potentially malignant disorders Flashcards by David Jack

What is a potentially malignant lesion?

Altered tissue which cancer is more likely to form

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What is a potentially malignant disorder?

Generalised state with increased cancer risk

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Give 4 examples of potentially malignant systemic conditions

Lichen planus
Oral submucous fibrosis
Iron deficiency - anaemia can lead to atrophy of oral epithelium so barrier function is diminished
Tertiary syphilis - can form white patch on tongue

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Describe chronic hyperplastic candidosis

Caused by C. albicans
Commissures seen at the angles of the mouth
Found in smokers
Dysplasia may be present

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How is chronic hyperplastic candidosis treated?

Systemic antifungal - fluconazole capsules, 50mg once daily for 14 days
Biopsy
Stop smoking
Observe

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Where do most oral carcinomas in the UK arise from?

Clinically normal mucosa

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How much more likely is leukoplakia to progress to cancer than clinically normal mucousa?

50 to 100 times

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What are the clinical predictors of malignancy in leukoplakia?

Age - older more likely
Gender - differs from country
Site - buccal mucosa is low risk, floor of mouth and tongue is high risk
Clinical appearance - if homogenous and smooth then less likely, non-homogenous, verrucous and ulcerated then mitre likely

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What are the histopathological predictors of malignant change?

Dysplasia
Atrophy
Candida infection
Biological markers eg - p53, HPV+ and HPV-

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What is dysplasia?

Disordered maturation (growth) in a tissue
A histopathological diagnosis, not clinical

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What is atypia?

Changes in cells

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What are the predictors for histopathology epithelial dysplasia?

Assess architectural changes then cytology
Architectural changes such as maturation (growth) and stratification (more layers)
Cytological abnormalities such as cellular atypia

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What is the WHO classification for grading of epithelial dysplasia?

Hyperplasia
Mild
Moderate
Severe
Carcinoma-in-situ

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How is staging and grading carried out?

Grading is done histopathologically
Staging is done clinically

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Describe basal hyperplasia

Increased number of basal cells, rest of epithelium is normal
Architecture - regular stratification, basal component is larger
No cellular atypia

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Describe mild dysplasia

Architectural changes in lower third
Cytology - mild atypia, pleomorphism and hyperchromatism

What is pleomorphism?

Difference in size and shape of a cell

What is hyperchromatism?

Darker staining of a cell due to more DNA present

Describe moderate dysplasia?

Architecture changes extends into middle third
Cytology - moderate atypia - hyperchromatism and pleomorphism

Describe severe dysplasia

Architecture changes extend into upper third
Cytology - severe atypia and numerous mitoses, abnormally high
- hyperchromatism and pleomorphism
- loss of polarity (lack of difference between different layers of cells)

Describe a carcinoma-in-situ

A theoretical concept
Malignant but not invasive
Abnormal architecture - full thickness or almost full of viable cell layers
Pronounced cytological atypia - mitotic abnormalities frequent

How may pathology be confirmed in the future?

Salivary biomarkers
Next generation sequencing
AI

What common diagnostic tests are used for potentially malignant lesions?

Vital staining
Oral cytology
Optical imaging

What are the 2 main factors of carcinogenesis?

Genetic
Environmental (carcinogens)

What is the molecular basis of cancer?

Damage leads to altered gene expression which leads to altered cell function

What is an oncogene?

A gene that has the potential to cause malignancy

What are tumour suppressor genes?

Genes that regulate cell division

What is miRNA?

Strands of RNA which can play a role in neoplastic transformation as they control the function of oncogenes and tumour suppressor genes

How can oncogene inactivation/mutation lead to malignancy?

If 1 of a pair is inactivated/mutated, the others function will not be enough and the cell will become malignant

How can tumour suppressor gene inactivation/mutation lead to malignancy?

Need both of a pair to be inactivated/mutated for the cell to become malignant This is called Knudson’s ‘two hit’ hypothesis of carcinogenesis

Give an example of a tumour suppressor gene and it’s role

Tp53 gene provides instructions for p53 protein

Give an example of a viral component in oral cancer genetics?

HPV

What are the 6 genetic changes of cancer?

Evading apoptosis Self-sufficiency in growth signals Insensitivity to anti-growth signals Tissue invasion and metastasis Limitless replication potential Sustained angiogenesis

What percentage of oral cancer is SCC?

95%

What is cohesive front and non-cohesive front in cancer spread?

Cohesive front - cells are together and advance at the same time Non-cohesive front - strong possibility of LN involvement even if no clinical signs of enlargement

What are the 3 methods of oral cancer spread?

Local extension of disease Lymphatic spread Haematogenous spread

How may oral cancer spread to bone?

Gaps in cortex in edentulous patients PDL if patient is dentate

Describe the subtypes of oral SCC?

Verrucous carcinoma - has the best outcome Basaloid squamous - aggressive and associated with HPV Spindle cell - aggressive and difficult to identify