White and red lesions
Leukoplakia - white patch that cannot be whipped off
Erythroplakia- red patch,
Both clinical descriptions not diagnoses
Oral cancer in white lesions
Incidence 0.2-4%
Unclear data (reliability)
Usually appear in “clinically normal mucosa” in the UK
Leukoplakia is more likely (50-100 times) to progress to cancer than clinically normal mucosa
Erythroplakia
Much less frequent than leukoplakia
Much greater risk of cancer
Greater dysplasia risk ( up to 50% become cancer)
Dysplasia
Based on cellular atypia and epithelial architectural organisation
Caterorisation (new)
Low, high grade or carcinoma in situ
Graded by different histological features
Cytological: abnormal varietion in- nuclear size and shape, cell size and shape, atypical mitosis figures, increased number and size of nucleoli, nuclear hypochromatism
Architectural: irregular epithelial stratification, loss of polarity of basal cells, drop-shaped rete ridges, increased and abnormal mitoses, premature keratinization in single cells, abnormal keratinization, keratin pearls in rete ridges, loss of epithelial cell cohesion/adhesion
High grade dysplasia
Little resemblance to a normal squamous epithelium
Architectural change upper third
Usually shows considerable atypia
Invade in non-cohesive pattern with fine cords, small islands and single cell infiltrating widely through the connective tissue
Mitotic figures are prominent and many many be abnormal
- Degree of differentiation is widely used to predict prognosis and shows a significant correlation to survival
Enlarged and hyperchromatic cells are visible and later of epithelium become less ordered
Marked loss of differentiation of epithelial cells, abnormal mitosis, marked cellular and nuclear pleomorphism
Low grade dysplasia
Easy to identify that the tumour originates from squamous epithelium
Architectural change into lower third
Shows a 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 the surface epithelium
Thin layer of parakeratin present
Structure, maturation, orderly differentiation of epithelial cells is largely unaffected
There is a degree of irregularities of the basal cells with an increase in the number
Carcinoma in situ
Theoretical concept
Cytologically malignant but not invading
Abnormal architecture -fill thickness, severe cytological atypia
Mitotic abnormalities frequent
Whole thickness of epithelium is involved but basement membrane is intact
No invasion of lamina propria
Histological prognostic factors
1.Pattern is invasion- bulbous rete ridges infiltrating at some level is considered of a better prognosis than widely infiltrating small islands and single cells
- Depth of invasion- risk of metastases for a tumour greater than 4 mm was 4x greater that for a tumour less than 4 mm
- Perineural invasion- is seen in up to 60% of OSCC but is most significant when a tumour is seen within a large nerve at a site nerve at a site some distance from the main tumour mass
- Invasion of vessels- widely thought to be associated with lymph node metastases and a poor prognosis
Multi stage promotion/stages of oral cancer
From normal ( hemostasis, normal keratinocyes) to potentially malignant (hyperplasia, genetic instability or aneuploidy,exposure to risk factors) to oral cancer (invasion)
Field cancerization concept
Not only the site with cancer was subjected to risk factors so the same changes (dysplasia) can be happening in other sites but just at a slower rate (if it becomes cancer, it is a new primary cancer not metastasis)
5 cm radius from original primary cancer is a high cancer risk field- field canceratisation
Examination of the whole field is necessary!! As many primary tumours can be in a single patient
Concept of field canceratisation - high cancer risk in 5 cm radius of the original primary - that is most of the mouth/pharynx
Metachronous lesions- come from the same field change and happen at the same time as the primary but on other site
Oral cancer staging
Site
Size (T)- TX- cannot be assessed, T0- no evidence of primary tumour,Tis- tumour in situ, T1- tumour 2 cm or less in greatest diameter , T2- tumour more than 2 cm but no more than 4 cm in greatest diameter, T3- tumour more than 4 cm, T4a- moderately advances local disease ( tumour invades through cortical bone into deep muscle of tongue- genioglossus, hyoglossus, palatoglossus, styloglossus), maxillary sinus, skin of the face, T4b- very advanced local disease (invades masticator space, pterygoid plates, skull base, internal carotid artery)
Spread (N&M)- N-regional lymph nodes, M- distant metastasis
Oral cancer prognosis
1/3 pt present at stage I/II
Stage I -80% cure rate
Stage II- 65% cure rate
If not in those stages, cure rate is 30%
Treatment options: surgery, radiotherapy, chemotherapy, immunotherapy - depends on pt choice and prognosis/tumour location/size and nutritional status
- For resectable tumours, primary surgery offers the best outcome+ post surgery radiotherapy and/or chemotherapy
Lip cancer
Commonly lower lip- manifests as bon healing ulcer or swelling
Risk: UV light (UV-B), smoking
It slowly grows, locally invasive, rarely metastasise to nodes
Good prognosis as early detection
Oral cancer detection
Difficult to do- judgement from experience
Oral cancer screening
Things to consider:
Benefits Vs harm
Undetected Vs false positive
Cost of screening Vs cost of disease
Cost of screening Vs disability of disease
HPVq16 screening
Toluidine blue ( shows change and dysplasia, but a lot of false positives)
VELscope (autofluoresence to tissues with blue light, loss of fluorescence equates to “change”)
Photodynamic diagnosis( PDD)
The most cost effective and reliable screening tool is the experienced dental practicioner
After smoking and alcohol as a risk factor for oral cancer what is the third highest risk factor ?
Poverty
Explain sensitivity and specificity associated with degrees of diagnostic accuracy
Sensitivity - proportion of true positives
Specificity - proportion of true negatives
The most cost-effective screening tool for detection of oral dysplasia and oral cancer in primary care
Clinical judgement of experienced clinician
What characteristics suggest enlarged lymph nodes are caused by a malignant neoplasm
Firm to palpation
Fixed to adjacent structures
No painful
Lymphatic spread of oral carcinomas
Metastatic spread is primarily via lymphatics to the regional lymph nodes
The specific sites of metastasis depend on the drainage of tumour site
Most of the carcinomas are in posterior, lower mouth, the submandibular and jugulodigastric nodes are most frequently involved
Lymphatic drainage from the top of the tongue is to the submental nodes and then to jugulo-omohyoid group, low down the neck
From the dorsum of the tongue, drainage is to submandibular nodes and then to the jugulodigastric group
Tobacco as a risk factor
Tobacco (smoked or chewed) releases a complex mixture of at least 50 compounds including polycyclic aromatic hydrocarbons such as benzpyrene, nitrosamines, aldehydes and aromatic amines which are carcinogens
The main cause of oral cancer
Alcohol as risk factor
Combined with tobacco is worse
Risk increases 80-fold in those with highest levels of smoking and alcohol consumption
Diet as risk factor
A diet low on fresh fruit and vegetables has been found to be associated with increased oral cancer risk
Histopathology of oral squamous cell carcinoma
Invasion into the basement membrane and destruction of surrounding rissue
When can OSCC be diagnoses
Once the basement membrane is breached
SSC.is infiltrating downward. The neoplastic squamous cells are still similar of the normal squamous cells, but are less orderly.
Some neoplastic epithelial cells can form keratin pearls
In general, neoplasms with less differentiation are more aggressive, growing more quickly, invading or metastasing
