Dysplasia and OC

Question 1

Common red flag sites for oral cancer?

Answer 1

Lateral border of Tongue
FOM

Question 2

What is oral cancer risk increased by in:

• smokers
• alcohol
• alcohol and smoking

Answer 2

2x

2x

5s

Question 3

What are some risk factors for oral cancer?

Answer 3

Smoking
Alcohol
DIet
Chewing betel nut
Chewing tobacco

Question 4

What is a potentially malignant disorder?

Answer 4

This is a term for a condition or disease that has an increased risk of becoming malignant (does not mean it will become malignant just higher chance)

Question 5

What are some examples of potentially malignant disorders?

Answer 5

Lichen planus
Leukoplakia
Erythroplakia

Question 6

What is lichen planus?

Answer 6

This is a chronic oral condition affecting mucosal membrane and skin that has 7 diff types:

Reticular
Atrophic
Papular
Plaque
Bullous
Ulcerative/Erosive

EROSIVE AND ULCERATIEV HAVE HIGHEST RISK

Question 7

What is luekopakia?

Answer 7

white patch with no attributable cause, does not rub off, higher risk than normal mucosa

Question 8

Wha is erythroplakia?

Answer 8

Red patch, no attributable cause - rare than leukoplakia but its due to a vascular change which can be a sign of malignancy

Question 9

Risk if white lesions progressing to cancer?

Answer 9

Low - 0.2-0.4% however have to warn pts there is a risk and it must be monitored

Question 10

What are the clinical predictors of malignancy? 5

Answer 10

Age - elder pts higher risk
Gender - females higher risk
Site - FOM, gingiva higher risk
Clinical Appearance - rolled, non homogenous, leuko-erythroplakia, verroucous, ulcerative
Idiopathic = if pt is non smoker, non drinkers etc then more concerned as to why it is therw

Question 11

What is the gold standard for assessing a lesion?

Answer 11

Histopathology

Question 12

What does histopathology do?

Answer 12

Assesses for dysplasia, atrophy and candida infection

Question 13

What can we also look fo run a tissue sample?

Answer 13

Biological markers - such as VEGF (this is a growth factor) and p53 which normally induces cell apoptosis when it notices something is off with cell however in 50% of cancers this is switched off

Question 14

What is dysplasia?

Answer 14

Disordered growth in tissue

Question 15

What is atypia?

Answer 15

Changes in cell at cellular level

Question 16

How do we diagnosis a potentially malignant lesion?

Answer 16

Cytological changes - cell size, cell shape, nuclear hyperchromatism (inc uptake of dye due to inc DNA content), nuclus size, nucleus shape, atypical mitotic figures

Architectural change - loss of epithelial cell adhesion, drop shaped rete ridges, irregular stratification, premature keratin in single cells, increasd and abnormal mitosis

Question 17

What architectural changes dowe look for ?

Answer 17

How much ep is involved - low, mid, upper 1/3rd
increased or atypical mitosis
loss of epithelial cell adhesion
dropped shaped rete ridges
irregular stratification
premature keratin in single cells

Question 18

What cytological changes do we look for?

Answer 18

Abnormal nucleus size
Abnormal nucleus shape
Abnormal cell size
Abnormal cell shape
Nucleus hyerpchromatism
Inc no and size of nucleus
Atypical mitotic figures

Question 19

What is the WHO classification for histopathological grading of lesions?

Answer 19

Hyperplasia
Mild dysplasia
Moderate dysplaisa
Severe dysplasia
Carcinoma in situ

NOW WE TEND TO USE LOW GRADE, HIGH GRADE, CIS

Question 20

Describe basal cell hyperplasia?

Answer 20

This is where there is INCREASED BASAL CELL NUMBERS

There is regular stratification

no cellular atypia

Question 21

What is mild dysplasia?

