Lichen Planus

What is it?

Lichen planus is a chronic inflammatory condition affecting the skin, mucous membranes, hair, and nails. The condition manifests as distinctive purple, flat-topped papules (small raised lesions) often covered by fine white lines called Wickham striae. Although the exact cause remains unknown, lichen planus is considered an autoimmune disorder in which the body's immune system mistakenly attacks cells in the skin and mucous membranes.

Who is affected?

Lichen planus affects approximately 0.5-1% of the adult population worldwide, with oral forms occurring in up to 2-4% of people.

• Prevalence: Cutaneous (skin) lichen planus affects approximately 1 in 200 to 1 in 100 adults (0.5-1%)
• Age demographics: Peak onset between ages 30-60 years; less than 5% of cases occur in children
• Gender distribution: More common in women than men (approximately 1.5:1 ratio)
• Risk factors: Hepatitis C virus infection (5-fold increased risk); certain medications (beta-blockers, NSAIDs, antimalarials); family history (approximately 10% of first-degree relatives may develop the condition); stress and anxiety

What causes it?

Lichen planus results from an abnormal immune response targeting the basal layer of the epidermis (the deepest layer of the outer skin):

• Autoimmune mechanism: Cytotoxic T-lymphocytes (immune cells) attack and destroy basal keratinocytes (skin cells), causing the characteristic inflammation
• Triggering factors: Viral infections (particularly hepatitis C), medications, dental materials (amalgam restorations), contact allergens
• Drug-induced forms: Certain medications can trigger lichenoid (lichen planus-like) eruptions, including beta-blockers, ACE inhibitors, thiazide diuretics, antimalarials, and NSAIDs
• Genetic component: Familial clustering suggests a genetic predisposition, though specific genes have not been definitively identified

What are the clinical features?

Lichen planus is classically described by the "6 Ps": purple, polygonal, planar (flat-topped), pruritic (itchy), papules, and plaques.

Cutaneous (skin) lichen planus:

• Flat-topped, violaceous (purple-red) papules ranging from 2-10 mm in diameter
• Fine white lines (Wickham striae) visible on the surface of lesions
• Intensely pruritic (itchy), sometimes with burning sensation
• Common locations: wrists, lower back, ankles, and shins
• May exhibit Koebner phenomenon (new lesions appearing at sites of skin trauma)

Oral lichen planus:

• Reticular pattern: Lacy white lines (most common presentation)
• Erosive form: Painful red, ulcerated areas affecting eating and drinking
• Affects inner cheeks (buccal mucosa), tongue, and gums

Other forms:

• Nail involvement (10% of patients): Ridging, thinning, splitting, or complete nail loss
• Scalp involvement: Lichen planopilaris causing permanent scarring hair loss
• Genital involvement: Painful erosions affecting quality of life

Disease progression:

Cutaneous lesions typically resolve within 1-2 years, though residual hyperpigmentation (darkening) often persists. Oral lichen planus tends to follow a chronic, relapsing-remitting course over many years.

How is it diagnosed?

Diagnosis is primarily clinical, based on the characteristic appearance of lesions:

• Clinical examination: Recognition of the typical purple, polygonal papules with Wickham striae; evaluation of distribution pattern
• Dermoscopy: Reveals characteristic white network pattern with peripheral red dots
• Skin biopsy: Confirms diagnosis showing interface dermatitis with a band-like lymphocytic infiltrate, "sawtooth" pattern of rete ridges, and colloid bodies (apoptotic keratinocytes)
• Direct immunofluorescence: Helps distinguish from lupus erythematosus when diagnosis is uncertain
• Hepatitis C screening: Recommended due to the strong association between the two conditions

What treatment options are available?

Treatment aims to relieve symptoms, promote healing, and prevent complications:

For limited cutaneous disease:

• High-potency topical corticosteroids (clobetasol propionate 0.05%) applied twice daily for 2-4 weeks
• Intralesional corticosteroid injections for resistant lesions
• Topical calcineurin inhibitors (tacrolimus, pimecrolimus) as steroid-sparing alternatives

For extensive or resistant disease:

• Oral corticosteroids (prednisone 30-60 mg daily, gradually tapered over 2-6 weeks)
• Phototherapy (narrowband UVB or PUVA)
• Systemic retinoids (acitretin) for hypertrophic variants
• Immunosuppressants (methotrexate, cyclosporine) for severe cases

For oral lichen planus:

• Asymptomatic cases may not require treatment
• Symptomatic cases: High-potency topical corticosteroids or tacrolimus
• Erosive oral disease may require systemic therapy

Prognosis:

• Cutaneous lesions typically resolve within 1-2 years
• Recurrence occurs in approximately 15-20% of patients
• Oral lichen planus is chronic but carries a small risk (1-2%) of malignant transformation to squamous cell carcinoma

Key points for patients

• Lichen planus is not contagious and cannot be spread to others
• Most skin lesions resolve within 1-2 years, though dark marks may persist temporarily
• Oral lichen planus requires long-term monitoring due to the small risk of cancer development
• When to seek medical attention: New oral ulcers that do not heal, rapidly spreading skin lesions, significant hair loss, or nail changes
• Prevention strategies: Avoid known triggers; maintain good oral hygiene; manage stress; regular dental and dermatological follow-up for oral disease
• Hepatitis C testing is recommended for all patients diagnosed with lichen planus