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Oral Med > Premalignant conditions > Flashcards

Premalignant conditions Flashcards

1
Q

What is a pre-malignant lesion?

A

Morphologically altered tissue in which cancer is more likely to occur than in its apparently normal counterpart

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2
Q

What is leukoplakia?

A

Predominantly white lesion of the oral mucosa that cannot be characterised as any other definable lesion (disease) & which is not associated with any physical or chemical causative agent except tobacco

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3
Q

What is erythroplakia?

A

Bright red velvety plaque which cannot be characterised as any other definable lesion (disease)

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4
Q

Normal anatomy causes of white patches?

A

o Fordyce spots
o Leucoedema

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5
Q

Developmental causes of white patches

A

o White sponge naevus

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6
Q

Traumatic causes of white patches?

A

o Frictional keratosis
o Cheek biting, trauma from dentures, cusps, fillings, orthodontic appliances

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7
Q

Chemical causes of white patches?

A

o Aspirin burns
o Smoker’s keratosis (on palate)

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8
Q

Autoimmune causes of white patches?

A

o Lichen planus
o Lupus erythematosus

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9
Q

Infective causes of white patches?

A

o Chronic hyperplastic candidosis
o Oral hairy leukoplakia

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10
Q

What is oral hairy leukoplakia associated with?

A
  • Associated with EBV
  • If associated with AIDS, resolves with HAART
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11
Q

Clinical features of OHL?

A
  • Painless
  • May mimic other oral mucosal diseases
  • Not premalignant
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12
Q

Clinical features & prevalence of Fordyce spots?

A
  • Common, benign
  • AKA Fordyce granules
  • Sebaceous glands
  • Creamy-yellow papules  may coalesce
  • Buccal/labial mucosa
  • Appear in childhood
  • Increase at late puberty & adult life
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13
Q

Management of Fordyce spots?

A
  • Reassurance
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14
Q

What is leucoedema?

A
  • Variation of normal
  • Bilateral, diffuse, translucent, greyish appearance to oral mucosa
  • Typically present in black people may also occur in white
  • Disappears on spreading affected mucosa
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15
Q

What are the 2 types of appearance of leukoplakia?

A

Homogenous
Non-homogenous

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16
Q

What is the appearance of homogenous leukoplakia?

A

Uniform, flat appearance that may exhibit shallow cracks & has a smooth, wrinkled or corrugated surface with a consistent texture throughout

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17
Q

What is the appearance of non-homogenous leukoplakia?

A

o Predominantly white or white & red lesion (erythroleukoplakia)
o Irregularly flat, nodular & exophytic:
- Nodular lesions have raised, rounded, red and/or white excrescences (protrusion)
- Exophytic (outward growth) lesions have irregular blunt or sharp projections

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18
Q

Epidemiology of leukoplakia?

A
  • Most diagnosed in middle age, increase with age
  • 10% of oral leukoplakias idiopathic
  • 90% associated with use of tobacco/areca nut
  • M>F (maybe due to greater prevalence of tobacco use by males)
  • Buccal mucosa affected in 25% cases, mandibular gingiva in 20%, tongue in 10% & floor of mouth in 10%
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19
Q

What surface features of leukoplakia is suggestive of an increased risk of malignant transformation?

A

Raised/nodular

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20
Q

Gender & age with increased risk of malignant transformation?

A

Advanced age
Females

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21
Q

What features of the colour of leukoplakia is suggestive of an increased risk of malignant transformation?

A

Red/white (speckled)

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22
Q

Which sites of leukoplakia are suggestive of malignant transformation?

A

o Floor of mouth
o Lateral border of tongue
o Retromolar region
o Buccal sulcus (paan chewers)
o Labial commissure

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23
Q

What is the rate of malignant change of leukoplakia & erythroplakia?

A
  • Leukoplakia – overall  1-5% (UK 4%)
    Homogenous  0%
    Non-homogenous  26%
  • Erythroplakia – overall  80%
24
Q

What is the risk of erythroplakia?

A
  • High risk lesion & ALWAYS associated with dysplasia or carcinoma
25
Q

Which premalignant conditions is erythroplakia associated with?

A

Syphilis
Sideropenic dysphagia (Patterson Kelly or Plummer Vinson Syndrome)
Oral submucous fibrosis
Actinic keratosis (cheilitis)
Lichen planus
Chronic hyperplastic candidosis

26
Q

Presentation of syphilis orally?

A

Leukoplakias on central dorsum of tongue
Glossitis with mucosal atrophy

27
Q

Clinical features of Sideropenic dysphagia (Patterson Kelly or Plummer Vinson Syndrome)

A

 Fe deficiency anaemia
 Generalised mucosal atrophy
 Oesophageal web
 Middle aged women

28
Q

Where do we see oral submucous fibrosis? And what is the risk of OSCC?

A

 Fibrosis of oral mucosa & difficulty opening mouth
 Paan, betel chewers
 30% may develop OSCC

29
Q

What is actinic keratosis (cheilitis)?

A

 Sunlight induced changes on the lip
 Increased risk of carcinoma

30
Q

Risk of OSCC developing in long-standing OLP?

