Oral carcinogenesis and oral epithelial dysplasia Flashcards

1
Q

What is a tumour?

A

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

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2
Q

What is cancer?

A
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3
Q

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

A

local tissue invasion and destruction

can also metastasise and reach far away tissues and organs

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4
Q

How does cancer get its name?

A

cancer = crab

crab like projections of abnormal epithelium into subcutaneous connective tissue

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5
Q

What causes cancer

A

carcinogenic substances or spontaneous mutation (possibly genetic factors)

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6
Q

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

A

SCC (90-95%)

minor salivary gland carcinoma

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7
Q

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

A
primary:
OSSC 
minor salivary gland carcinomas 
lymphoma 
malignant melanoma 
sarcoma

secondary:
metastatic adenocarcinomas

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8
Q

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

A

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
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9
Q

Mechanisms and markers of oral carcinogenesis

A
tumour suppressor genes (p53)
oncogenes 
loss of cell adhesion 
viruses
immortalisation
angioneogenesis 
cell cycle disruption 
genetic abnormalities (DNA aneuploidy)
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10
Q

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

A

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
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11
Q

What does epidermal proliferative unit consist of?

A

stem cells
amplifying cells
non-proliferative supra- basal cells

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12
Q

What is dysplasia?

A

a spectrum of tissue DYSMATURATION and DISORGANISATION

associated with increased risk of malignant transformation

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13
Q

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

A

cytology (changes in cell)

tissue architecture

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14
Q

NAME histological changes in SCC

A
pleomorphisms 
drop shaped rete ridges 
keratin pearls in rete ridges 
dyskeratinisation 
loss of polarity of basal cells
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15
Q

WHO grading of dysplasia

A

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

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16
Q

Binary system classification of dysplasia

A

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

17
Q

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

A

mild/mod 10.3%

severe/carcinoma in situ 24.1%

overall 12.3

18
Q

OPMD?

A

clinically recognisable disorders with increased risk of carcinoma

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