Lichen Planus
Dermatology · Papulosquamous · lean revision notes
Lichen Planus
Lichen planus (LP) is a chronic, idiopathic, T-cell-mediated inflammatory dermatosis affecting the skin, mucous membranes, nails, and hair. It is the prototype of the papulosquamous group and a perennial NEET PG favourite because of its classic morphology (the "six Ps"), Wickham striae, hepatitis C link, the malignant potential of oral LP, and its many clinical variants.
Definition & classification
Lichen planus is defined as a cell-mediated immune reaction in which CD8+ cytotoxic T-lymphocytes attack basal keratinocytes that express an altered self-antigen, producing the histological hallmark of band-like lymphocytic infiltrate with basal cell degeneration. The word "lichen" reflects the flat, lichen-on-a-rock appearance of the papules.
Clinical (morphological) variants — high yield:
| Variant | Key feature | Site / clue |
|---|---|---|
| Classic (papular) | Violaceous, flat-topped, polygonal papules | Flexor wrists, ankles, shins |
| Hypertrophic | Thick, verrucous, intensely pruritic plaques | Shins/ankles; chronic; risk of SCC |
| Annular | Ring-shaped with central clearing | Glans penis, axillae |
| Atrophic | Few atrophic lesions, white-blue hue | Resolved hypertrophic lesions |
| Follicular (LP pilaris) | Keratotic follicular papules → scarring alopecia | Scalp; Graham-Little syndrome |
| Bullous / LP pemphigoides | Vesicles over LP lesions; BP180 antibodies | Lower limbs |
| Actinic | Annular hyperpigmented plaques | Sun-exposed areas; tropics, darker skin |
| Linear | Lesions along Blaschko lines | Children; Koebner-related |
| Pigmentosus | Diffuse grey-brown macules | Face/flexures; Indians, common in exams |
| Lichen planopilaris | Perifollicular erythema + scarring alopecia | Scalp |
High-yield: The classic LP lesion is described by the six Ps — Purple (violaceous), Polygonal, Planar (flat-topped), Pruritic, Papules, with Plaques. Add a seventh P for Pterygium (nails).
Etiology & pathophysiology
LP is idiopathic but driven by a T-cell autoimmune mechanism. The current model:
Antigen alteration in basal keratinocytes → presentation to CD8+ cytotoxic T cells → keratinocyte apoptosis → basal layer destruction → reactive epidermal changes.
Key immunological and associated factors:
- CD8+ cytotoxic T lymphocytes are the principal effectors; CD4+ cells assist. Apoptosis is mediated via Fas–FasL and granzyme/perforin pathways.
- Hepatitis C virus (HCV) — the most exam-tested association, especially with oral LP and in Mediterranean/Asian populations. Screen for HCV in widespread or oral LP.
- Drug-induced LP (lichenoid drug eruption): remember the mnemonic — "GOLD ACT-B" style list — Gold, Oral hypoglycaemics, beta-blockers, Antimalarials (hydroxychloroquine, quinine), Captopril/ACE inhibitors, Thiazides, NSAIDs, penicillamine, and antimalarials. Lichenoid drug eruptions are often photodistributed, more eczematous, and lack Wickham striae.
- Contact LP: dental amalgam (mercury) causing oral lichenoid lesions adjacent to fillings; colour-film developers (para-phenylenediamine).
- Graft-versus-host disease produces lichenoid lesions histologically identical to LP.
- Associations: autoimmune diseases (alopecia areata, vitiligo, myasthenia gravis, ulcerative colitis, primary biliary cholangitis), dyslipidaemia, and possibly diabetes.
High-yield: Hepatitis C association is strongest for oral lichen planus. Always think HCV serology in an exam vignette of erosive/reticulate oral LP.
Clinical features
Skin
- Symmetrical, violaceous, shiny, flat-topped polygonal papules with fine white lacy lines (Wickham striae) on the surface, best seen after applying oil/mineral oil or on dermoscopy.
- Favoured sites: flexor surfaces of wrists and forearms, ankles, shins, lower back, genitalia.
- Intensely pruritic — yet patients characteristically rub rather than scratch, so excoriations are uncommon.
- Koebner phenomenon (isomorphic response): new lesions appear in lines of trauma/scratching — shared with psoriasis, vitiligo, warts.
- Resolves with characteristic post-inflammatory hyperpigmentation, prominent in Indian skin.
Mucosal LP
- Affects ~50% of cutaneous LP patients; may occur in isolation.
- Buccal mucosa is the commonest site; presents as a lacy, reticulate white network (Wickham striae) — the reticular form is most common and asymptomatic.
- Erosive/atrophic form is painful, persistent, and carries the malignant potential.
- Genital mucosa: vulvovaginal-gingival syndrome (erosive LP of vulva, vagina, gingiva) and peno-gingival syndrome in males.
