Dysplasia and Oral Cancer- Oral lesions and Therapy Options

Question 1

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

Answer 1

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

Question 2

What are the different types of potentially malignant lesions?

Answer 2

White lesions (leukoplakia)

Red lesions (erythroplakia)

Lichen planus
-> Candidal Leukoplakia
-> Chronic Hyperplastic Candidiasis

Oral Submucous Fibrosis

Question 3

What is Leukoplakia?

(clinical description)

Answer 3

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)

Question 4

What is erythroplakia?

Answer 4

Red patch, not attributable to any other disease

-> More commonly associated with malignant change

Question 5

What does erythema in erythroplakia suggest?

Answer 5

Erythema suggests vascular change consequent to malignancy developing

Question 6

What should we tell patients about white lesions?

Answer 6

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)

Question 7

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

Answer 7

Most carcinomas arise in clinically normal mucosa

*in UK- in other areas most arise from PMLs

Question 8

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

Answer 8

Biopsy to check for dysplasia

Question 9

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

Answer 9

Occurs less frequently

Higher chance of Cancer

Greater dysplasia risk

Question 10

Which factors in dysplasia are risk of cancer based off?

Answer 10

Cellular atypia

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

Question 11

What are the categories in dysplasia?

Answer 11

Low grade

High Grade

Carcinoma-in-situ

Question 12

Why was moderate dysplasia removed from the categories?

Answer 12

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

Question 13

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

Answer 13

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

Question 14

What do the cytological changes during dysplasia represent?

Answer 14

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

Question 15

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

Answer 15

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

Question 16

What are the typical features of low grade dysplasia?

Answer 16

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

Question 17

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

Answer 17

Look at level of atypia to decide if low or high

Question 18

What are the typical features of high grade dysplasia?

Answer 18

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

Question 19

What is degree of differentiation used to predict?

Answer 19

Prognosis as level correlates with long term survival

Question 20

What are the features of carcinoma in situ?

Answer 20

Cytologically malignant but not invading

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

Severe cytological atypia

Mitotic abnormalities frequent

Question 21

When is the term carcinoma in situ used?

Answer 21

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

Question 22

What are histological prognostic factors used for?

Answer 22

Reported to clinicians to help inform management of cancer for MDT

Question 23

What are the histological prognostic factors associated with poor prognosis?

Answer 23

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)

Question 24

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

Answer 24

 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

Question 25

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

Answer 25

Normal mucosa- normal keratinocytes Genetic instability/Aneuploidy- hyperplasia, low grade dysplasia -> potentially malignant Adaptive advantages- high grade dysplasia Invasion- carcinoma

Question 26

What is field cancerisation?

Answer 26

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)

Question 27

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

Answer 27

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)

Question 28

What is a synchronous tumour?

Answer 28

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)

Question 29

What is a metachronous tumour?

Answer 29

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

Question 30

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

Answer 30

They must be continuously followed up and reviewed

Question 31

How are tumours staged?

Answer 31

 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)

Question 32

Why is the TMN staging system used?

Answer 32

Correlates with survival rates and treatment options are based off staging

Question 33

How many patients present at stage 1 or 2?

Answer 33

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

Question 34

What is the cure rates in stage 1 and 2?

Answer 34

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

Question 35

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

Answer 35

As most believe they will outlive 5 years

Question 36

What are the treatments available for oral cancer?

Answer 36

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

Question 37

How does lip cancer present?

Answer 37

As non-healing ulcer or swelling -> not an OCC/OPC

Question 38

Which factors are involved in aetiology of lip cancer?

Answer 38

Smoking Sunlight

Question 39

What are the characteristics of lip tumours?

Answer 39

slow growth local invasion rarely metastasise to nodes

Question 40

Which treatment does lip cancer usually respond well to?

Answer 40

Responds well to surgery- good prog if removed early

Question 41

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

Answer 41

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

Question 42

Why would oral cancer screening be helpful?

Answer 42

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

Question 43

What are examples of oral cancer screening methods?

Answer 43

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

Question 44

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

Answer 44

 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)

Question 45

How does velscope work?

Answer 45

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

Question 46

How does Photodynamic diagnosis work?

Answer 46

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

Question 47

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

Answer 47

Smoking cessation advice Alcohol reduction advice Healthy diet promotion

Question 48

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

Answer 48

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

Question 49

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

Answer 49

MaxFacs department

Question 50

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

Answer 50

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