Lichen Planus

Lichen planus (LP) is a chronic, inflammatory, papulosquamous disorder affecting skin, mucous membranes, hair, and nails. It presents most commonly with pruritic, flat-topped, violaceous papules and plaques with Wickham striae. Mucosal involvement, particularly oral LP, can be chronic and erosive. Pathogenesis involves T cell–mediated cytotoxicity against basal keratinocytes, with genetic, infectious, and drug-related triggers. Management depends on site and severity, ranging from potent topical corticosteroids to systemic immunomodulators. Longstanding erosive mucosal disease carries a small risk of malignant transformation, warranting surveillance.

Epidemiology

  • Affects adults most commonly; slight female predominance in mucosal LP.
  • Prevalence ~0.2–1%; oral LP ~1–2% in dental clinic populations.
  • Associations: hepatitis C virus (geographic and population variability), metabolic syndrome, autoimmune thyroid disease; drug-induced lichenoid eruptions are common mimics.

Pathophysiology

  • CD8+ T cell–mediated interface dermatitis targeting basal keratinocytes; apoptosis via perforin/granzyme and Fas-FasL.
  • Triggers: infections (HCV in selected regions), medications (e.g., antimalarials, thiazides, beta-blockers, ACE inhibitors, NSAIDs, TNF inhibitors), contact allergens (amalgam), trauma (Koebner), and stress.

Clinical Features

  • Cutaneous LP: “6 Ps” — planar (flat-topped), purple, polygonal, pruritic papules/plaques, with Wickham striae and Koebnerization; flexor wrists, forearms, ankles, lumbar; may be generalized.
  • Hypertrophic LP: hyperkeratotic plaques, especially shins; intense pruritus; risk of squamous cell carcinoma in chronic lesions is rare but reported.
  • Mucosal LP: oral (reticular, erosive/ulcerative, atrophic, plaque-like), genital; painful erosions impact quality of life and nutrition.
  • Nail LP: longitudinal ridging, thinning, trachyonychia, pterygium formation; can lead to scarring.
  • Scalp LP (lichen planopilaris): perifollicular erythema and scale with scarring alopecia; frontal fibrosing alopecia variant.

Differential Diagnosis

  • Cutaneous: psoriasis, pityriasis rosea, prurigo nodularis, secondary syphilis, lichenoid drug eruption, lichen simplex chronicus.
  • Oral: leukoplakia, candidiasis, mucous membrane pemphigoid, pemphigus vulgaris, lupus.
  • Scalp: central centrifugal cicatricial alopecia, discoid lupus, folliculitis decalvans.

Diagnosis

  • Clinical supported by dermoscopy (white reticular lines, vascular dots).
  • Biopsy: interface dermatitis with saw-tooth acanthosis, Civatte bodies, wedge-shaped hypergranulosis.
  • Consider HCV screening based on local epidemiology/risk; rule out lichenoid drug eruption via medication review.
  • For oral LP: exclude candidiasis and dysplasia with targeted biopsies.

Management

  1. Cutaneous LP
  • Topical high- to super-potent corticosteroids for limited disease; occlusion for hypertrophic lesions.
  • Intralesional triamcinolone for hypertrophic plaques or resistant papules.
  • Antihistamines for itch; sedating agents at night if needed.
  • Phototherapy: NB-UVB/PUVA for widespread disease.
  • Systemic therapy for extensive/refractory: short course oral corticosteroids for flares; steroid-sparing agents include acitretin, methotrexate, cyclosporine, mycophenolate mofetil, hydroxychloroquine; consider JAK inhibitors or biologics in select refractory cases per emerging evidence.
  1. Mucosal LP (oral/genital)
  • High-potency topical steroids (e.g., clobetasol gel/ointment), dexamethasone mouth rinse; consider topical calcineurin inhibitors (tacrolimus/pimecrolimus) as steroid-sparing.
  • Manage superimposed candidiasis with topical/oral antifungals.
  • Systemic agents for erosive, refractory disease: short course oral corticosteroids, acitretin, methotrexate, mycophenolate, cyclosporine; evidence supports flexibility based on comorbidities.
  1. Nail LP
  • Intralesional steroids to matrix; systemic agents often needed early to prevent scarring (e.g., acitretin, cyclosporine).
  1. Lichen planopilaris and frontal fibrosing alopecia
  • Aim to halt progression: high-potency topical/IL steroids, topical calcineurin inhibitors; systemic options include hydroxychloroquine, doxycycline, pioglitazone, low-dose naltrexone; immunosuppressants for rapidly progressive disease.

Monitoring and Prognosis

  • Cutaneous LP often resolves within 1–2 years but may recur; postinflammatory dyspigmentation common in skin of color.
  • Oral erosive LP can be chronic; small but real risk of oral squamous cell carcinoma—recommend regular oral examinations (e.g., every 6–12 months) and biopsy of suspicious areas.
  • Monitor labs per systemic agent; screen for medication triggers.

References (recent guidelines and key reviews)

  • European/British guidelines on LP and oral LP management, 2022–2024.
  • AAD/International consensus statements on lichen planopilaris and frontal fibrosing alopecia, 2022–2024.
  • Systematic reviews of systemic therapies for LP, 2021–2024.
  • Associations with HCV and malignant transformation risk in oral LP, 2022–2024.

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