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OverviewAetiologyPathophysiologyClinical features and red flagsInvestigationsDifferential diagnosisManagementComplicationsMonitoring and follow-upSpecial situationsCommon pitfallsQuestionsSources
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Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

Lichen planus

Dermatology · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

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Time-critical presentation

Rapid painful mucosal erosion causing dehydration, dysphagia, urinary obstruction, severe genital adhesion or ocular involvement requires urgent specialist assessment and supportive care.

Overview

Recognise cutaneous, mucosal, scalp, nail and pigmentary lichen planus, confirm atypical disease safely, protect scarring sites, and monitor persistent lesions for malignant change.

Lichen planus is one disease family with very different consequences by site. Ordinary cutaneous papules often self-resolve, whereas scalp, nail and erosive mucosal inflammation can scar and requires a lower threshold for biopsy, treatment and follow-up.

The diagnostic method is morphology plus a complete site inventory and medication timeline. Wickham striae support the diagnosis, but lichenoid medicines and alternative mucosal diseases must be considered when the course or distribution is atypical.

Treatment aims to relieve itch and pain, stop inflammatory activity and prevent permanent structural damage. Residual pigmentation may need time and photoprotection rather than ongoing high-potency corticosteroid.

Key points

  • Classic cutaneous lichen planus is an itchy eruption of flat-topped shiny papules, often violaceous or darker than surrounding skin, with fine pale Wickham striae on wrists, ankles and lower back.
  • Examine mouth, genital skin, scalp and nails with explanation and consent: specialised-site disease can scar even when the ordinary skin eruption is modest.
  • In darker skin, papules may be deep brown or subtly purple, pale striae remain useful, and grey-brown post-inflammatory pigment can persist long after active inflammation.
  • Lichen planus is usually diagnosed clinically; biopsy a representative lesion when diagnosis is uncertain and promptly sample any persistent indurated, ulcerated or enlarging focus.
  • Asymptomatic limited skin disease can be observed. Symptomatic cutaneous disease usually starts with a potent or very potent topical corticosteroid applied carefully once daily under BAD guidance.
  • Face, flexures and long-term mucosal use need specialist-selected steroid-sparing or site-specific formulations; much lichen-planus prescribing is off-label and should be stated as such.
  • Scalp follicular loss, rapidly progressive nail change and erosive oral or genital disease merit early specialist referral because permanent damage and low malignant risk alter monitoring.

Aetiology

01

Immune-mediated interface disease

The precise cause is uncertain. Lichen planus reflects an abnormal cell-mediated immune response against basal keratinocytes and is not infectious or usually inherited.

02

Lichenoid triggers

Medicines including some antihypertensives, antimalarials and other agents can cause a lichenoid eruption. Dental metals and contact exposures occasionally contribute to local oral disease, so timing and distribution matter.

03

Infection associations

Hepatitis viruses have reported associations whose strength varies by population. Test according to clinical and epidemiological risk rather than applying untargeted screening to every typical eruption.

Pathophysiology

  1. 1
    Basal-cell injury

    Cytotoxic lymphocytes damage the epidermal basal layer, producing an interface dermatitis. Hypergranulosis and altered keratin create the fine pale Wickham striae seen on close inspection.

  2. 2
    Koebner response

    Trauma and scratching can recruit new lesions along injured skin. The resulting linear papules are a pattern clue and a reason to control itch and avoid rubbing.

  3. 3
    Scarring at specialised sites

    Inflammation around scalp follicles, nail matrix or erosive mucosa can destroy permanent structures. The treatment threshold is therefore lower than for asymptomatic papules on ordinary skin.

  4. 4
    Post-inflammatory pigment

    Interface injury releases pigment into the dermis, so grey-brown macules can persist after active papules resolve. This change is often more conspicuous and prolonged in darker skin.

Clinical features and red flags

Cutaneous papules

Clusters of flat-topped, shiny, polygonal papules favour flexor wrists, ankles and lower back. Fine white or pale Wickham striae and linear Koebner lesions can be seen with close light and magnification.

Oral diseaseRed flag

Reticular white lacy lines may be asymptomatic, while erosive gingival or buccal disease is painful and affects eating. Examine the full mouth and palpate persistent ulcerated or indurated areas.

Genital erosionsRed flag

Glazed painful erythema, white border, erosion and scarring may affect vulva, vagina, glans or foreskin. Use trauma-informed consent, offer a chaperone and avoid assuming infection or sexual transmission.

