BAMS - Potentially malignant lesions Flashcards
What is the gold standard for diagnosing potentially malignant lesions?
histopathology/biopsy
How do we stage potentially malignant lesions? what do we use?
Via clinical examination
T - tumour size (width)
N - lymph node involvement
M - distant metastesis
How do we grade potentially malignant lesions? what do we use?
histopathology/biospy
- well differentiated
- moderately differentiated
- poorly differentiated
What does the term potentially malignant disorder encompass? (2)
- Potentially malignant lesion
- Potentially malignant conditions
What is a potentially malignant lesion?
An area of altered tissue in which cancer is more likely to form
What is a potentially malignant condition?
Generalized systemic condition that a patient has that increases cancer risk
What are systemic conditions which increase the risk of oral cancer? (4)
- lichen planus – erosive/ulcerative variant especially on tongue and gingivae
- oral submucous fibrosis - chewing of beetlenut
- iron deficiency – due to the oral epithelium being thinner, this is an important pathogen/carcinogen barrier
- tertiary syphilis (rare)
What types of lichen planus increases the oral cancer risk?
erosive/ulcerative variant especially on tongue and gingivae
How much more likely is it for leukoplakia to undergo malignant change than normal mucosa?
Leukoplakia is 50 to 100 times more likely to progress to cancer than clinically normal mucosa
What indicators are used to predict malignant change to leucoplakia? (5)
- age– OC risk increases with age
- gender - females more at risk of OC
- idiopathic
- site - floor of mouth, tongue and gingivae = high risk
sublingual keratosis = extremely high risk of OC - clinical appearance - non-homogeneous verrucous, ulcerated, leuko-erythroplakia
What are the disadvantages of biopsy? (2)
Can’t screen patients = unpleasant/painful and invasive
Can’t monitor tissue response to treatment
What are biopsied samples asssessed for? (3)
- dysplasia
- atrophy (thinning)
- candida infection – chronic hyperplastic candidiasis/candida leukoplakia has malignant potential
Why is leucoplakia tested for candida infection?
candidiasis/candida leukoplakia has malignant potential
What is the function of a p53 gene?
what is the relationship between this gene and cells that undergo malignant change?
gene helps prevents cell division in cells where there is irreparable cellular damage
In a larger percentage of malignant cells, this gene has been deleted/ inactivated = allows the defective cells to proliferate
What protein degrades the p53 gene and in which circumstances is this gene present?
Those with HPV 16&18
HPV16&18 Produces E6 protein which degrades p53
What is the difference between epithelial dysplasia and cellular atypia?
Dysplasia is disordered maturation (growth) in a tissue
changes that occur at an individual cellular levels (not the tissues)
What is the criteria for diagnosis (via histopathology) of a PM lesion? (2)
- Assess architectural changes
- boundaries between categories not well defined
- architectural changes = abnormal maturation and stratification - Cytological abnormalities
- individual cells – look for atypia
List the grades of epithelial dysplasia. (5)
- hyperplasia
- mild
- moderate
- severe
- carcinoma-in-situ
What occurs in basal hyperplasia (grade 1 epithelial dysplasia).
Increased basal cell numbers in the basal cell compartment.
Describe the architectural changes and the cytological abnormalities of a grade 1 epithelial dysplasia/basal hyperplasia.
Architecture:
- regular stratification
- basal compartment is larger
No cytological changes - Only affects the basal cell numbers, No basal cell atypia
Describe the architectural changes and the cytological abnormalities of a grade 2 mild epithelial dysplasia. (3 + 1)
Architecture:
changes in lower third only
- pleomorphism: variety of shapes and sizes in nucleus and/or cell
- hyperchromatisim: has an increased DNA content = nucleus stains darker
- basal cell hyperplasia (increased no.s)
cytology:
mild atypia of cells
How much of the cell layers are involved in grade 2 mild epithelial dysplasia.
the lower 1/3rd only
Describe the architectural changes and the cytological abnormalities of a grade 3 moderate epithelial dysplasia. (3)
Architecture:
changes in 2/3rds of cell layers
- pleomorphism
- hyperchromatisim
cytology:
moderate atypia of cells
How much of the cell layers are involved in grade 3 mild epithelial dysplasia.
