potentially malignant disorders Flashcards
What is a potentially malignant lesion?
Altered tissue which cancer is more likely to form
What is a potentially malignant disorder?
Generalised state with increased cancer risk
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
Describe chronic hyperplastic candidosis
Caused by C. albicans
Commissures seen at the angles of the mouth
Found in smokers
Dysplasia may be present
How is chronic hyperplastic candidosis treated?
Systemic antifungal - fluconazole capsules, 50mg once daily for 14 days
Biopsy
Stop smoking
Observe
Where do most oral carcinomas in the UK arise from?
Clinically normal mucosa
How much more likely is leukoplakia to progress to cancer than clinically normal mucousa?
50 to 100 times
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
What are the histopathological predictors of malignant change?
Dysplasia
Atrophy
Candida infection
Biological markers eg - p53, HPV+ and HPV-
What is dysplasia?
Disordered maturation (growth) in a tissue
A histopathological diagnosis, not clinical
What is atypia?
Changes in cells
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
What is the WHO classification for grading of epithelial dysplasia?
Hyperplasia
Mild
Moderate
Severe
Carcinoma-in-situ
How is staging and grading carried out?
Grading is done histopathologically
Staging is done clinically
Describe basal hyperplasia
Increased number of basal cells, rest of epithelium is normal
Architecture - regular stratification, basal component is larger
No cellular atypia
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
