Lichen planus

Affects ~0.2–1% of the general population. Peak age 30–60 years. Slightly female predominance. Oral LP is more common in women (2:1). Hepatitis C association is well established, particularly in Mediterranean and Middle Eastern populations — prevalence of HCV in LP patients may reach 10–20% in endemic areas; consider HCV screening in at-risk patients.

CD8+ T cells target an unknown antigen on basal keratinocytes, causing apoptosis (Civatte bodies) and interface dermatitis (vacuolar change at the dermo-epidermal junction with a band-like lymphocytic infiltrate — 'lichenoid'). Triggers include:

• Medications (lichenoid drug eruption — β-blockers, ACE inhibitors, thiazides, antimalarials, gold, NSAIDs, imatinib, checkpoint inhibitors, many others).
• Hepatitis C (especially oral LP).
• Dental amalgam (oral LP adjacent to amalgam restoration — consider replacement in localized disease).
• Vaccines (hepatitis B; rare).
• Contact allergens (flavorings, cinnamon — oral LP mimic).

Purple, Pruritic, Polygonal, Papules — plus Planar (flat-topped) and Peripheral distribution (flexor wrists, forearms, ankles, shins, lumbosacral).

• Wickham striae: fine white/grey lines on the surface of papules — pathognomonic. Best seen with dermoscopy or side lighting; can appear on oral mucosa as a reticulate pattern.
• Koebner phenomenon: new lesions along sites of skin trauma (scratches, scars).
• Mucosal involvement: oral (buccal reticulate > erosive > atrophic > plaque > papular > bullous), genital (vulvar or penile, often erosive and overlapping with lichen sclerosus), esophageal (rare but important — dysphagia, strictures).
• Nail LP: longitudinal ridging, trachyonychia (rough, sandpaper nails), pterygium (scarring fusion of cuticle onto nail plate → permanent loss), 20-nail dystrophy (all nails involved, often in children).
• Scalp LP = lichen planopilaris (LPP): scarring alopecia with perifollicular erythema/scale; frontal fibrosing alopecia is a clinical variant with frontotemporal hairline recession and eyebrow loss (post-menopausal women most commonly).

Critical SoC content.

• Classic LP papules appear violaceous-grey or dusky rather than purple/pink in Fitzpatrick V–VI. The 'P' for purple is often a brown-grey color.
• Post-inflammatory hyperpigmentation after LP is prominent, sharply demarcated, and persistent — can last years. This is a major patient concern and distinct from active disease.
• Lichen planus pigmentosus (LPP — not the same as lichen planopilaris): a distinct variant strongly associated with darker skin tones:

- Asymptomatic or mildly pruritic.

- Dark brown, slate-grey, or blue-grey macules and patches on the face (forehead, temples, preauricular), neck, upper chest, and flexures.

- Lichen planus pigmentosus-inversus: flexural distribution (axillae, inframammary, inguinal) — confusing because LP classically avoids flexures.

- Often misdiagnosed as melasma, Riehl's melanosis, or post-inflammatory hyperpigmentation from another cause.

- Biopsy shows lichenoid interface dermatitis with pigment incontinence.

- Treatment is unsatisfying; topical tacrolimus, hydroquinone for pigment, photoprotection, avoidance of scented products and hair oils (implicated triggers).

• LP pigmentosus in facial distribution should be distinguished from Riehl's melanosis (contact-mediated, pattern matches the contactant — often fragrance or hair dye) and Hori's nevus (ABNOM — bilateral blue-grey on cheeks, distinct histology, laser-responsive).
• Ashy dermatosis (erythema dyschromicum perstans) overlaps significantly with LP pigmentosus — some authorities consider them on a spectrum.

