Lichen Planus Flashcards
1
Q
What are the 6 main types of lichen planus
A
- reticular
- papular
- plaque like
- atrophic
- erosive ulceration
- bullous
2
Q
Which types of lichen planus are often symptom free
A
- reticular
- papular
- plaque like
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
4
Q
What is bullous lichen planus
A
it is preceded by bulla
the rarest form
5
Q
How does erosive/ulcerative lichen planus present
A
- persistent irregular and painful erosions with a yellow slough
6
Q
Which type of lichen planus is seen in desquamative gingivitis
A
atrophic
7
Q
What does plaque like lichen planus resemble
A
leukoplakia
8
Q
How does reticular lichen planus present
A
- a network of raised white lines creating a lacy pattern called striae
9
Q
What may bullous lichen planus possibly caused by
A
- superficial mucoceles
10
Q
Where can lichen planus occur in the mouth
A
- buccal mucosa (most common site)
- tongue
- palate
- lips
- gingiva
11
Q
Which type of lichen planus is this
A
plaque like
12
Q
Which type of lichen planus is this
A
Papular
13
Q
Which type of lichen planus is this
A
reticular
14
Q
Which type of lichen planus is this
A
atrophic
15
Q
Which type of lichen planus is this
A
Bullous
16
Q
Which type of lichen planus is this
A
erosive
17
Q
What type of hypersensitivity reaction is lichen planus
A
type 4
T cell mediated
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
19
Q
What type of t cell are cd8+
A
cytotoxic
20
Q
What type of cells are cd4 cells
A
helper cells
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
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
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
24
Q
What drugs are associated with lichen planus
A
NSAIDS
betablockers
ace inhibitors
diuretics
25
When a cause such as drugs or dental materials is implicated, what is this called
lichenoid tissue reaction
26
What is E and C
E = Epitheliotropism
C = area of basal cell destruction
27
What is epitheliotropism
* lymphocytes are drawn up into deeper layers of the epithelium
* they sit among the deeper keratinocytes
28
What is D
civatte bodies
29
What are civatte bodies
cells with eosinophilic cytoplasma and very dark staining nuclear remnants
they are surrounded by a clear halo
**they have undergone apoptosis**
30
What is B
lymphocytes
31
What is a
band of inflammatory cells within the lamina propria
32
What is B
Perivascular infiltration
33
What is perivascular infiltration
deeper infiltration of the lymphocytes
there is mononuclear inflammatory cell infiltrate around the venules
indicates a delayed hypersensitivtiy reaction
34
What is perivascular infiltration a sign of
* lichenoid tissue reaction or lupus erythematous
35
What can be seen in this slide
* saw tooth rete ridges
* patchy acanthosis
* parakeratosis
36
Summarise the process of lichen planus at a histopathological level
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
What are the usual symptoms of lichen planus
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
Where else in the body may the patient see lesions
skin
scalp
genitals
hair and nails
39
What is the benefit of buccal lichen planus
it is an easy biopsy site
40
What is gingival lichen planus often termed
desquamative gingivitis
41
What does gingival lichen planus resemble
gingival pemphigoid
plasma cell gingivitis
can only differentiate via histology
42
What is the presentation of gingival lichen planus
* v red looking gingiva - can worry px
* can be very patchy
* in some forms, typical reticular pattern seen
43
What is important in settling gingival lichen planus
good OH
44
Why is biopsy difficult for gingival lichen planus
* risk of damaging adjacent attachment area of gingiva/tooth
* adherent attached mucosa damaged lifting from bone
* take care when deciding biopsy
45
What is usually the reason behind LP on the dorsal tongue
idiopathic
often asymptomatic
results in loss of papillae and smooth tongue surface
46
What is the usual cause of lichen planus on the lateral surface of the tongue
* drug/amalgam trigger
* amalgam most likely if isolated lesion
* look at tongue position at rest, is it in contact with amalgam
47
Is the tongue easy to biopsy
yes but painful healing
48