A

0.5-2% rate over 5-year period

31
Q

When would OLP need further specialist opinion & possible biopsy?

A
  • Isolated areas of increasing whiteness, speckling (areas of redness & whiteness)/ solitary ulceration unlikely to reflect local trauma
32
Q

What must all pts with OLP be advised of?

A

Controversial malignant potential

To avoid tobacco & alcohol

Have diet rich in vitamins A, C & E/antioxidants

Maintain good OH with regular dental care

33
Q

What is chronic hyperplastic candidosis related to?

A
  • Uncommon
  • Associated with tobacco use
  • Occasionally related to immunodeficient states
  • Resistant to anti-fungal therapy
34
Q

What does histology tell us in regard to malignancy of lesion?

A

More reliable indication than clinical exam

But dependent on site of lesion biopsied

35
Q

Definition of keratosis?

A

Keratinisation in an epithelium that is not normally keratinised

36
Q

What is hyperkeratosis?

A

Increased thickness of the keratinised layer

37
Q

What is orthokeratosis?

A

Flat, anucleate superficial cells with homogenous eosinophilic cytoplasm

38
Q

What is parakeratosis?

A

Flat, homogenous eosinophilic superficial cells BUT with pyknotic nuclei

39
Q

What is acanthosis?

A

o Increased number of cells in prickle layer
o Broadening of rete ridges
o Thicker epithelium

40
Q

What is atrophy?

A

o Decreased epithelial thickness
o Loss of rete ridges
o Epithelium may be roughly equal thickness throughout

41
Q

What is atypia?

A

Changes to individual cell

42
Q

What is dysplasia?

A

Changes in whole epithelium

43
Q

Histological features of oral dysplasia

A
  • Nuclear hyperchromatism (increased DNA content)
  • Nuclear & cellular pleomorphism (variation in size & shape)
  • Increased nuclear to cytoplasmic ratio
  • Increased number & bizarre mitoses
  • Mitosis in prickle cell layer
  • Premature keratinisation in the prickle cell layer
  • Loss of polarity of basal cells
  • Loss of epithelial stratification
  • Drop shaped rete ridges
  • Loss of cell adherence
44
Q

Grading of dysplasia

A
  • None - epithelial cells appear normal
  • Mild - few epithelial cells in the basal layers show atypia
  • Moderate - Most cells in the basal layers & some suprabasally show atypia
  • Severe - Almost all cells show atypia but there is no evidence of invasion into the underlying tissues; ‘carcinoma in situ’
45
Q

What makes leukoplakias appear white clinically?

A

Hyperkeratosis or parakeratosis

46
Q

Why are erythroplakias red?

A

Atrophy

47
Q

Histological features of leukoplakia?

A
  • Hyperkeratosis or parakeratosis
  • Variable hyperplasia & acanthosis (increased thickness of prickle cell layer)
  • Atrophy
  • Candidal hyphae – up to 30% of leukoplakias
  • Inflammation
  • Some leukoplakias may show one or more features of dysplasia
48
Q

Histological features of erythroplakia?

A
  • Atrophy
  • Dysplasia
  • Inflammation
49
Q

Risk of malignant change in epithelial dysplasia?

A

10-36%

50
Q

Aetiology of leukoplakia?

A

Tobacco - chewing tobacco (paan - betel quid), reverse smoking, pipe smoking, smoking (bidi smoking, cigarettes)

Smokeless tobacco & oral epithelial dysplasia (snuff, tobacco chewing)

Candida albicans (30% of leukoplakias may contain candida)

51
Q

Management of leukoplakia in gdp?

A
  • Determine the level of risk – site, size, colour, surface, habits
  • Refer to local oral & maxillofacial department – don’t biopsy yourself!
  • If lesion very suspicious, mark the letter as urgent or treat within 2 week rule & phone relevant consultant; fax letter & send through post
52
Q

What is survival rate of oral cancer?

A

40%

53
Q

Hospital setting management of leukoplakias?

A
  • Biopsy lesion to establish the level of risk
  • Incisional biopsy for a large lesion, multiple biopsies if necessary
  • Always biopsy most suspicious part & include margin of normal tissue
  • Multiple biopsies may be required
  • Excisional biopsy if the lesion is small
54
Q

How to manage erythroplakia in gdp/hospital?

A

Refer urgently from gdp

In hospital, these lesions are always biopsied & excised

55
Q

Management of mild/moderate dysplasia?

A
  • Keep under review – every 3-6 months
  • Advice on tobacco, alcohol cessation
  • Nutritional assessment – Fe/B12/folate deficiency
  • Biopsy at 3 months to reassess dysplasia
  • Further biopsy within 2-3 years
56
Q

Management of moderate dysplasia?

A

Surgical excision
- If lesion is small
- If patient if unlikely to modify risk habits
Candidal leukoplakia
- Fluconazole up to 6 weeks treatment
- Smoking cessation advice
- Re-biopsy after 3 months & reassess dysplasia

57
Q

Management of severe dysplasia?

A

Surgical excision
- Scalpel, laser or cryotherapy
Photodynamic therapy
- 5 aminolaevulinic acid
- Multiple lesions
- Topical
- Systemic - Patient will need to stay in darkened room

Oral Med (1 decks)

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