• Hypertrophic LP: thick, verrucous plaques on shins and ankles; intensely pruritic; difficult to treat.
• Atrophic LP: late-stage, few flat atrophic lesions.
• Annular LP: ring-shaped plaques, favors axilla and penis.
• Actinic LP: photodistributed, ring-like or pigmented; more common in Middle Eastern, Indian, African populations; springtime flares.
• Lichen planus pigmentosus: SoC variant — see above.
• Bullous LP: blistering within LP plaques.
• LP pemphigoides: autoimmune bullous disease overlap — tense bullae on and around LP lesions; BP180 antibodies.
• Oral LP: reticulate, atrophic, erosive, plaque, papular, bullous subtypes.
• Lichen planopilaris (scalp): scarring alopecia; frontal fibrosing alopecia variant.
• Nail LP: 20-nail dystrophy in children; isolated nail disease possible.
• Lichenoid drug eruption: resembles LP but often more extensive, photodistributed; identify and stop culprit drug.

• Lichenoid drug eruption — history of new medication; often more diffuse; resolves with drug discontinuation.
• Lichen simplex chronicus — single thickened plaque from chronic scratching; no Wickham striae.
• Hypertrophic LP vs. prurigo nodularis — both pruritic, hyperkeratotic; biopsy differentiates.
• Cutaneous lupus (DLE) — photodistributed, scale, scarring, follicular plugging; DIF positive.
• Lichen planus pigmentosus vs. melasma — melasma is symmetric centrofacial (malar, forehead, upper lip), lighter brown, and worsens with sun; LPP is slate-grey, may involve temples, nape, flexures.
• Lichen planus pigmentosus vs. ashy dermatosis — significant overlap; many authorities consider them variants.
• Erosive oral LP vs. mucous membrane pemphigoid / pemphigus — DIF and histology differentiate.
• Oral LP vs. candidiasis, geographic tongue, leukoplakia — biopsy if uncertain; oral leukoplakia is premalignant and should not be missed.
• Scalp LPP vs. CCCA vs. discoid lupus — all scarring alopecias; histology (horizontal sections) differentiates.

• Clinical diagnosis usually sufficient for classic cutaneous LP with Wickham striae.
• Biopsy for atypical, hypertrophic, or pigmentosus variants, or for scalp/nail/mucosal disease.
• Hepatitis C screening in patients from endemic areas or with risk factors.
• Direct immunofluorescence to differentiate from lichenoid bullous disorders (LP pemphigoides, mucous membrane pemphigoid).
• Medication review — identify lichenoid drug triggers.
• Oral exam + photo documentation for all LP patients; baseline and annual surveillance for erosive oral LP.
• Patch testing if oral LP is localized to an amalgam restoration or adjacent to a specific contactant.

Classic LP (cutaneous):

• Compact hyperkeratosis without parakeratosis.
• Wedge-shaped hypergranulosis underlies clinical Wickham striae.
• Sawtooth rete ridges — pointed, not rounded.
• Band-like lymphocytic infiltrate at the dermo-epidermal junction (lichenoid).
• Vacuolar change of the basal layer; colloid/Civatte bodies (apoptotic keratinocytes).
• Pigment incontinence in the upper dermis (melanophages) — prominent in SoC and in LP pigmentosus.

Variant histology:

• Hypertrophic LP: marked acanthosis, pseudoepitheliomatous hyperplasia; can mimic SCC at low power.
• Lichen planus pigmentosus: subtle interface change, prominent pigment incontinence — the dermal melanin dominates.
• Lichenoid drug eruption: eosinophils, parakeratosis, deep perivascular infiltrate (beyond the lichenoid band).
• Lichen planopilaris: perifollicular lichenoid infiltrate, loss of sebaceous glands, follicular scarring.

Cutaneous LP (most clears in 1–2 years; treatment aimed at symptom control and accelerating resolution):

• Class I topical corticosteroid (clobetasol 0.05%) BID under occlusion for thick lesions; taper as improving.
• Intralesional triamcinolone 5–10 mg/mL for hypertrophic, localized, or recalcitrant plaques.
• Topical calcineurin inhibitors (tacrolimus 0.1%) for face, genital, and maintenance.
• Oral antihistamines for itch (sedating at night).

