white lesions part 2 (PMD) Flashcards

1
Q

3 types of potentially malignant disorders

A

1) leukoplakia
2) oral lichen planus
3) lichenoid reactions

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2
Q

characteristics of leukoplakia
- what it looks like
- female/male
- cause
- predisposing factors

A
  • is a white plaque that cannot be characterised clinically/ pathologically as another disease
  • male predomincance, >40 yo, increase with age
  • is uncommon, but the most common premalignant lesion
  • unknown cause
  • predisposing factors are the 6S:
    sunlight, sex, syphilis, smoking, spirits (alcohol), spices (betel nut)
    same factors as SCC and erythroplakia
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3
Q

6 types of clinical presentation of leukoplakia

A

1) early/ mild/ thin
2) nodular/ granular
3) homogenous/ thick
4) speckled/ erythroleukoplakia
5) verruciform
6) proliferative verrucous

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4
Q

what does early/ mild leukoplakia look like

A
  • grey/ white plaque
  • flat to slightly elevated
  • soft with sharply demarcated borders
  • may be translucent, fissured, wrinkled
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5
Q

clinical presentation of nodular/ granular leukoplakia

A

increase surface irregularities

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6
Q

clinical presentation of homogenous/ thick leukoplakia

A
  • distinctly white plaque
  • thickened/ leathery
  • deepened fissures
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7
Q

clinical presentation of speckled/ erythroleukoplakia

A
  • white plaque with scattered patches of redness
  • epithelial cells so immature and atrophic that they cant produce keratin
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8
Q

clinical presentation of verruciform

A

sharp/ blunt wart-like projections

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9
Q

clinical presentation of proliferative verrucous

A
  • multiple, slowly spreading, keratotic plaques
  • rough surface projections
  • exhibit persistent growth, eventually become exophytic and verrucous (wart-like)
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10
Q

location of leukoplakia

A
  • lip vermillion, buccal mucosa and gingiva ( more common)
  • lip vermillion, tongue, floor of mouth (accounts for >90% of those that show dysplasia/ carcinoma)
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11
Q

how to diagnose leukoplakia

A

clinical + histo (must take biopsy) + elimination of other lesions that appear as white plaque

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12
Q

histopatho findings of leukoplakia
- hyperkeratosis and ____
- variable number of ____ cells in subjacent _____
- keratin layer will have ____
- no/ got dysplasia?

A
  • may have acanthosis
  • chronic inflammatory cells, in aubjacent CT
  • hyperorthokeratosis/ hyperparakeratosis or both
  • may have dysplasia
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13
Q

management of leukoplakia that exhibit moderate dysplasia or worse

A
  • complete removal
  • recurrence rate 10-35%
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14
Q

mx of leukoplakia with no/minimal dysplasia

A
  • mx should be guided by lesion size and response to tobacco cessation
  • may diminish in size after smoking cessation
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15
Q

ddx of leukoplakia

A

white lesions:
- leukoedema
- BARK, frictional keratosis (linea alba, morsicato buccarum)
- nicotinic stomatitis, smokeless tobacco lesions
- OLP, lichenoid reactions
- pseudomembranous candidiasis
- OHL

not white lesions:
- syphilis (secondary mucous patches)
- squamous papilloma, condyloma acuminatum

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16
Q

what layers of epithelium are affected and what histo is observed in MILD epithelial dysplasia in leukoplakia

A
  • basal and parabasal layers
  • nuclear hypochromatism and slight pleomorphism
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17
Q

what layers of epithelium are affected and what histo is observed in MODERATE epithelial dysplasia in leukoplakia

A
  • basal layer to mid portion of spinous layer
  • nuclear hypochromatism and pleomorphism
  • cellular crowding
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18
Q

what layers of epithelium are affected and what histo is observed in SEVERE epithelial dysplasia in leukoplakia

A
  • basal layer to a level above midpoint of epithelium
  • marked nuclear hyPER chromatism and pleomorphism
  • scattered mitotic figures
  • atypical cells involve most of epithelial thickness
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19
Q

what layers of epithelium are affected and what histo is observed in carcinoma in situ epithelial dysplasia in leukoplakia

