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BDS4 VIROLOGY > Potentially Malignant Disorders and Oral Cancer > Flashcards

Potentially Malignant Disorders and Oral Cancer Flashcards

1
Q

what is a potentially malignant lesion?

A

altered tissue in which cancer is more likely to form

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2
Q

what is a potentially malignant condition?

A

generalized state with increased cancer risk

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3
Q

What systemic conditions make a person more likely to develop cancer? [potentially malignant conditions]

A
  • lichen planus [erosive variety]
  • oral submucous fibrosis
  • iron deficiency [causes atrophy of oral epithelium]
  • tertiary syphilis [develops white patch on tongue]
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4
Q

What can cause oral submucous fibrosis?

A

Chewing betel nut which causes
- atrophy
- abnormal collagen
- restricted mouth opening
- xerostomia
- increased cancer risk

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5
Q

what type of leukoplakia can be potentially malignant?

A
  • chronic hyperplastic candidoses
  • proliferative verrucous leukoplakia
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6
Q

Where is chronic hyperplastic candidosis found? What causes it?

A
  • caused by Candida albicans
  • found on the commissures of the mouth
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7
Q

What typically causes chronic hyperplastic candidosis?

A

smokers

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8
Q

What investigation should you do when a pt has chronic hyperplastic candidosis?

A

Biopsy!!
- check for dysplasia as these lesions can become malignant

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9
Q

How does hyperplastic candidosis appear under microscope?

A
  • excessive keratin deposits (where epithelium is generally not keratinised)
  • acanthosis of epithelium (stratum spinosum layer)
  • inflammatory cells within the lamina propria (macrophages, neutrophils etc)
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10
Q

What specific stain is needed to demonstrate candida albicans hyphae clearly?

A

Periodic Schiff Stain (PAS)

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11
Q

How is chronic hyperplastic candidosis treated?

A
  1. systemic antifungal
    - Fluconazole 1x 50mg everyday for 2 weeks
  2. biopsy
  3. smoking cessation
  4. observe
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12
Q

do all cases of oral cancer have potentially malignant lesions beforehand?

A

NO
- most oral carcinomas in UK arise in clinically normal mucosa

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13
Q

What sites of oral cavity are higher risk of leukoplakia becoming malignant?

A
  • floor of mouth
  • tongue
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14
Q

What sites of oral cavity are lower risk of leukoplakia becoming malignant?

A

buccal mucosa

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15
Q

Not every leukoplakia will develop into cancer, what markers may suggest that a lesion will?

A
  • age and gender (older)
  • idiopathic
  • site [tongue & FoM]
  • non-homogenous lesions
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16
Q

What predictor markers do we look for in histopathology that suggest malignant change?

A
  • dysplasia
  • atrophy
  • candida infection
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17
Q

what molecular markers may determine if a lesion will become malignant?

A

HPV & p53 (apoptosis)

18
Q

What is dysplasia ?

A

disordered maturation (growth) in a tissue

19
Q

What is atypia?

A

changes in cells

20
Q

For a potentially malignant lesion, what is the criteria for diagnosis?

A
  • abnormal architectural changes
  • cytological abnormalities (cellular atypia)
21
Q

What does grading refer to?

A

Histopathology

22
Q

What does staging refer to?

A

Clinical assessment

23
Q

What is basal hyperplasia?

A

increased basal cell numbers

24
Q

How does histopathology appear in mild dysplasia?

A
  • changes in architecture of lower third
  • mild atypia [pleomorphism and hyperchromatisim]
25
Q

How does histopathology appear in moderate dysplasia?

A
  • architectural changes extend into middle third
  • moderate atypia
26
Q

How does histopathology appear in severe dysplasia?

A
  • architectural changes extending into upper third
  • severe atypia & numerous mitosis
27
Q

How would a carcinoma-in-situ appear under the microscope?

A
  • abnormal architecture = full thickness of viable cell layers
  • pronounced cytological atypia
28
Q

How are potentially malignant lesions / oral cancer detected?

A

Visual oral examination alongside biopsy & histopathological investigation

29
Q

What common diagnostic tests are used in clinical practise to investigate potentially malignant lesions?

A
  • vital staining
  • oral cytology
  • optical imaging
30
Q

What are the two main factors that contribute to carcinogenesis?

A
  • genetic predisposition
  • environmental factors
31
Q

what are oncogenes?

A

normal genes that produce growth factors in cells
- in cancer these can become activated and contribute to tumour growth

32
Q

Explain Knudsons two hit theory:

A

First hit = Individuals inherit one mutated copy of a tumor suppressor gene from one of their parents. This mutation is present in all cells of the body and predisposes the individual to cancer development.

Second hit = A second, somatic mutation occurs in the remaining functional copy of the tumor suppressor gene within a specific cell or tissue. This second mutation results in the complete loss of function of the tumor suppressor gene in the affected cell, leading to uncontrolled cell growth and tumor formation.

33
Q

What genes are involved in driving oral cancer?

A
  • oncogenes
  • tumour suppressor genes
  • Tp53 mutation
  • genes that regulate apoptosis
  • genes involved in DNA repair
  • miRNA
34
Q

What are epigenetic changes?

A

chemical changes in DNA, such as methylation and modification of the histones that package DNA

35
Q

What are the six genetic hallmarks of cancer?

A
  • self sufficiency and growth signals
  • evading apoptosis
  • insensitivity to anti-growth signals
  • tissue invasion and metastasis
  • sustained angiogenesis
  • limitless replicative potential
36
Q

What % of oral cancer is squamous cell carcinoma?

A

95% of oral cancer cases

37
Q

How does oral cancer spread?

A
  1. local extension of disease
  2. lymphatic spread
  3. haematogenous spread
38
Q

If a histopathological view of oral cancer has a non-cohesive front, what may this suggest?

A

The cancer has spread to the lymph nodes

39
Q

What system is used for clinical staging of oral cancer?

A

TNM staging
- T = size
- N = lymph node involvement
- M = metastasis

40
Q

What are some subtypes of oral squamous cell carcinomas?

A
  • basaloid squamous (associated with HPV)
  • verrucous carcinoma
  • spindle cell

BDS4 VIROLOGY (5 decks)

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