Oral LP (reticulate/asymptomatic may not need treatment):

• Topical clobetasol gel or triamcinolone in Orabase for erosive and symptomatic forms.
• Topical tacrolimus 0.1% ointment off-label — effective for oral LP; discuss malignancy surveillance.
• Intralesional triamcinolone for recalcitrant erosive lesions.
• Dental amalgam replacement if disease is localized to amalgam contact.

Scalp LPP (scarring alopecia):

• Class I topical steroid + intralesional triamcinolone as in CCCA.
• Hydroxychloroquine 200 mg BID — first-line oral for LPP/FFA.
• Minoxidil adjunct.

Nail LP:

• Intralesional triamcinolone to the proximal nail fold; 2–5 mg/mL monthly.
• Systemic steroids or MTX if multiple nails with scarring risk.

• Phototherapy (nbUVB; PUVA for severe disease) — effective for generalized cutaneous LP.
• Oral retinoids (acitretin 10–30 mg/day) — effective for hypertrophic and palmoplantar LP; teratogenic (3-year avoidance post-dose).
• Methotrexate 10–25 mg weekly — generalized cutaneous or mucosal disease.
• Hydroxychloroquine 200 mg BID — mucosal LP and LPP/FFA; ophthalmology screening.
• Cyclosporine 2.5–5 mg/kg/day — short-term; severe erosive mucosal disease.
• Mycophenolate mofetil — refractory mucosal disease.
• Biologics (anti-TNF, anti-IL-17/23) — case series and emerging evidence for refractory disease.
• JAK inhibitors (tofacitinib, baricitinib, upadacitinib) — emerging evidence, especially for LPP/FFA and erosive oral LP.
• Lichen planus pigmentosus specifically: difficult to treat; topical tacrolimus, topical hydroquinone ± tretinoin for pigment, strict photoprotection, avoidance of scented products and oils (implicated triggers in some reports).

Cutaneous LP self-limits in 1–2 years for most; post-inflammatory hyperpigmentation in SoC can persist for additional 1–2 years. Oral LP often chronic (years–decades); erosive oral LP carries small but established SCC risk (~1–2% cumulative) — lifelong surveillance indicated. Nail LP may cause permanent nail loss via pterygium. Scalp LPP/FFA is scarring and irreversible; early aggressive treatment preserves remaining follicles. Lichen planus pigmentosus is chronic and resistant — pigment clearance is slow.

• Wickham striae are pathognomonic. Look with dermoscopy or tangential light before biopsy.
• Review the medication list — lichenoid drug eruption is common and resolves with discontinuation.
• Lichen planus pigmentosus ≠ lichen planopilaris. Pigmentosus = skin macules; planopilaris = scarring alopecia. Both are LP variants; the similar names confuse residents.
• Erosive oral LP needs SCC surveillance — dentist + ENT follow-up; photograph baseline and serial exams.
• Nail LP can irreversibly scar within weeks — don't delay systemic treatment for rapidly progressive nail disease.
• HCV screening in LP patients from endemic areas.
• Koebner phenomenon — avoid unnecessary procedures over LP-prone sites; new lesions will form at scars.
• PIH in SoC is the disease, not a cosmetic issue. Discuss at baseline; set realistic timeline (months to years for resolution).
• Hypertrophic LP on shins can mimic SCC histologically (pseudoepitheliomatous hyperplasia) — communicate clinical context to pathology.

Lichen planus is an immune-mediated skin condition — your body's T cells are attacking the top layer of skin. On the body it usually clears by itself in 1–2 years with treatment. The color changes it leaves behind can take additional months to fade, especially in darker skin. The mouth version can last longer and requires dental/oral medicine follow-up because of a small long-term cancer risk. On the scalp and nails, treatment is urgent because damage can be permanent. Itch and discomfort respond well to the prescribed cream. I'll review your medication list — sometimes a pill you're taking for blood pressure or something else can trigger this. If you're at risk for hepatitis C, we'll test you. In the meantime: don't scratch or pick (it can spread the rash), protect your skin from strong sun, and use gentle skincare.