Oral cancer - Dysplasia

Question 1

What are the two classifications of head and neck cancers?

Answer 1

oral cavity cancer

oropharyngeal cancer

Question 2

List high risk areas for oral cancer. (7)

Answer 2

● Floor of the mouth – increased risk to this site in drinkers and smokers

● Lateral border of the tongue - increased risk to this site in drinkers and smokers

● Retromolar regions

● Soft palate - increased risk to this site in drinkers and smokers

● hard palate
● Gingivae
● Buccal mucosa

Question 3

What are the risk factors for oral cancer? (9)

Answer 3

Smoking
Drinking
smoking and drinking
Socioeconomic status
Diet
Betel quid (paan)
oral health
family history
sexual activity

Question 4

How much does smoking increase your risk of OCC?

Answer 4

X2

Question 5

How much does drinking (3-4 drinks/day) increase your risk of OCC?

Answer 5

x2

Question 6

How much does smoking and drinking increase your risk of OCC?

Answer 6

x5

Question 7

How much does Betel paan increase your risk of OCC?

Answer 7

x3

Question 8

How much does SE status increase your risk of OCC?

Answer 8

x2
(even without other risk factors you have the sane risk as those who smoke or drink)

Question 9

What specific type of cancer has the greatest risk of developing if a px smokes?

Answer 9

larynx cancer

Question 10

What specific type of cancer has the greatest risk of developing if a px drinks? (2)

Answer 10

oral cavity

oropharyngeal

Question 11

What factors contribute to the OCC risk from smoking? (3)

what patter of use increases the risk?

Answer 11

Quantity
duration
frequency

fewer cigarettes for longer duration

Question 12

What factors contribute to the OCC risk from drinking? (1)

what patter of use increases the risk?

Answer 12

Frequency
(more important than duration) – more drinks each day key

Question 13

How do we reduce the risks of OCC? (3)

Answer 13

Stop smoking

stop drinking

Healthy diet

Question 14

when are the benefits of stopping smoking seen?

Answer 14

benefits of quitting smoking are seen one to four years after stopping

• After quitting for 20 years: you’re at the same risk as someone who has never smoked

Question 15

when are the benefits of stopping drinking alcohol seen?

Answer 15

Benefits of quitting heavy alcohol consumption emerge 20 years after quit

Question 16

what advice would you give px’s regarding reducing the risk of OCC if only a limited health education message can be conveyed?

Answer 16

In the short term, if a px is going to change either their smoking or drinking habits, they are going to get an improvement in oral cancer risk quickest by reducing their smoking (rather than drinking) however should be encouraged to reduce/stop both

Question 17

In terms of diet how can we reduce our OCC risk (by 1/2) ?

Answer 17

high intake of fresh fruits and vegetables

Question 18

Why is the incidence of oropharyngeal cancer increasing?

Answer 18

Due to the HPV epidemic

Question 19

What are potentially malignant lesions? (6)

Answer 19

• White lesions - leukoplakia
• Red lesions - erythroplakia
• Lichen planus
• Candidal Leukoplakia
• Chronic Hyperplastic Candidiasis
• Oral Submucous Fibrosis

Question 20

describe the risks associated with leukoplakia.

Answer 20

• Higher risk of malignant transformation compared to normal healthy mucosa
  (however most OCC arise from healthy mucosa)
• not all white patches have the same level of risk

Question 21

Describe what colour of lesion is more commonly associated with malignant transformation.

Answer 21

Erythroplakia
- More Commonly associated with malignant change, erythema due to the vascular changes that occur as a consequence to malignant change

Question 22

What is the criteria for dysplasia based on? (2)

Answer 22

Cellular atypia

epithelial architectural organisation

Question 23

How do we categorise dysplasia? (3)

Answer 23

• Low grade
• high grade
• carcinoma-in-situ

based on the cellular atypia and epithelial architectural organisation

Question 24

What cytological changes are associated with dysplasia? (8)
Not all have to be present to mean its dysplastic

Answer 24

Abnormal variation in nuclear size

Abnormal variation in nuclear shape

Abnormal variation in cell size

Abnormal variation in cell shape

increased/altered nuclear/cytoplasmic ratio

atypical mitosis figures

increased number and size of nucleoli

nuclear hyperchromatism

Question 25

What epithelial architectural changes are associated with dysplasia? (8) Not all have to be present to mean its dysplastic

Answer 25

irregular epithelial stratification loss/disturbed of polarity basal cells drop-shaped rete ridges increased and abnormal mitoses premature keratinisation in single cells abnormal keratinisation keratin pearls within rete ridges loss of epithelial cell cohesion or adhesion

Question 26

List the criteria for a low grade dysplasia. (8)

