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BDS4 Oral Medicine > Lichen Planus > Flashcards

Lichen Planus Flashcards

1
Q

What are the 6 main types of lichen planus

A
  • reticular
  • papular
  • plaque like
  • atrophic
  • erosive ulceration
  • bullous
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2
Q

Which types of lichen planus are often symptom free

A
  • reticular
  • papular
  • plaque like
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3
Q

Which types of lichen planus often occur together

A

atrophic and erosive
usually have a red glazed appearance with areas of superficial ulceration

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4
Q

What is bullous lichen planus

A

it is preceded by bulla
the rarest form

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5
Q

How does erosive/ulcerative lichen planus present

A
  • persistent irregular and painful erosions with a yellow slough
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6
Q

Which type of lichen planus is seen in desquamative gingivitis

A

atrophic

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7
Q

What does plaque like lichen planus resemble

A

leukoplakia

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8
Q

How does reticular lichen planus present

A
  • a network of raised white lines creating a lacy pattern called striae
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9
Q

What may bullous lichen planus possibly caused by

A
  • superficial mucoceles
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10
Q

Where can lichen planus occur in the mouth

A
  • buccal mucosa (most common site)
  • tongue
  • palate
  • lips
  • gingiva
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11
Q

Which type of lichen planus is this

A

plaque like

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12
Q

Which type of lichen planus is this

A

Papular

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13
Q

Which type of lichen planus is this

A

reticular

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14
Q

Which type of lichen planus is this

A

atrophic

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15
Q

Which type of lichen planus is this

A

Bullous

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16
Q

Which type of lichen planus is this

A

erosive

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17
Q

What type of hypersensitivity reaction is lichen planus

A

type 4
T cell mediated

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18
Q

What is the pathogenesis of lichen planus

A
  • cell mediated immune response to an external antigen or internal antigenic changes in the epithelial cells
  • this induces the release of cytokines
  • t cells become attracted to the basement membrane and stratum basale
  • CD8 and CD4 cells become present and cause damage
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19
Q

What type of t cell are cd8+

A

cytotoxic

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20
Q

What type of cells are cd4 cells

A

helper cells

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21
Q

What are the possible aetiologies/predispositions to lichen planus

A
  • genetic
  • stress
  • idiopathic - most common
  • trauma
  • systemic viral infections
  • graft vs host disease
  • drugs
  • dental materials
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22
Q

What systemic viral infection is associated with lichen planus and why

A

hepatitis C
virus may modify the self antigens on the surface of the basal keratinocytes

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23
Q

Why does graft vs host disease result in lichen planus-type reaction

A
  • oral and cutenaous lesions are seen
  • transplanated t lymphocytes react to antigens in the host epithelial cells which they regard as foreign
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24
Q

What drugs are associated with lichen planus

A

NSAIDS
betablockers
ace inhibitors
diuretics

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25
Q

When a cause such as drugs or dental materials is implicated, what is this called

A

lichenoid tissue reaction

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26
Q

What is E and C

A

E = Epitheliotropism
C = area of basal cell destruction

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27
Q

What is epitheliotropism

A
  • lymphocytes are drawn up into deeper layers of the epithelium
  • they sit among the deeper keratinocytes
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28
Q

What is D

A

civatte bodies

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29
Q

What are civatte bodies

A

cells with eosinophilic cytoplasma and very dark staining nuclear remnants
they are surrounded by a clear halo
they have undergone apoptosis

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30
Q

What is B

A

lymphocytes

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31
Q

What is a

A

band of inflammatory cells within the lamina propria

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32
Q

What is B

A

Perivascular infiltration

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33
Q

What is perivascular infiltration

A

deeper infiltration of the lymphocytes
there is mononuclear inflammatory cell infiltrate around the venules
indicates a delayed hypersensitivtiy reaction

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34
Q

What is perivascular infiltration a sign of

A
  • lichenoid tissue reaction or lupus erythematous
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35
Q

