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BDS4 Oral Medicine > Dysplasia and Oral Cancer- Oral lesions and Therapy Options > Flashcards

Dysplasia and Oral Cancer- Oral lesions and Therapy Options Flashcards

1
Q

What are potentially malignant lesions? What has this terminology replaced and why?

A

Lesions that may become cancer
 Prev. premalignant/precancerous- but this suggests that it will become cancer at some point

-> In PML- most lesions do not change to malignancy

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2
Q

What are the different types of potentially malignant lesions?

A

White lesions (leukoplakia)

Red lesions (erythroplakia)

Lichen planus
-> Candidal Leukoplakia
-> Chronic Hyperplastic Candidiasis

Oral Submucous Fibrosis

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3
Q

What is Leukoplakia?

(clinical description)

A

White patch cannot rub off, not attributable to any other disease

-> has higher risk of cancer developing than normal mucosa (but not all white patches have same level of risk)

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4
Q

What is erythroplakia?

A

Red patch, not attributable to any other disease

-> More commonly associated with malignant change

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5
Q

What does erythema in erythroplakia suggest?

A

Erythema suggests vascular change consequent to malignancy developing

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6
Q

What should we tell patients about white lesions?

A

Incidence of cancer is very small
 Wide variation in populations- studies have different criteria
 Variations also exist in genetics, diet, smoking habits
 Be guarded about giving patient information about %chance of malignant changes (make them aware there is a small risk and that lesion should be monitored)

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7
Q

Why is it important not to focus on only red and white lesions when screening for oral cancer?

A

Most carcinomas arise in clinically normal mucosa

*in UK- in other areas most arise from PMLs

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8
Q

What should be done if a patient presents with a white lesion?

A

Biopsy to check for dysplasia

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9
Q

What are the features of erythroplakia that mean that referrals are given more credence in OM?

A

Occurs less frequently

Higher chance of Cancer

Greater dysplasia risk

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10
Q

Which factors in dysplasia are risk of cancer based off?

A

Cellular atypia

Epithelial architectural organisation- changes in organisation of maturation and normal layering within epithelium

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11
Q

What are the categories in dysplasia?

A

Low grade

High Grade

Carcinoma-in-situ

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12
Q

Why was moderate dysplasia removed from the categories?

A

Moderate dysplasia was not well catered for in terms of Tx (difficult choices in whether excision or biopsy was required)
 Much clearer distinctions- much clearer guidance for clinician and patient in

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13
Q

What are the cytological features to look out for when carrying out a histological grading of dysplastic tissue?

A

Abnormal nucleus shape or size

Abnormal cell shape or size

Increased or altered nucleus:cytoplasm ratio

Atypical mitotic features

Nuclear hyperchromatism

Increased number and size of nucleoli

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14
Q

What do the cytological changes during dysplasia represent?

A

Changes in individual cells reflecting abnormal DNA content in the nucleus, failure to mature/keratinise as normal and increased proliferation

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15
Q

What are the architectural features to look out for when carrying out a histological grading of dysplastic tissue?

A

Irregular epithelial stratification

Lost/disturbed polarity of basal cells

Drop-shaped rate ridges

Increased and abnormal mitosis

Premature keratinisation in single cells

Abnormal Keratinisation

Keratin pearls in rete ridges

Loss of epthelial cell cohesion/adhesion

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16
Q

What are the typical features of low grade dysplasia?

A

Tumour originates from squamous epithelium

Architectural change into lower third

Cytological atypia or dysplasia may not be prominent

Considerable amount of keratin production

Evidence of stratification

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

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17
Q

How is it decided what classification to apply when dysplasia extends into middle third of epithelial layer?

A

Look at level of atypia to decide if low or high

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18
Q

What are the typical features of high grade dysplasia?

A

Little resemblance to a normal squamous epithelium

Architectural change upper third

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

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19
Q

What is degree of differentiation used to predict?

A

Prognosis as level correlates with long term survival

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20
Q

What are the features of carcinoma in situ?

A

Cytologically malignant but not invading

Abnormal architecture:
-> Full thickness (or almost full)

Severe cytological atypia

Mitotic abnormalities frequent

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21
Q

When is the term carcinoma in situ used?

A

When pathologist strongly suspects carcinoma is present but cannot demonstrate any evidence of invasion through basement membrane

22
Q

What are histological prognostic factors used for?

A

Reported to clinicians to help inform management of cancer for MDT

23
Q

What are the histological prognostic factors associated with poor prognosis?

A

Pattern of invasion- widely infiltrating small island and single cells have worse prognosis

Depth of invasion- tumours >4mm have greater risk of metastases

Perineural invasion

Invasion of vessels- associated with LN spread (poor prognosis)

24
Q

What are the genetic and environmental effects on cells that can result in oral cancer?

A

 Can cause cells to have tendency to form unusual divisions ( as they get aggravated by smoking, drinking, other factors)
-> resulting altered cell expression progresses to malignancy and invasion (takes time)

 Occurs at different stages in different parts of the mouth depending how environmental stimuli are applied

25
Q

What are the different aspects involved in multi-stage promotion in oral cancer?

