Dysplasia & OC P2 Flashcards

1
Q

Potentially malignant lesions

A
  • previously termed premalignant/ precancerous
  • important to inform pt so they know if they can turn malignant
  1. are they en-route to becoming cancer?
  2. much more likely to be cancer?
  3. potentially malignant?
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2
Q

Examples of potentially malignant lesions?

A
  1. White lesions- leukoplakia
  2. Red lesion- erythroplakia
  3. Lichen planus
    - ulcerative and erosive LP
    - candidal leukoplakia??
    - chronic hyperplastic candidiasis??
  4. Oral submucous fibrosis
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3
Q

Leukoplakia

A
  • white patch that cannot be rubbed off
  • undiagnosed white patch, higher risk of cancer developing than normal mucosa
  • not all white patches have the same levels of malignancy

** clinical description and should not be used as a pathological diagnosis for pt

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4
Q

Erythroplakia

A
  • red patch
  • much more common to malignant change
  • erythema may represent vascular change consequent to malignant change

** clinical description and should not be used as a pathological diagnosis for pt

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5
Q

Incidence of OC in white lesions

A

0.2 - 4%
- very small

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6
Q

Oral cancer in White lesions

A
  • 0.2 - 4%
  • wide variation in different pop
  • diet, smoking habits, genetics
  • malignant change is at most 4%
  • 2.5% in 10 years and 4% in 20 years

**pt needs to know there is a risk of malignant change, and lesions need to be monitored.

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7
Q

OC in white lesions in UK

A
  • most arise initially as clinically normal mucosa
  • most cancer in higher incidence areas are from potentially malignant lesions
  • worldwide leukoplakia is 50-100 times more likely to progress to cancer than clinically normal mucosa
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8
Q

White lesions example

A
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9
Q

Erythroplakia

A
  • higher risk of malignancy
  • much less frequent than leukoplakia which does not have an explaination
  • higher risk of cancer
  • greater dysplasia risk
  • no good followup studies
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10
Q

Dysplasia to assess cancer risk?

A
  1. Based on
    - cellular atypia
    - epithelial architectural organisation
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11
Q

Previous categorisation of dysplasia

A
  • mild
  • moderate
  • severe
  • carcinoma- in- situ

** moderate sometimes can proceed to severe or mild -> affecting tx

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12
Q

New categorisation

A
  • low grade
  • high grade
  • carcinoma-in-situ
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13
Q

Histological grading of Oral Mucosa Dysplasia

A
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14
Q

Low grade dysplasia

A
  1. easy to identify that tumour originates from squamous epithelium
  2. architectural change into lower third
  3. cytological atypia/ dysplasia may not be prominent
  4. considerate amount of keratin production
  5. evidence of stratification
  6. well formed basal cell layer surrounding tumour islands
  7. tumour islands are usually well defined and often continuous with surface epithelium
  8. invasion pattern with intact large branching rete pegs pushing into underlying CT

**when there is architectural changes into middle 3rd, depending on level of cytological atypia, will then be classified either into low/ high grade

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15
Q

High grade dysplasia

A
  1. show little resemblance to a normal squamous epithelium
  2. architectural change upper third
  3. show considerable atypia
  4. invade in a non-cohesive pattern with fine cords, small islands and single cells infiltrating widely through CT
  5. mitotic figures are prominent and many may be abnormal
  6. loss of stratification

Degree of differentiation is widely used to predict prognosis and shows a significant correlation to survival

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16
Q

Carcinoma in situ

A
  • cytologically malignant but not invading
  • abnormal architecture
  • full thickness
  • severe cytological atypia
  • Mitotic abnormalities frequent
17
Q

Prognostic factors

A
  1. Pattern of invasion
    - Bulbous rete pegs infiltrating at same level is considered of a better prognosis than widely infiltrating small islands and single cells
  2. Depth of invasion
    - risk of metastases for a tumour greater than 4mm was 4x greater than a tumour less than 4mm
  3. Perineural invasion
    - up to 60% of OSCC, most significant when a tumour is seen within a large nerve at a site some distance from main tumour mass
  4. Invasion of vessels
    - associated with lymph node metastases and poor prognosis
18
Q

How does cancer happen?

