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Oral Medicine > Dysplasia and Oral Cancer > Flashcards

Dysplasia and Oral Cancer Flashcards

1
Q

Incidence of oral cavity cancer?

male vs female

A

male 2:1 female

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2
Q

What are the high risk sites for oral cancer?

(6)

A
  • floor of mouth
  • lateral border of the tongue
  • retromolar regions
  • soft and hard palate
  • gingivae
  • buccal mucosa
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3
Q

Incidence of oro-pharyngeal cancer

male vs female

A

male 4.8:1 female

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4
Q

Oro-pharyngeal cancer rates are rapidly rising, especially in high income areas (north america). What is this suggested to be linked to?

A

Rise in HPV epidemic

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5
Q

According to the Scottish Cancer Registry, what is the increase for oro-pharyngeal cancer?

A

85% inncrease from 2001-2012

highest increase for any cancer

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6
Q

According to the Scottish Cancer Registry, what is the increase for oral cavity cancer?

A

10% inncrease from 2001-2012

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7
Q

What are the main risk factors for oral cancer?

(2)

A

Tobacco-use (smoking)

Drinking alcohol

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8
Q

What is the risk of oral cancer for smokers?

A

Risk of oral cancer is doubled in smokers.

The risk increases with quantity, duration and frequency of tobacco use.

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9
Q

What is the risk of oral cancer in those who drink alcohol?

3-4 drinks a day

A

Risk of oral cancer is doubled in those who drink alcohol.

Frequency is more important that duration (those who drink more per day have greater risk).

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10
Q

What is the risk of oral cancer in those who smoke and drink alcohol?

A

Risk of oral cancer in those who smoke and drink alcohol is 5 times more.

This risk increases with frequency and duration of smoking and alcohol consumption.

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11
Q

What is the risk of oral cancer for betel quid (paan)?

A

Risk is 3 times more.

Betel quid is a mixture of substances including arecca nut with or without tobacco wrapped in a betel leaf and placed in the mouth.

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12
Q

What are the benefits of stopping smoking and drinking alcohol?

A

Smoking cessation benefits:
* demonstrable benefits within 1-4 years after stopping smoking
* risks reduced and reached a similar level to those who had never smoked after 20 years of quitting

Stopping alcohol consumption benefits:
* takes 20 years

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13
Q

What is considered to be potentially malignant lesions?

A
  • white lesions (leukoplakia)
  • red lesions (erythroplakia)
  • lichen planus (candidal leukoplakia, chronic hyperplastic candidiasis)
  • oral submucous fibrosis
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14
Q

What is the incidence of leukoplakia becoming malignant?

A

0.2-4%

2.5% in 10 years
4% in 20 years

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15
Q

What is the incidence of erythroplakia becoming malignant?

A

Higher risk of cancer compared to leukoplakia.

Risk of dysplasia is 50%.

However, erythroplakia is less frequent than leukoplakia.

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16
Q

How is dysplasia categorised?

A

Categorised based on:
* cellular atypia
* epithelial architectural organisation

17
Q

What are the histological gradings of oral mucosal dysplasia?

A
  • low grade
  • high grade
  • carcinoma-in-situ
18
Q

What is low-grade oral mucosa dysplasia?

histological grading

A
  • 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
  • well formed basal cell layer
  • tumour islands are usually **well define **and are often continuous with the surface epithelium
  • invasion pattern with intact large branching rete pegs pushing into underlying CT
19
Q

What is high-grade oral mucosa dysplasia?

histological grading

A
  • show little resemblance to a normal squamous epithelium
  • architectural change upper third
  • usually show considerable atypia
  • invade in a non-cohesive pattern with fine cords, small islands and single cells infiltrtating widely through the CT
  • mitotic figures are prominent and many may be abnormal
20
Q

What are the histological prognostic factors?

oral cancer and dysplasia

A

Pattern of invasion:
* bulbous rete pegs infiltrating at same level is considered of a better prognosis than widely infiltrating small islands and single cells

Depth of invasion:
* risk of metastases for a tumour greater than 4mm was 4x greater than for a tumour less thhan 4mm

Perineural invasion:
* most signnificant when a tumour is seen within a large nerve at a site some distance from the main tumour mass

Invasion of vessels:
* associated with lymph node metastases and a poor prognosis

21
Q

Describe the Field Cancerisation Concept.