Answer 26

- Easy to identify that the tumour originates from squamous epithelium - Architectural change into lower third - Cytological atypia or dysplasia may not be prominent - Shows a considerable amount of keratin production - Evidence of stratification (2 or more cell layers) - Well formed basal cell layer surrounding the tumour islands - Tumour islands are usually well defined and are often continuous with the surface epithelium - Invasion pattern with intact large branching rete pegs ‘pushing’ into underlying CT

Question 27

List the criteria for a high grade dysplasia. (5)

Answer 27

- Show little resemblance to a normal squamous epithelium - Architectural change reaches the upper third - Usually show considerable atypia - Invade in a non-cohesive pattern with fine cords, small islands and single cells infiltrating widely through the CT - Mitotic figures are prominent and many may be abnormal

Question 28

How do we classify a dysplasia which has changes in the middle 1/3rd?

Answer 28

depending on the level of cytological atypia = will be classified into low grade or high grade

Question 29

Describe a carcinom - in - situ dysplasia. (4)

Answer 29

A lesion which the pathologist strongly suggests a carcinoma is present but cant provide evidence that invasion through the basement membrane has occurred; * Cytologically malignant but not invading * Abnormal architecture - Full thickness (or almost full) - Severe cytological atypia *Mitotic abnormalities frequent

Question 30

What factors determine how cancer should be managed? (4)

Answer 30

1. Pattern of Invasion 2. Depth of Invasion 3. Perineural Invasion 4. Invasion of Vessels

Question 31

Describe pattern of invasion in relation to cancer prognosis.

Answer 31

Good prognosis = Bulbous rete pegs infiltrating at same level is considered poor prognosis = widely infiltrating small islands and single cells

Question 32

Describe depth of invasion in relation to cancer prognosis.

Answer 32

Risk of metastases for a tumour which is greater than 4mm in size = 4x greater than for a tumour less than 4mmm

Question 33

Describe invasion of vessels in relation to cancer prognosis.

Answer 33

poor prognosis = thought to be associated with lymph node metastaes

Question 34

Describe field cancerisation of the oral cavity.

Answer 34

Where the cancer has developed in the mouth Is not the only area which has been subject to the cellular changes and to the environmental stimuli which have caused the cancer – the same changes progress in other parts of the mouth at a slower rate but can also produce OCC in the future = a new primary and not reoccurrence.

Question 35

Why should we continue to review not only the site of the oral cancer but the whole mouth in patients who have a history of OCC?

Answer 35

Field cancerisation tells us that patients presenting with an OCC in one area have a risk of developing other tumours in other parts of the mucosa - High cancer risk in 5cm radius of original primary = that’s most of the mouth/pharynx. Therefore we consider the whole mouth as a risk and the whole mouth should be reviewed each time.

Question 36

What is the cure rate of a stage 1 early lesion?

Answer 36

80% cure rate

Question 37

what is the cure rate for stage 2?

Answer 37

65% cure rate

Question 38

what is the cure rate for stage 3 or worse?

Answer 38

less than 30% cure rate 5 year survival is < 50%

Question 39

what is the survival time (in months) for an untreated lesion with metastases?

Answer 39

around 4 months

Question 40

How do we determine how to treat the cancer?

Answer 40

Based on the TNM staging and findings - N&M cannot be fully assessed until excised and sent for pathological examination

Question 41

Does lip cancer come under OCC or OPC

Answer 41

none - separate type

Question 42

How does lip cancer present? (2)

Answer 42

as a on-healing ulcer or swelling

Question 43

what can cause lip cancer? (2)

Answer 43

- Sunlight UV-B - Smoking

Question 44

Describe the behaviour of a lip cancer. (5)

Answer 44

- slow growth - local invasion - rarely metastasise to nodes - Good prognosis as usually detected early - Responds well to surgery

Question 45

What methods do we use to screen for oral cancer? (5) which is the most effective?

Answer 45

* HPV16 screening * Toluidene blue * VELscope – (Autofluorescence of tissues with blue light) Loss of fluorescence = ‘change’, Change may be cancer but can be other changes * Photodynamic Diagnosis (PDD) * Clinical judgement of experienced clinician – most efficient

Question 46

what is an advantage of using toluidene blue for oral cancer screening?

Answer 46

Can detect areas within lesions which are more likely to become maliganant – determines biopsy site

Question 47

What is a GDP's role in relation to oral cancer? (7)

Answer 47

- Smoking cessation advice - Alcohol reduction advice - Healthy diet promotion - Dentist has to make decision about their referral threshold for potentially malignant lesions - Monitor with photographs - Remove local factors where ulcer may be due to trauma, then review - Monitor PML & if they undergo changes = refer