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
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2
Q

Aetiology of lichen planus

A

unknown

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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
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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
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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)
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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
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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
  1. Reticular - meshwork pattern of striae that criss cross
  2. Papular
  3. Plaque-type - solid areas of keratinisation
  4. Atrophic (erythematous): red areas caused by inflamed submucosa showing though thin epithelium
  5. Erosive
  6. Bullous: results from separation of epithelium forming blisters that break down into ulcers
  7. 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
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8
Q

Management of oral lesions

A
  • Difficult to treat

- Oral lesions for life, although severity may reduce with age

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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
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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
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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
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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
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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
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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
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15
Q

Mechanism of lichenoid reactions

A
  • Type IV hypersensitivity reaction (delayed)
  • Contact allergy
  • Cell mediated immune reaction
  • Burning/itching sensation
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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