What can be seen in this slide

A
  • saw tooth rete ridges
  • patchy acanthosis
  • parakeratosis
36
Q

Summarise the process of lichen planus at a histopathological level

A
  1. Earliest features = changes in basal epithelium + appearance of Langerhan’s cells
  2. A band like dense mononuclear inflammatory cell infiltrate in the upper lamina propria
  3. T-cell cytokines cause apoptosis in the epithelial basal keratinocytes
  4. Basal keratinocytes degenerate and die
  5. Civatte bodies appear in the epithelial spinous layer
  6. Rest of the epithelium reacts with thickening of spinous layer and parakeratosis and this accounts for the clinical white lesion
  7. Rete ridges adopt saw tooth configuration
  8. Epithelial atrophy and erosions can appear and this leads to discomfort, redness and ulceration
37
Q

What are the usual symptoms of lichen planus

A

usually none
may feel sensitive to hot and spicy food
likely due to thinning of oral epithelium
may get lesions in other sites of the body

38
Q

Where else in the body may the patient see lesions

A

skin
scalp
genitals
hair and nails

39
Q

What is the benefit of buccal lichen planus

A

it is an easy biopsy site

40
Q

What is gingival lichen planus often termed

A

desquamative gingivitis

41
Q

What does gingival lichen planus resemble

A

gingival pemphigoid
plasma cell gingivitis
can only differentiate via histology

42
Q

What is the presentation of gingival lichen planus

A
  • v red looking gingiva - can worry px
  • can be very patchy
  • in some forms, typical reticular pattern seen
43
Q

What is important in settling gingival lichen planus

A

good OH

44
Q

Why is biopsy difficult for gingival lichen planus

A
  • risk of damaging adjacent attachment area of gingiva/tooth
  • adherent attached mucosa damaged lifting from bone
  • take care when deciding biopsy
45
Q

What is usually the reason behind LP on the dorsal tongue

A

idiopathic
often asymptomatic
results in loss of papillae and smooth tongue surface

46
Q

What is the usual cause of lichen planus on the lateral surface of the tongue

A
  • drug/amalgam trigger
  • amalgam most likely if isolated lesion
  • look at tongue position at rest, is it in contact with amalgam
47
Q

Is the tongue easy to biopsy

A

yes but painful healing

48
Q

Describe the clinical presentation of lichenoid drug reactions

A
  • usually widespread lesions that are bilateral and mirrored
  • often poor response to steroid tx
49
Q

How should management of lichenoid drug reactions be decided

A
  • consider symptoms
  • consider benefit of causative drug and risk of stopping it
  • is maximum tx required for the LP
  • contact GP - is the drug still needed and are there alternatives
50
Q

What is a good alternative for ACE inhibitors

A

AT2 blockers

51
Q

What is the management of amalgam related lesions

A
  • patch testing not hepful
  • if not symptomatic may want to leave in situ
  • can replace with composite but ensure removed under dam, avoid removal in pregnancy and warn px that it may not resolve the lesions
52
Q

What investigations should be done for lichen planus

A
  • biopsy unless good reason not to
  • bloods - haematinics, FBC, antibody screen if suspected lupus
53
Q

What is the treatment for mild intermittent lesions (lichen planus)

A

Topical OTC tx
* CHX mouthwash
* benzodamine mouthwash
Avoid SLS containing toothpaste

54
Q

What is the management for persisting symptomatic lichen planus in primary care

A
  • topical steroids
  • as per oral ulcers
  • beclomethasone MDI
  • betamethasone rinse
55
Q

What is the dose for beclomethasone inhalers

A

0.5mg / puff
2-3times daily

56
Q

What is the mangement for persisting symptomatic lichen planus in secondary care

A
  • higher strength topical steroid
  • may use skin steroid cream called clobetasol which can be applied using trays for gingival lesions
  • topical tacrolimus
  • hydroxychloroquine
  • systemic immunomodulators e.g azathioprine, mycophenolate
57
Q

