Oral carcinogenesis and oral epithelial dysplasia

Question 1

What is a tumour?

Answer 1

abnormal, uncoordinate tissue growth which persists after initiating stimulus is gone

Question 2

What is cancer?

Answer 2

Question 3

What affect can cancer have on surrounding structures and further away?

Answer 3

local tissue invasion and destruction

can also metastasise and reach far away tissues and organs

Question 4

How does cancer get its name?

Answer 4

cancer = crab

crab like projections of abnormal epithelium into subcutaneous connective tissue

Question 5

What causes cancer

Answer 5

carcinogenic substances or spontaneous mutation (possibly genetic factors)

Question 6

What are the 1st and 2nd most common oral cancer?

Answer 6

SCC (90-95%)

minor salivary gland carcinoma

Question 7

Name some primary (5) and secondary (2) oral tumours.

Answer 7

primary:
OSSC 
minor salivary gland carcinomas 
lymphoma 
malignant melanoma 
sarcoma

secondary:
metastatic adenocarcinomas

Question 8

Principal signs and symptoms that could help identify oral cancer (pneumonic)

Answer 8

Oral ulceration, non healing for >2weeks
Red or white patches
Abnormal growths/swellings
Loss of tongue mobility

Cauliflower like growths 
Abnormal localised tooth mobility 
Non-healing sockets
Colour changes to mucosa (brown/blue) 
Erosions in mucosa 
Reduced or altered sensation

Question 9

Mechanisms and markers of oral carcinogenesis

Answer 9

tumour suppressor genes (p53)
oncogenes 
loss of cell adhesion 
viruses
immortalisation
angioneogenesis 

cell cycle disruption 
genetic abnormalities (DNA aneuploidy)

Question 10

Explain the changes and types of cells from normal to epithelial dysplasia to invasive SCC

Answer 10

in normal: (2)
growth promoting and inhibiting factors IN BALANCE
-> cells: oral keratinocytes and stem cells

dysplasia: (5)
- some factor (carcinogen, spontaneous) over-ride normal control mechanisms and cause stem cells to be overactive
- keratinocyte stem cells change to become tumour initiating stem cells
- there is dysregulated cell proliferation (causes unrestricted growth)
- > phase of pre/potential malginancy, process can be halted

invasive SCC (4)

• immortalisation of cells
• neovascularisation
• cell migration
• local invasion and then metastasis

Question 11

What does epidermal proliferative unit consist of?

Answer 11

stem cells
amplifying cells
non-proliferative supra- basal cells

Question 12

What is dysplasia?

Answer 12

a spectrum of tissue DYSMATURATION and DISORGANISATION

associated with increased risk of malignant transformation

Question 13

What two types of changes is the pathologist going to look for?

Answer 13

cytology (changes in cell)

tissue architecture

Question 14

NAME histological changes in SCC

Answer 14

pleomorphisms 
drop shaped rete ridges 
keratin pearls in rete ridges 
dyskeratinisation 
loss of polarity of basal cells

Question 15

WHO grading of dysplasia

Answer 15

mild - architectural changes limited to lower 1/3 of epithelium accompanied by atypical cytology
moderate - limited to middle 1/3, possibly upgrade if high atypia
severe - extending above 2/3s of epithelium
carcinoma in situ - FULL or almost full thickness architectural abnormalities accompanied by high degree of cytological atypia but not invaded through basement membrane

Question 16

Binary system classification of dysplasia

Answer 16

high risk lesions: atleast 4 architectural changes + 5 cytological changes
low risk: less than ^

Question 17

What are the malignant transformation rates of mild, mod and severe dysplasia and carcinoma in situ. AND overall?

Answer 17

mild/mod 10.3%

severe/carcinoma in situ 24.1%

overall 12.3

Question 18

OPMD?

Answer 18

clinically recognisable disorders with increased risk of carcinoma

the more severe the dysplasia, the greater the chance of malignancy