Describe the clinical presentation of lichenoid drug reactions
* usually widespread lesions that are bilateral and mirrored
* often poor response to steroid tx
49
How should management of lichenoid drug reactions be decided
* 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
What is a good alternative for ACE inhibitors
AT2 blockers
51
What is the management of amalgam related lesions
* 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
What investigations should be done for lichen planus
* biopsy unless good reason not to
* bloods - haematinics, FBC, antibody screen if suspected lupus
53
What is the treatment for mild intermittent lesions (lichen planus)
Topical OTC tx
* CHX mouthwash
* benzodamine mouthwash
Avoid SLS containing toothpaste
54
What is the management for persisting symptomatic lichen planus in primary care
* topical steroids
* as per oral ulcers
* beclomethasone MDI
* betamethasone rinse
55
What is the dose for beclomethasone inhalers
0.5mg / puff
2-3times daily
56
What is the mangement for persisting symptomatic lichen planus in secondary care
* 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
What are conditions that result lichen-like lesions
* graft vs host disease
* lupus erythematous
58
What is graft vs host disease
* chronic GVHD presents with lichenoid lesions
* recent BM/Stem cell transplant
* systemic immunosuppressants required
59
What are the types of lupus erythematous
* chronic discoid LE
* systemic LE
60
What is the usual presentation of chronic discoid LE
* localized
* discoid area of erythema/ulceration surrounded by a white keratotic border sometimes with radiating striae
61
What is the histology of chronic discoid LE
* subepithelial/deeply situated perivascular foci of lymphocytes present in connective tissue
* liquefactive degeneration of basal cells as per lichen planus
62
How do bloods present for chronic discoid LE
* no autoantibodies
63
What is the systemic LE presentation
* skin rashes
* oral lesions variable
64
What is the histology for systemic LE
*diffuse infiltration of lymphocytes
65
What appears in the bloods for systemic LE
* autoantibodies
* ANA, RO, dsDNA
66
What is the management of LE
* refer
* treat oral symptoms as if symptomatic LP
67
Why is it important to monitor lichen planus
* risk of malignant transformation
68
What is the risk of malignant transformation of LP
1%
risk of SCC
69
What do NICE guidelines state around lichen planus
* monitor for oral cancer as part of routine dental exam
* can be carried out by GDP
70
What features should cause a dentist to refer in concern of malignant transformation
Isolated areas of increasing whiteness, speckling (areas of redness and whiteness) or solitary ulceration unlikely to reflect local trauma
Lumpd
71
What should px be told about malignant risk of LP
* should be advised of it
* reduced other risk factors e.g smoking and alcohol, ensure good diet etc
72
What classification is used to describe hypersensitivity reactions
Gell and Coombs
73
What is type 1 hypersensitivity
IgE mediated
allergic response
74
What are examples of type 1 hypersensitivity reactions
* atopy
* anaphylaxis
75
What is type 2 hypersensitivity reaction
* non-IgE mediated
* cytotoxic
76
What are examples of type 2 hypersensitivity reactions
pemphigus/pemphigoid
77
What is type 3 hypersensitivtiy reaction
non-IgE mediated
immune complex
78
What is an example of a type 3 hypersensitivity reaction
serum sickness
erythema multiforme
systemic LE
79
What is type 4 hypersensitivity
* T cell mediated
80
Describe the process of type 1 hypersensitivity
* 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
What is atopy
when someone has a genetic predisposition to an allergy
82
What are the 3 fatal reactions of anaphylaxis
* laryngeal oedema
* bronchial constriction
* peripheral oedema
83
Explain the pathogenesis of type 2 hypersensitivity reaction
* activation of complement by IgM or IgG binding to antigenic cell
* cells are lysed (cell death)
84
Describe the pathogenesis of type 3 hypersensitivity reaction
* 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
Describe the pathogenesis of type 4 hypersensitivity
* 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