What are conditions that result lichen-like lesions

A
  • graft vs host disease
  • lupus erythematous
58
Q

What is graft vs host disease

A
  • chronic GVHD presents with lichenoid lesions
  • recent BM/Stem cell transplant
  • systemic immunosuppressants required
59
Q

What are the types of lupus erythematous

A
  • chronic discoid LE
  • systemic LE
60
Q

What is the usual presentation of chronic discoid LE

A
  • localized
  • discoid area of erythema/ulceration surrounded by a white keratotic border sometimes with radiating striae
61
Q

What is the histology of chronic discoid LE

A
  • subepithelial/deeply situated perivascular foci of lymphocytes present in connective tissue
  • liquefactive degeneration of basal cells as per lichen planus
62
Q

How do bloods present for chronic discoid LE

A
  • no autoantibodies
63
Q

What is the systemic LE presentation

A
  • skin rashes
  • oral lesions variable
64
Q

What is the histology for systemic LE

A

*diffuse infiltration of lymphocytes

65
Q

What appears in the bloods for systemic LE

A
  • autoantibodies
  • ANA, RO, dsDNA
66
Q

What is the management of LE

A
  • refer
  • treat oral symptoms as if symptomatic LP
67
Q

Why is it important to monitor lichen planus

A
  • risk of malignant transformation
68
Q

What is the risk of malignant transformation of LP

A

1%
risk of SCC

69
Q

What do NICE guidelines state around lichen planus

A
  • monitor for oral cancer as part of routine dental exam
  • can be carried out by GDP
70
Q

What features should cause a dentist to refer in concern of malignant transformation

A

Isolated areas of increasing whiteness, speckling (areas of redness and whiteness) or solitary ulceration unlikely to reflect local trauma

Lumpd

71
Q

What should px be told about malignant risk of LP

A
  • should be advised of it
  • reduced other risk factors e.g smoking and alcohol, ensure good diet etc
72
Q

What classification is used to describe hypersensitivity reactions

A

Gell and Coombs

73
Q

What is type 1 hypersensitivity

A

IgE mediated
allergic response

74
Q

What are examples of type 1 hypersensitivity reactions

A
  • atopy
  • anaphylaxis
75
Q

What is type 2 hypersensitivity reaction

A
  • non-IgE mediated
  • cytotoxic
76
Q

What are examples of type 2 hypersensitivity reactions

A

pemphigus/pemphigoid

77
Q

What is type 3 hypersensitivtiy reaction

A

non-IgE mediated
immune complex

78
Q

What is an example of a type 3 hypersensitivity reaction

A

serum sickness
erythema multiforme
systemic LE

79
Q

What is type 4 hypersensitivity

A
  • T cell mediated
80
Q

Describe the process of type 1 hypersensitivity

A
  • IgE producing B cells are activated to haptens on first exposure
  • IgE on next exposure binds rapidly to mast cells and causes immediate degranulation
81
Q

What is atopy

A

when someone has a genetic predisposition to an allergy

82
Q

What are the 3 fatal reactions of anaphylaxis

A
  • laryngeal oedema
  • bronchial constriction
  • peripheral oedema
83
Q

Explain the pathogenesis of type 2 hypersensitivity reaction

A
  • activation of complement by IgM or IgG binding to antigenic cell
  • cells are lysed (cell death)
84
Q

Describe the pathogenesis of type 3 hypersensitivity reaction

A
  • reaction against soluble antigens circulating in serum
  • antibody-antigen immune complexes formed and deposited in organs
  • in erythema multiforme (oral), the IgM complexes are deposited in the microvasculature of the oral mucosa membrane
85
Q

Describe the pathogenesis of type 4 hypersensitivity

A
  • t cell mediated - no antibodies
  • sometimes called delayed hypersensitivity as takes time to recruit t cells
  • localised t cell reaction at site of encounter of contact antigen
  • CD4 cause inflammation induced damage, CD8 cause direct damage

BDS4 Oral Medicine (17 decks)

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