A

whole thickness of epithelium

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20
Q

what is the cause of oral lichen planus

A

chronic t cell mediated disorder of stratified squamous epithelium (SSE), unknown cause

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21
Q

which demographic is more affected by OLP

A

middle aged adults, females

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22
Q

predisposing factors for OLP

A

drugs, restorative materials, microbes (hep C), systemic disorders, stress

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23
Q

pathogenesis of OLP

A
  • antigen specific cd8+ cytotoxic t cells trigger keratinocyte apoptosis, destroy the basal keratinocytes above basement membrane
  • mast cell granulation and MMP activation -> prolongs antiinflam reaction
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24
Q

7 forms of OLP

A

PAPERBD

papular: raised
atrophic: red, thin
plaque: white, flat
erosive: break in epithelium
reticular: striated
bullous: bubble appearance (less common)
desquamative gingivitis: red, painful, involve free gingi margin to mucogingival fold

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25
Q

histopatho findings for OLP

  • varying degree of ___ and ___ on surface epithelium
  • thickness of ___ layer varies
  • ___, ____ rete ridges
  • degeneration of ___ cell layer of epithelium
  • degenerating ___ (Civatte bodies) between epithelium and ___
  • intense, band like infiltrate of predominantly ____ in lamina propria
  • got/ no dysplasia?
A
  • varying degree of orthokeratosis and parakeratosis
  • thickness of spinous layer
  • pointed, saw toothed rete ridges
  • degen of basal cell layer
  • degenerating keratinocytes, between epithelium and CT
  • infiltrate of predominantly t lymphocytes
  • no dysplasia
26
Q

forms and characteristics of erosive LP

A

AEBD forms:
- atrophic
- erythematous
- bullous (only if erosive component is severe and there is epithelial separation from the underlying CT)
- desquamative gingivitis (if the atrophy and ulceration is confined to gingiva mucosa)

characteristics:
- got central ulceration of varying degrees
- periphery bordered by fine, white radiating striae

27
Q

2 types of OLP

A

1) erosive LP (AEBD forms)
2) reticular LP (PPR forms)

28
Q

forms and characteristics of reticular LP

A

PPR: papules, keratotic plaques on tongue, reticular (striated)

characteristics:
- lace like network, striated pattern of slightly raised grey white lines (wickham striae)
- usually asymptomatic

29
Q

symptoms of erosive LP

A
  • erythematous and desquamative gingiva
  • ulceration
  • bleeding and irritation with tooth brushing
  • oral pain and soreness, worse with acidic and spicy food
  • sensitivity to hot, acidic, spicy food
  • altered/ blunted taste sensation (if the tongue is affected)
30
Q

location of OLP

A
  • bilateral, mostly symmetrical
  • posterior buccal mucosa > dorsal and lateral border of tongue > gingiva and alveolar ridge > lower lip
  • floor of mouth, palate, upper lip (uncommon)
  • skin, genital mucosa, scalp, nails (uncommon)
31
Q

what are the 3 key histo points impt for the dx of OLP

A
  • degeneration of basal cell layer of epithelium
  • intense, band like infiltrate of predom t lymphocytes in lamina propria
  • no dysplaisa
32
Q

comparing leukoplakia and OLP

A

leukoplakia: single, well demarcated and non striated

OLP: bilateral, diffuse, striated

33
Q

ddx of OLP

A

lichenoid reactions (have identical clinical and histo findings)

34
Q

3 types of therapy that can be done under management of OLP

A

1) Symptomatic therapy
2) adjunctive therapy
3) maintenance therapy

35
Q

symptomatic therapy for OLP

A
  • control inflammation, decrease pain with minimal side effects
  • change erosive OLP to non erosive
  • 1st line: topical corticosteroids
  • 2nd line: systemic corticosteroids for severe/ recalcitrant lesions resistant to topical. OR topical calcineurin inhibitors to block activation and prolif of t lymphocytes
36
Q

example of topical calcineurin inhibitor

A

tacrolimus

37
Q

adjunctive therapy for OLP

A
  • control candida using topical anti fungals eg nystatin, miconazole
  • maintain good OH
  • manage salivary gland hypofunction if present
38
Q

maintenance therapy for OLP

A
  • low potency topical corticosteroids
  • long term follow up
39
Q

ddx for OLP

A

lichenoid reactions

40
Q

what are lichenoid reactions

A

antigen fixation in epithelial cells causing these cells to be destroyed by immune system

these lesions resemble OLP clinically and histologically but have identifiable aetiology