changes in 2/3rds of cell layers
How much of the cell layers are involved in grade 4 severe epithelial dysplasia.
most cells affected
- changes extend to the upper 1/3rd
Describe the architectural changes and the cytological abnormalities of a grade 4 severe epithelial dysplasia. (5)
Cytology:
Severe atypia
- Hyperchromatism affecting the majority of cells
- Mitotic cells above the basal cell layer = abnormal = malignant changes
- pleomorphism
- hyperchromatisim
Describe a lesion which has carcinoma in situ.
A Malignant but non-invasive lesion = Still confined to epithelium however all cells affected (cellular atypia)
List the 4 stages of carcinogenesis.
initiation
promotion
transformation
progression
Describe what occurs in the initiation stages of carcinogenesis.
spontaneous change or triggers (carcinogens) causes mutation to occur that isn’t repaired however doesn’t form a malignant cell
Describe what occurs in the promotion stages of carcinogenesis.
mutated cells continue to grow and reproduce and there is a fault in the repair genes
Describe what occurs in the transformation stages of carcinogenesis.
malignant conversion of the cell
(preneoplastic to malignancy)
Describe what occurs in the progression stages of carcinogenesis. (3)
= expression of the malignant phenotype
= genetic instability and uncontrolled growth
= activation of oncogenes and loss of tumour suppressor genes
List 3 changes to chromosomes (contain genes) that can occur.
- aneuploidy: missing or extra chromosomes
- translocations: sections of the chromosome break off and attach to another chromosome
- amplifications: extra copies of genes
List 3 changes to genes (sections of DNA) that can occur.
- mutations
- deletions
- amplifications
List epigenetic changes that can occur. (2)
chemical changes in DNA - such as methylation (silence genes)
modification of the histones that package DNA
What is the function of Tp53 gene? What is the relationship between this and carcinogenesis?
most important tumour suppressant genes (come in pairs)
in cancer these genes are mutated or inactivated
Describe Knudson’s “two-hit” hypothesis of carcinogenesis.
2x tumour suppressant genes (come in pairs) e.g. Tp53 must be damaged to become malignant
If only 1 is damaged the cell will remain benign
List the 6 hallmarks of cancer.
self sufficiency in growth signals
insensitviety to anti-growth signals
tissue invasion and metastasis
limitless replicative potential
sustained angiogenesis
evading apoptosis
Describe field change theory.
Which sites are commonly affected. (3)
The formation of multiple patches of premalignant disease with a higher-than-expected rate of multiple local second primary tumors forming - not metastasis.
commonly - Pharynx, larynx and respiratory tract.
What is included on an oral cancer pathology report? (3)
- differentiation and grading using histopathology
- well differentiated
- moderately differentiated SCC
- poorly differentiated SCC - pattern of invasive front (related to nodal spread)
- cohesive (cells advance like a wave)
- non-cohesive: has correlation with lymph node involvements - local extension of the disease
What are the ways in which oral cancer can spread? provide examples. (6)
Local extension of disease
- mucosal extension
- muscle (tongue etc)
- bone
- nerve
- Lymphatic spread
- Haematogenous spread
Describe how oral cancer would spread to bone in edentulous patients.
via gaps in cortex
Describe how oral cancer would spread to bone in dentate patients.
what must we investigate further?
along the PDL and into the jaw bone
In patients with good OH and no reason for mobility of teeth
In terms of perineural spread, which type of spread can predict nodal spread?
If malignancy has spread to small nerves at the advancing edges
In terms of perineural spread, which type of spread can predict reoccurence?
If there is extensive spread of the malignancy related to the inferior alveolar nerve
List and describe haematogenous spread of cancer. (3)
- Permeation = Grow inside vessels
- Via embolism
- Via extracapsular spread
List 3 types of rare SCC.
- Verrucous - rarely metastasises and better prognosis
- Basaloid – associated with HPV
- Spindle cell – aggressive