A

Normal mucosa- normal keratinocytes

Genetic instability/Aneuploidy- hyperplasia, low grade dysplasia
-> potentially malignant

Adaptive advantages- high grade dysplasia

Invasion- carcinoma

26
Q

What is field cancerisation?

A

Cancer which develops in mouth is not the only part that has been subjected to carcinogenic stimuli which has lead to a cancer
 These stimuli have been coalescent in cancer area to produce change at this time
 Same changes may progress in other parts of mucosa at slower rate and may result in new primary cancer at another time (not a recurrence of original tumour)

27
Q

What is considered the high risk zone in patients who have presented with dysplasia or carcinoma? How may this change the management?

A

Within 5cm radius of original cancer (which includes most of mouth and pharynx)

-> consider whole mouth as at risk (keep reviewing- ensure other lesions have not been missed)

28
Q

What is a synchronous tumour?

A

Lesions arise at same time in different places (if patient presents with oral cancer- look at whole digestive tract as if second lesion is missed it is pointless to treat the first one only)

29
Q

What is a metachronous tumour?

A

Develops subsequent to original cancer in same field change region and are a result of same interaction with genetic and environmental factors

30
Q

What is the issue with the management of patient with oral cancer due to field cancerisation concept?

A

They must be continuously followed up and reviewed

31
Q

How are tumours staged?

A

 Site

 T- size of tumour

 Spread (N&M)- nodes and metastases
->cannot fully be assessed until sample is excised and sent for pathological examination (adjuvant treatment to help with spread may be indicated post operative once these findings have come to light)

32
Q

Why is the TMN staging system used?

A

Correlates with survival rates and treatment options are based off staging

33
Q

How many patients present at stage 1 or 2?

A

A third

-> good outcomes for these patients but ideally picked up and removed at dysplastic stage

34
Q

What is the cure rates in stage 1 and 2?

A

Stage I - 80% cure rate
Stage II – 65% cure rate

35
Q

Why is a 5 year survival rate less helpful for patients?

A

As most believe they will outlive 5 years

36
Q

What are the treatments available for oral cancer?

A

Surgery- treatment of choice for head and neck cancer if resection is possible

Chemo, immune and radio be used in addition as tumour markers dictate and spread is identified/assessed

-> General health, location, tumour size nutrition status influence treatment choice

37
Q

How does lip cancer present?

A

As non-healing ulcer or swelling

-> not an OCC/OPC

38
Q

Which factors are involved in aetiology of lip cancer?

A

Smoking

Sunlight

39
Q

What are the characteristics of lip tumours?

A

slow growth

local invasion

rarely metastasise to nodes

40
Q

Which treatment does lip cancer usually respond well to?

A

Responds well to surgery- good prog if removed early

41
Q

What must be considered before carrying out an oral cancer screening programme?

A

Benefits vs Harm (anxiety, unnecessary tx)

Undetected lesions vs False positive

Cost of Screening vs Cost of disease

Cost of Screening vs Disability from disease

42
Q

Why would oral cancer screening be helpful?

A

It would pick up lesions before they became malignant or at early stage where tx would be more successful

43
Q

What are examples of oral cancer screening methods?

A

HPV16 screening

Toluidene blue- dye applied to mucosa

VELscope

Photodynamic Diagnosis (PDD)

Clinical judgement of experienced clinician
-> likely better than inexperienced HCW using above methods

44
Q

What are the features of toluidene blue screening? What are its strengths and weaknesses?

A

 Stains markers within cells

 Good at showing areas of dysplasia, but also trauma, inflammation (false positives and negatives)

 Fairly widespread result- may not be helpful

 May be beneficial with known lesions- can detect areas which are more likely to be malignant (helps determine biopsy site)

45
Q

How does velscope work?

A

Causes autofluorescence of tissues with blue light
 Identifies areas of lack of fluorescence but doesn’t tell us cause (may or may not be cancerous change)
 May lead to needless biopsy

46
Q

How does Photodynamic diagnosis work?

A

Uses solerin which fluoresces in contact with UV light and is attracted to area of dysplasia

47
Q

What can a dentist do to deliver primary prevention of oral cancer?

A

Smoking cessation advice

Alcohol reduction advice

Healthy diet promotion

48
Q

What may a dentist do before they refer to OM under suspicion of oral cancer?

A

Monitor with photographs and education

Remove local factors where ulcer may be due to trauma, then review

-> Suspicious lesions- refer no matter the risk factors

49
Q

If a PML undergoes a change who should the dentist refer to?

A

MaxFacs department

50
Q

What pathway should a patient be referred on if they are deemed urgent suspicion of cancer?

A

2 WEEK RULE for referral to clinic for the hospital
-> Patient must be initially seen within this time

62 day referral to treatment time for cancer patients

BDS4 Oral Medicine (28 decks)

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