Answer 21

This is where there are changes in the lower 1/3rd of the epithelium
Often due to reactive change due to smoking, infection, inflammation, trauma etc
May see nuclear hyperchromatism
Pleomorphism
few cells show atypia (pleomorphism, hyperchromatism)
rest of cells look normal

Question 22

What is moderate dysplasia?

Answer 22

This is where there are changes into the mid 1/3rd of epithelium

Architecture - Loss of cohesion of epithelial cells (non cohesive pattern)

cytology - hyperchromaism, pleomorphism

rete pegs more round and bulbous

Question 23

What is severe dysplasia?

Answer 23

This is where the upper 1/3rd is affected, so majority of layers are affected and there is little resemblance to the normal Strat squamous ep , non cohesive

cytology = severe atypic of cells (size and shape), pleomorphism, hyperchroatism, presence of mitotic figures further up (should only be in basal layer), inc no of mitotic figures

Question 24

What is severe dysplasia?

Answer 24

This is where the upper 1/3rd is affected, so majority of layers are affected and there is little resemblance to the normal Strat squamous ep , non cohesive W

cytology = severe atypic of cells (size and shape), pleomorphism, hyperchroatism, presence of mitotic figures further up (should only be in basal layer), inc no of mitotic figures

Question 25

What is carcinoma in situ?

Answer 25

This is a theoretical concept all layers are involved (including upper third) sample is malignant but not yet invasive a sit hasn't breached the connective tissue - needs removal!!

Question 26

What are the 4 histological prognostic factors of cancer?

Answer 26

Pattern of invasuon depth of invasion perineurial invasion invasion of vessels

Question 27

What are the main factors in carcinogens?

Answer 27

Genetics Envuronement (alcohol, tobacco, betel nut chewing, diet which promote change from altered cell exp to malignancy and invasion)

Question 28

WHat is the process of carcinogenesis?

Answer 28

INITIATION (this is where the DNA mutation occurs and this DNA mutation inactivates the tumour suppression gene) PROMOTION (this is where the cell proliferations with the mutation and inactivates DNA repair gene) TRANSFORMATION (this is where cell undergoes further mutations that cant repair PROGRESSION - cell undergoes further mutations, inactivates several more tumour suppressor genes and has the hallmarks of malignancy

Question 29

What is an oncogene?

Answer 29

This is a gene that when normal regulates and promotes cell proliferation however when it becomes mutated it has the potential to cayse cancer as there is inappropriate proliferation

Question 30

What isa tumour suppressor gene?

Answer 30

This supresses cell growth

Question 31

What does Tp53 do?

Answer 31

Ptoetein that induces cell apoptosis when mutation is recognised however in50% of cancer its inactivated so mutated cell profilerates

Question 32

What are the hallmarks of cancer? 6

Answer 32

Evades apoptosis Angiogenesis Insenstive to anti-growth signals Has its own growth signals invades tissues and metastasises replicates uncontrollably

Question 33

What is the fild cancerisation concept?

Answer 33

This is the theory that it is no just the tissue that has the malignant change that as been exposed to the changes and stimuli leading to the cancer - the surrounding tissue has also been exposed and may be occurring at a slower rate there is a big risk in 5cm radio from original primary and may actually get a second new primary tumour rather than as secondary tumour §

Question 34

What is a synchronous slesion?

Answer 34

Second primary within 6 months

Question 35

What is a metachronu lesion?

Answer 35

Second primary more than 6 months after first and due to same field change

Question 36

How do we stage cancer?

Answer 36

T - tumour primary T0 = no primary found T1 = <2cm T2 = 2-4cm T3 = >4cm N - lymph node involvement N0 = no regional LN involvement N1 = ipsilateral single, <3cm N2 = <6cm, ipsilateral single, multiple or bilateral N3 = >6cm M = metastasius N0 = no M1 = metastasised

Question 37

Risk factors for lip cancer?

Answer 37

Sunlight Smoking

Question 38

What is good about lip cancer ?

Answer 38

Slow growth rarely metastasis to nodes local invasion responds well to xt