41
Q

4 types of lichenoid reactions that we learn

A

1) oral lichenoid drug reaction/ eruption
2) oral lichenoid contact lesions
3) oral lichenoid lesions of GVHD
4) systemic lupus erythematous

42
Q

what are some drugs causing OLDR (oral lichenoid drug rxn)

A

methyldopa, anti malarias, NSAIDs, diuretics, ACE inhibitors, B blockers

43
Q

what is the clinical presentation of OLDR

A
  • unilateral lesions of reticular striae
  • erosive lesions
  • e/o lesions
44
Q

location of OLDR in mouth

A
  • palate
  • labial mucosa
  • floor of mouth
45
Q

how do we dx OLDR

A
  • need to establish when the lesion onset and when the offending drug was used
  • see whether there is resolution of symptoms upon withdrawal of the agent
46
Q

what are the histopatho findings of OLDR

A
  • variable, non diagnostic
  • lymphocytic infiltrate is mixed, more diffuse. this extends deeper into lamina propria, got perivascular distribution
47
Q

mx for OLDR?

A

1) substitute drug after consulting physician
2) decrease dose of offending drug
3) topical corticosteroids (+/- anti fungals)

do these in order

48
Q

ddx of OLDR and oral lichenoid contact lesions

A

OLDR: erosive OLP
OLCL: reticular OLP

49
Q

where are oral lichenoid contact lesions found?

A

adjacent to dental materials
possible materials are Ni, composite, gic

usually buccal mucosa, ventral and lateral borders of tongue

50
Q

clinical presentation of oral lichenoid contact lesions

A
  • white or erythematous
  • peripheral striae
51
Q

histopatho findings of oral lichenoid contact lesions and oral lichenoid lesions of GVHD

A
  • similar to OLP aka varying degree of ortho and parakeratosis on surface epithelium. pointed saw toothed rete ridges, degen of basal cell layer of epithelium, infiltrate of predom t lymphocytes in lamina propria
  • lymphocytic infiltrated mixed
52
Q

how do oral lichenoid lesions of GVHD come about

A
  • hx of bone marrow transplant
  • immunocompetent t cells from donor (graft) attack tissue in immunocompromised host (recipient)
  • increased risk of developing solid tumours (eg SCC)
53
Q

clinical presentation of oral lichenoid lesions of GVHD

A
  • fine, reticular network of white striae
  • may have atrophy of mucosa
  • burning sensation of oral mucosa
54
Q

where will oral lichenoid lesions of GVHD be located in mouth

A
  • buccal and labial mucosa
  • tongue
55
Q

mx of oral lichenoid lesions of GVHD

A
  • systemic therapy since it is a multi organ disease
    1) give high dose systemic corticosteroids
    2) supplement w cyclosporin, tacrolimus
  • topical corticosteroids (+/- anti fungals)
  • long term follow up
56
Q

ddx of oral lichenoid lesions of GVHD

A

reticular OLP

57
Q

which are the lichenoid reactions that have ddx of reticular OLP and which have ddx of erosive OLP

A

reticular OLP:
1) oral lichenoid contact lesions
2) oral lichenoid lesions of GVHD

erosive OLP:
1) OLDR
2) SLE

58
Q

clinical presentation of SLE

A
  • central atrophic area with radiating white striae
  • erythematous lesions on palate
  • slit like gingival ulcerations
59
Q

location of SLE in oral cavity

A
  • palate (most common, 80%)
  • buccal mucosa, lips, gingiva

vs OLP on palate is uncomon

60
Q

how to dx SLE

A

must be by histo

61
Q

histopatho findings of SLE

A

similar to OLP
may have deep perivascular distribution