A

Multiple primary cancers possible over time.

High cancer risk in 5cm radius of the original primary tumour.

22
Q

How is oral cancer clinically staged?

A

Variables:
* site
* size (T)
* spread (N&M)

23
Q

Describe Stage 1 cancer.

TNM

A

T1 tumour ≤2cm in greatest dimension
N0 no regional lymph node metastasis
M0 no distant metastasis

24
Q

Describe Stage 2 cancer.

TNM

A

T2 tumour 2<T≤4cm in greatest dimension
N0 no regional lymph node metastasis
M0 no distant metastasis

25
Q

Describe Stage 3 cancer.

TNM

A

T3 (enough alone), T2 or T1
T3 tumour >4cm in greatest dimension
T2 tumuor 2<T≤4cm in greatest dimension
T1 tumour ≤2cm in greatest dimension

N1 metastasis in a single ipsilateral lymph node, ≤3cm in greatest dimension
M0 no distant metastasis

26
Q

Describe Stage 4A cancer

TNM

A

T4a moderately advanced local disease. Lip: tumour invades through cortical bone, inferior alveolar nerve, FoM, or skin (chinne or nose). Oral cavity: tumour invades through cortical bone, into deep/extrinsic muscles of tongue, maxillary sinus, or skin of face.
N0 or N1
No regional lymph node metastasis; OR
Metastasis in a single ipsilateral lymph node, ≤3cm in greatest dimension.
M0 no distant metastasis

T1, T2 or T3
T1 tumour ≤2cm in greatest dimension
T2 tumour 2cm<T≤4cmm in greatest dimension
T3 tumour >4cm in greatest dimension
N2
metastasis in:
N2a single ipisilateral lymph node 3cm<N≤6cm in greatest dimension
N2b multiple ipsilateral lymph nodes, none >6cm in greater dimension
N2c bilateral or contralateral lymph nodes, none >6cm in gratest dimension
M0 no distant metastasis

T1, T2 or T3
N2
M0

T4a
N0 or N1
M0

27
Q

Describe Stage 4B cancer

A

any T
N3 metastasis in a lymph node >6cm in greatest dimension
M0 no distant metastasis

T4b very advanced local disease. Lip and oral cavity: tumour invades masticator space, pterygoid plates, or skull base; or encases internal carotid artery
any N
M0

T4b
any N
M0

any T
N3
M0

28
Q

Describe Stage 4C cancer

A

any T
any N
M1 distant metastasis

29
Q

What is the prognosis for Stage 1 cancer?

A

80% cure rate

30
Q

What is the prognosis for Stage 2 cancer?

A

65% cure rate

31
Q

What is the prognosis for Stage 3 and Stage 4 cancer?

A

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

32
Q

What is the prognosis of cancer if left untreated, with metastases?

A

4 months survival

33
Q

What is the aetiology for lip cancer?

A
  • sunlight UV-B
  • smoking
34
Q

What is the behaviour of lip cancer?

A
  • slow growth
  • local invasion
  • rarely metastasis to nodes
35
Q

How can oral cancer be detected?

(6)

A

Oral cancer is difficult to detect, experience helps.
Oral Cancer Recognition Toolkit can be utilised to help detection.

Oral Cancer Screening can be done:
* HPV16 screening
* Toluidene blue
* VELscope
* PhotoDynamic Diagnosis (PDD)
* Clinical judgement of experienced clinician

36
Q

What are the harms for using Toluidine blue for detecting cancer?

A
  • false positives in inflammatory lesions
  • 50% false negatives
37
Q

How does VELscope work in cancer screening?

A

VELscope is the autofluorescence of tissues with blue light.
A loss of fluorescence suggests “change”. This change may be cancer but also be other changes.

Not enough evidence to support.

38
Q

What are the predictors of malignancy in leukoplakia?

clinical

A
  • age and gender
  • idiopathic
  • site (buccal mucosa low risk; FoM and tongue high risk)
  • clinical appearance
39
Q

What are the histopathological predictors of malignant change?

A
  • dysplasia
  • atrophy
  • candida infection

Oral Medicine (11 decks)

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