Nail LP (~10%)
- Longitudinal ridging, thinning, fissuring, and the hallmark pterygium formation (dorsal pterygium = scarring overgrowth of proximal nail fold onto the nail bed).
- Twenty-nail dystrophy (trachyonychia) can be a presentation, especially in children.
- Anonychia = complete and permanent nail loss in severe cases.
Hair / scalp
- Lichen planopilaris → perifollicular erythema, follicular hyperkeratosis, and scarring (cicatricial) alopecia.
- Graham-Little-Piccardi-Lassueur syndrome: triad of scarring scalp alopecia + non-scarring axillary/pubic hair loss + follicular keratotic papules on body.
High-yield: Wickham striae (lacy white lines) on the papule surface and on buccal mucosa are pathognomonic. Pterygium of the nail and scarring alopecia indicate permanent damage.
Diagnosis & investigation of choice
Diagnosis is usually clinical, supported by skin biopsy (histopathology) — the investigation of choice.
Diagnostic approach:
- Identify the six Ps + Wickham striae clinically (use dermoscopy/oil immersion).
- Examine mucosa, nails, scalp, genitalia for occult involvement.
- Biopsy ambiguous, hypertrophic, erosive, or non-resolving lesions.
- Screen for hepatitis C (anti-HCV) in oral/extensive disease.
- Direct immunofluorescence (DIF) if bullous or to exclude autoimmune blistering disease.
- Review drug history to exclude lichenoid drug eruption.
Histopathology — classic findings
| Feature | Description |
|---|---|
| Hyperkeratosis | Orthokeratosis (without parakeratosis — unlike psoriasis) |
| Granular layer | Wedge-shaped hypergranulosis (corresponds to Wickham striae) |
| Epidermal pattern | Irregular acanthosis → "saw-tooth" rete ridges |
| Basal layer | Liquefactive (vacuolar) degeneration of the basal cell layer |
| Dermo-epidermal junction | Band-like (lichenoid) lymphocytic infiltrate hugging the junction |
| Apoptotic keratinocytes | Civatte / colloid / hyaline bodies (apoptotic keratinocytes) |
| Clefting | Max-Joseph spaces (subepidermal clefts from basal damage) |
Direct immunofluorescence: shaggy fibrinogen deposition along the basement membrane zone and globular IgM deposits on colloid bodies.
High-yield mnemonic for histology — "HHIVB" / remember the buzzwords: Hyperkeratosis (ortho), Hypergranulosis (wedge), Irregular acanthosis (saw-tooth rete pegs), Vacuolar basal degeneration, Band-like infiltrate, plus Civatte bodies and Max-Joseph spaces.
Management / drug of choice
LP is self-limiting in many cutaneous cases (often resolving within 1–2 years) but mucosal and hypertrophic disease is chronic.
Stepwise management:
First line → potent/super-potent topical corticosteroids (clobetasol propionate 0.05%, betamethasone) → topical calcineurin inhibitors (tacrolimus/pimecrolimus, especially for mucosal/genital LP) → intralesional triamcinolone for hypertrophic plaques and nails → systemic corticosteroids or phototherapy for widespread disease → oral retinoids / methotrexate / mycophenolate for refractory disease.
| Scenario | Drug of choice |
|---|---|
| Localised cutaneous LP | Potent topical corticosteroid (clobetasol) |
| Hypertrophic LP | Intralesional triamcinolone ± occlusion |
| Widespread/eruptive LP | Systemic corticosteroids (short course) or NB-UVB phototherapy |
| Oral reticular LP (asymptomatic) | Reassurance + oral hygiene; no treatment |
| Erosive oral/genital LP | Topical corticosteroid (in orabase) ± topical tacrolimus |
| Lichen planopilaris | Potent topical/intralesional steroid; oral hydroxychloroquine |
| Refractory/severe | Acitretin, methotrexate, mycophenolate, ciclosporin |
| Nail LP | Intralesional or systemic corticosteroids (to prevent pterygium) |
Supportive: antihistamines for pruritus; sun protection in actinic LP; stop the offending drug in lichenoid drug eruption; replace amalgam fillings in contact-induced oral LP.
High-yield: Drug of choice for typical cutaneous LP = potent topical corticosteroids. For erosive oral LP unresponsive to steroids, topical tacrolimus is preferred. NB-UVB/PUVA is used for extensive disease.
Complications
- Malignant transformation: Erosive/atrophic oral LP can progress to oral squamous cell carcinoma (overall risk ~1%); the WHO classifies oral LP as a potentially malignant disorder. Hypertrophic LP of the legs can also undergo SCC change in long-standing lesions. → Mandates long-term follow-up and biopsy of suspicious areas.
- Scarring sequelae: cicatricial alopecia (lichen planopilaris), nail pterygium/anonychia, oesophageal/vaginal strictures from erosive mucosal LP.
