Lichen Planus Flashcards
1
Q
Description of Lichen Planus
A
- Common chronic inflammatory disease of skin and mucous membranes (1-2% of population)
- Middle age or older (40+)
- 1/3 have skin lesions only
- 1/3 have oral lesions only
- 1/3 have both oral and skin lesions
2
Q
Aetiology of lichen planus
A
unknown
3
Q
Pathogenesis of lichen planus
A
- Immunologically mediated process
- Cytotoxic T cells and few T helper cells migrate into basal laters of epidermis and mucosal epithelium
- They destroy basal cells by direct cytotoxicity using perforin and enzymes released into the cell or through the secretion of TNF-alpha or cytokines
- Basal cells die via apoptosis
- Epithelium now has fewer proliferating cells to renew itself, so becomes thinner. Attachment of epithelium becomes weaker and can separate
- Damage to epithelium causes recruitment of lymphocytes to form band of infiltrate below epithelium
- Process in state of balance
1. when basal cell destruction dominates, epithelium becomes atrophic or ulcerates - symptoms increase
2. when immunological reaction decreases, remaining basal cells proliferate and recover, epithelium thickens and more keratinised - symptoms may vanish
3. cause of cyclical cycle is unclear
4
Q
Clinical presentation of skin lesions? How do you manage?
A
- Purplish papules 2-3mm across - usually itchy
- Sites: flexor surface of forearms, wrist, shins and back
- Easy to treat with steroids
- Suffer for a few years
5
Q
Clinical presentation of oral lesions? How do you manage?
A
- Lesions are usually bilateral and often symmetrical
- Lesions can comprise of: striae, atrophic area, ulcers, plaques
- Sites: buccal mucosa (most common), tongue (lateral margins or dorsum), gingiva (affected by desquamative gingivitis: full width of attached gingiva)
6
Q
If found in what intraoral areas, should the diagnosis of lichen planus never be accepted? and why?
A
- When affected ventral tongue, floor of mouth or palate should not be accepted unless typical changes elsewhere
- Involvement raises suspicion of malignant dysplastic process or drug reaction
7
Q
How can lichen planus be physically classified? Why is there a range of appearances?
A
- depending on balance of destruction and resolution, there can be a range of appearances
- Reticular - meshwork pattern of striae that criss cross
- Papular
- Plaque-type - solid areas of keratinisation
- Atrophic (erythematous): red areas caused by inflamed submucosa showing though thin epithelium
- Erosive
- Bullous: results from separation of epithelium forming blisters that break down into ulcers
- Ulcerative: basal cell destruction to extent that epithelium cannot renew itself and ulcers develop. Raised yellow layers of fibrin - usually surrounded by atrophic areas with striae
- Can be simply classified as ulcerative/erosive or non-ulcerative/non-erosive
8
Q
Management of oral lesions
A
- Difficult to treat
- Oral lesions for life, although severity may reduce with age
9
Q
Histopathology of lichen planus
A
- Dense band-like lymphocytic infiltrate under epithelium
- Saw tooth rete pegs (looks like a saw) (common in skin)
- Hyperkeratosis and acanthosis (increase in thickness of prickle cell layer) - although in atrophic forms the epithelium is thinner
- Apoptotic degeneration of basal cells
- Widening of BM zone
- Sometimes melanin dropout/post inflammatory hyperpigmentation
10
Q
Diagnosis of LP
A
- Usually can be made on history, appearance and distribution of lesions
- Check for drugs that can cause lichenoid reaction
- Ideally confirmed by biopsy - required for all white lesions to exclude dysplasia
- biopsy avoided if typical LP and follow up appt is given
- Biopsy given if plaque-type or unusual lesion as it is difficult to distinguish from leukoplakia
11
Q
management of LP
A
- No curative tx - aims to relieve pain and promote healing (good symptomatic response to corticosteroids)
1. Reassurance and education
2. Optimise oral hygiene - sensitivity prevents tooth brushing but plaque accumulation can worsen inflammation
- CHX mouthwash and non-astringent toothpaste
3. Analgesic for pain relief - Benzydamine hydrocholoride, 5% lignocaine gel
4. Topical steroids - adhesive tablets (mild), steroid gel in vacuum formed tray (medium potency), mouthwash preparation (generalised)
5. Intralesional steroids
6. systemic steroids - Corticosteroids, cyclosporine, azathioprine, hydroxychloroquine
7. disease modifying agents - e.g. anti-TNF therapy
12
Q
What could the the possible reason for LP worsening?
Why does this happen?
what is the tx?
A
- When inflammation worsens or symptoms become more severe consider the possibility of superimposition of candida
- Increased keratinisation and steroid tx = increased candida
- Tx: anti fungal
13
Q
When should lesions be followed up, and why?
A
- Follow up associated with reddening, and if unusual site, appearance or severity
- Squamous carcinoma may develop in lesions rarely (0.03-1.8%) particularly oral lichen planus can turn into oral squamous carcinoma
14
Q
What are lichenoid reactions?
A
- Lichen planus-like lesions (erythema, vesicle formation/ulceration) caused by a trigger - usually a drug
- Cannot be confidently distinguished from lichen planus
- Lichenoid reactions are often more severe
1. onset closely associated with potential cause
2. Unilateral/asymmetrical/unusual distribution
3. Unusal severity
4. widespread skin lesions
5. localised lesion in contact with potential cause
15
Q
Mechanism of lichenoid reactions
A
- Type IV hypersensitivity reaction (delayed)
- Contact allergy
- Cell mediated immune reaction
- Burning/itching sensation
16
Q
What is the histopathology of lichenoid reactions
A
- Subepithelial infiltrate
- More eosinophils and plasma cells
- More diffuse than LP
- Extends more deeply
- Otherwise no specific test
17
Q
Which drugs can cause lichenoid reactions
A
Colloidal gold beta blockers oral hypoglycaemics allopurinol NSAIDs antimalarials methyldopa penicillamine some tricyclic antidepressants thiazide diuretics captopril
18
Q
How long can drug lichenoid reactions persist after administration
A
months to years
19
Q
Cause of drug lichenoid reactions?
A
- unclear cause
- Either: drug binds to epithelial cells and elicits and antigen-specific response
- Or: drug is metabolised differently in the epithelium of susceptible pts triggering immune response
20
Q
Diagnosis of lichenoid drug reactions
A
- Resolution on removal of stimulus, followed by relapse on replacement
- Biopsy: histologically very subtle difference between lichenoid and LP but needed to exclude other conditions
21
Q
Treatment of lichenoid drug reactions
A
- Withdrawal of drugs if possible
- Changing to another drug may be helpful but same class of drugs may cause same reaction
- reaction does not disappear immediately after withdrawal e.g. with amalgam takes 2-3 years
22
Q
Topical restoration lichenoid reactions clinical presentations
A
- usually amalgam but can be due to polymeric materials
- Clinical appearance close to LP but localised to mucosa close to restoration
- Common sites: posterior buccal mucosa, posterior ventral tongue
- Lesions composite only striae or plaque - more severe have ulceration/atrophy centrally
- amalgams that have corroded more likely to cause reason
- healing follows removal of restorations confirms lichenoid reaction
23
Q
Clinical presentation of cinnamon stomatitis and plasma cell gingivitis
A
- cinnamon (toothpaste/gum/food) can cause topical lichenoid reaction
- histological features similar to LP
- Clinically more likely to be patchy irregular keratosis without significant erythema
- Gingival and adjacent mucosa may be bright red
- Diagnosis based on resolution after withdrawal of allergen