A
  • it is a multi-stage promotion
19
Q

Field Cancerisation concept

A

Definition
- where a cancer develops inside the mouth, it is not the only part of mouth which has been subject to changes and stimuli that lead to cancer
- coalesce in cancer area and produce change at the time
- may be progressing at other parts at a slower stage

** has a risk of developing cancer in a later time at diff parts
- higher risk in 5cm radius of original primary
- hence important to consider the whole mouth
- review pt
- look for other lesions that may have been missed

20
Q

Synchronous/ Metachronous lesions

A
  • can occur at the same time as primary but different places at a later times
21
Q

Oral cancer staging

A

Multiple variables for clinical staging of oral cancer

  1. site
  2. size (T)
  3. spread (N & M)
22
Q

Oral cancer prognosis

A

1/3 patients present at stage1/2

  • Stage 1: 80% cure rate
  • Stage 2: 65% cure rate
  • later than this is 5 year survival of <50%, cure 30%
  • if untreated, with metastases, survival is about 4 months

Surgery/ radiotherapy/ chemo/ immunotherapy
- choice will depend on pt choice and health/ prognosis
- tumour location, size and nutritional status

For resectable tumours, primary surgery offers best outcome
- post surgical radiotherapy/ chemotherapy

23
Q

Lip cancer

A

Lower lip
- non- healing ulcer/ swelling
- normally detected early as it is visible, hence good prognosis
- Aetiology is sunlight UVB or smoking
- slow growth
- local invasion
- rarely metastasise to nodes

24
Q

Oral cancer detection

A
  • difficult process
  • Oral cancer Recognition Toolkit by Cancer Research UK and British Dental Association
25
Q

Oral Cancer Screening

A
  • looking specific for a lesion at early stage or before lesion is malignant
  • benefit vs harm
  • undetected lesions vs false positive
  • cost of screening vs cost of disease
  • cost of screening vs disability from disease
26
Q

Different forms of screening processes

A
  • HPV16 screening
  • Toluidine blue
  • VELscope
  • Photodynamic diagnosis (PDD)
  • clinical judgement of experienced clinician
  • oral brush cytology
27
Q

Toluidine Blue

A
  • which apply to oral mucosa
  • stain particular markers within cells
  • show areas of change in dysplasia
  • also shows area of inflammation and trauma
  • not particularly helpful, as it widespread
  • false positive in inflammatory lesions
  • not a good tool to detect oral malignant lesions
28
Q

VELscope

A
  • autofluorescence of tissues with blue light
  • loss of fluorescence equates to change
  • change can be cancer or can be other changes
  • ie: show area with reduce fluorescence, but with no cause why, may lead to biopsy of false positive test
29
Q

PDD

A
  • Photodynamic diagnosis
  • use Psoralen, UV light which can be attracted to area of dysplasia/ cancer
30
Q

Oral cancer screening

A
  • most cost effective and reliable screening tool is experienced dental practitioner
31
Q

Oral cancer in primary care

A
  • part of general CPD requirement now
  • primary prevention in pts attending for regular oral care

Dentist must be familiar with and competent in
1. smoking cessation advice
2. alcohol reduction advice
3. healthy diet promotion- will help in long term

  • can present in any age in any pt
32
Q

Referral for OC

A
  • dentist has to make decision about the referral threshold for potentially malignant lesions
  • monitor with photographs and education, ie: smoking and alcohol reduction
  • remove local factors where ulcer may be due to trauma and review

2 week rule for referral to clinic for hospital (maxillofacial department- local health board pathway- suspicion of cancer)
- pt must be initially seen within this time- lesion can be promptly assess
- 62 days referral to tx time for cancer pt

33
Q

Desquamative gingivitis

A
  • OHI
  • Topical Tacrolimus: topical immunosuppressant