- Post-inflammatory hyperpigmentation — cosmetically significant, especially in Indian/darker skin.
- Psychological morbidity from chronic pruritus and visible lesions.
High-yield: Oral erosive LP is a premalignant condition → squamous cell carcinoma. This is one of the single most repeated facts in NEET PG dermatology.
Key differentials
| Condition | Distinguishing point from LP |
|---|---|
| Psoriasis | Silvery scale, Auspitz sign, parakeratosis + Munro microabscess histology; extensor surfaces |
| Lichenoid drug eruption | Photodistributed, eczematous, parakeratosis + eosinophils on biopsy, no Wickham striae; drug history |
| Pityriasis rosea | Herald patch, Christmas-tree distribution on trunk, self-limiting in weeks |
| Lichen nitidus | Tiny pinhead skin-coloured papules; "ball-in-claw" histology; grouped on penis/forearms |
| Lichen sclerosus | Porcelain-white atrophic plaques, anogenital, figure-of-eight distribution |
| Discoid lupus erythematosus | Follicular plugging, scarring, photodistribution; oral LE on palate |
| Secondary syphilis | Copper-coloured papules on palms/soles, serology positive, mucous patches |
| Leukoplakia (oral) | Homogeneous white plaque, cannot be rubbed off, no reticulate pattern |
| Graft-versus-host disease | Identical lichenoid histology; transplant context |
High-yield: Lichen nitidus — multiple tiny, shiny, flesh-coloured papules; histology shows a focal lymphohistiocytic infiltrate clutched by elongated rete ridges ("claw clutching a ball"). Frequently paired with LP in MCQs.
Comparison with psoriasis (frequently paired)
| Feature | Lichen planus | Psoriasis |
|---|---|---|
| Colour | Violaceous | Salmon-pink/red |
| Scale | Minimal, adherent | Silvery, loose |
| Distribution | Flexor (wrists, ankles) | Extensor (elbows, knees) |
| Surface | Wickham striae | Auspitz sign |
| Keratin | Orthokeratosis | Parakeratosis |
| Granular layer | Hypergranulosis (wedge) | Absent/diminished granular layer |
| Infiltrate | Band-like (lichenoid) | Munro microabscesses (neutrophils) |
| Koebner | Positive | Positive |
| Nails | Pterygium, ridging | Pitting, oil-drop, onycholysis |
Recently asked / exam angle
- Six Ps identification from a clinical photo of violaceous flat-topped papules on the wrist — classic image-based MCQ.
- Wickham striae — definition, where seen (papule surface + buccal mucosa), and its histological correlate (wedge-shaped hypergranulosis).
- Histology buzzwords: saw-tooth rete ridges, band-like lymphocytic infiltrate, Civatte (colloid) bodies, Max-Joseph spaces, orthohyperkeratosis — and contrast with parakeratosis of psoriasis.
- Hepatitis C as the systemic association of (oral) LP.
- Oral erosive LP → squamous cell carcinoma (potentially malignant disorder).
- Nail pterygium as a sign of LP; twenty-nail dystrophy in children.
- Graham-Little syndrome triad and lichen planopilaris as a cause of scarring alopecia.
- Lichenoid drug eruption drug list (beta-blockers, antimalarials, thiazides, ACE inhibitors, gold, NSAIDs).
- Drug of choice = potent topical corticosteroid; tacrolimus for resistant oral LP.
- Differentiating lichen nitidus ("claw clutching a ball") from LP.
- DIF findings: shaggy fibrinogen at the BMZ, IgM on colloid bodies.
Rapid revision
- Six Ps: Purple, Polygonal, Planar (flat-topped), Pruritic Papules/Plaques — add Pterygium (nail).
- Wickham striae = lacy white lines on papules/buccal mucosa; histological correlate = wedge hypergranulosis.
- Sites: flexor wrists, ankles, shins; oral LP commonest on buccal mucosa.
- Mediated by CD8+ cytotoxic T cells against basal keratinocytes.
- Strongest systemic association = hepatitis C (esp. oral LP).
- Histology: orthokeratosis, hypergranulosis, saw-tooth rete ridges, basal vacuolar degeneration, band-like infiltrate, Civatte bodies, Max-Joseph spaces.
- DIF: shaggy fibrinogen at BMZ + IgM on colloid bodies.
- Erosive oral LP → squamous cell carcinoma (potentially malignant disorder).
- Nail signs: pterygium, longitudinal ridging, trachyonychia, anonychia.
- Scalp: lichen planopilaris → scarring alopecia; Graham-Little syndrome triad.
- Drug of choice = potent topical corticosteroid; tacrolimus for resistant oral/genital LP; NB-UVB/PUVA for extensive disease.
- Lichen nitidus = tiny papules, "claw clutching a ball" histology — classic LP differential.