Scalp follicular lossRed flag

Perifollicular scale, erythema and loss of follicular openings indicate lichen planopilaris and active scarring alopecia. Symptoms can include itch, tenderness or burning before visible loss is extensive.

Nail matrix injuryRed flag

Longitudinal ridging, thinning, fissuring and dorsal pterygium may progress to irreversible nail loss. Distinguish from fungal disease and psoriasis, especially when change is asymmetric.

Pigmentary phenotype

Grey-brown macules on face, neck, trunk or flexures may occur without preceding obvious papules and are more frequent in darker skin. Seek activity at borders and exclude medicine or contact triggers.

Red flags requiring action

  • A persistent indurated, ulcerated, bleeding or enlarging lesion within oral, genital or hypertrophic disease needs urgent biopsy assessment for squamous cell carcinoma.

Investigations

  1. 01
    First-line complete skin and specialised-site examinationFirst stepFirst line
    Why
    Map cutaneous, oral, genital, scalp and nail involvement and identify sites at risk of scarring or cancer.
    Interpretation and limitations
    Pale striae and concordant lesions support lichen planus; loss of follicular openings, nail pterygium, erosion or induration increases urgency regardless of total skin extent.
  2. 02
    Dated medicine and exposure review
    Why
    Identify a lichenoid drug eruption or local contact contributor before labelling disease idiopathic.
    Interpretation and limitations
    Latency can be prolonged and improvement after withdrawal slow. Do not stop essential medicines abruptly; discuss probability and alternatives with the original prescriber.
  3. 03
    Skin or mucosal biopsy with histology
    Why
    Confirm interface dermatitis when clinical diagnosis is uncertain and exclude dysplasia or malignancy in a changing lesion.
    Interpretation and limitations
    Choose an active representative edge rather than an eroded centre where possible. State the anatomical site, medicine history and differential to pathology, and obtain explicit procedure consent.
  4. 04
    Direct immunofluorescence when blistering disease is considered
    Why

Differential diagnosis

01

Lichenoid drug eruption

A symmetric widespread rash after a compatible medicine may be more eczematous or photodistributed and have fewer classic wrist or mucosal signs. Resolution can lag for months after safe withdrawal.

02

Psoriasis and eczema

Psoriasis is more scaly and often extensor or scalp-predominant; eczema is frequently less sharply bordered and more exudative or lichenified. Histology helps when treatment response and morphology conflict.

03

Mucosal alternatives

Candidiasis, leukoplakia, lupus, mucous-membrane pemphigoid, lichen sclerosus, aphthae and dysplasia can resemble oral or genital lichen planus. Erosion or scarring should not be diagnosed from a photograph alone.

04

Scalp and nail mimics

Discoid lupus, frontal fibrosing alopecia, alopecia areata, psoriasis, fungal infection and trauma can produce overlapping loss or dystrophy. Examine follicular openings and choose biopsy site carefully.

05

Pigmentary disorders

Lichen planus pigmentosus causes grey-brown face, neck or flexural macules, especially in darker skin, but melasma, drug pigment, post-inflammatory change and erythema dyschromicum require consideration.

Management

01First-lineLimited cutaneous lichen planusFirst stepFirst lineTypical skin papules without scarring-site disease, significant erosion or malignant warning features.+
  1. 1Explain the often self-limiting course, avoid skin injury, use emollient or soap substitute for comfort, and document active papules separately from residual pigment.
  2. 2Observe asymptomatic limited disease; for itch or active inflammation, apply a prescribed potent or very potent topical corticosteroid carefully once daily to papules.
  3. 3Review within the defined course for flattening, itch, atrophy and diagnostic fit; stop active steroid when lesions become flat pigment rather than continuing to chase colour.
  4. 4Refer widespread, persistent or treatment-resistant disease for phototherapy or systemic options selected by dermatology.
02Scarring sitesScalp and nail protection

Complications

01

Squamous cell carcinoma

BAD describes a low cancer risk in persistent severe hypertrophic or erosive mucosal disease. New induration, ulceration, bleeding or growth requires biopsy rather than stronger empirical anti-inflammatory treatment.

02

Scarring alopecia

Lichen planopilaris can permanently destroy follicles. Loss of ostia and perifollicular scale signal active damage, so early control is more important than waiting for extensive hair loss.

03

Permanent nail dystrophy

Matrix scarring can split or thin plate and form dorsal pterygium, eventually destroying the nail. Rapid progression warrants treatment even when only a few nails are involved.

04

Mucosal stenosis and pain

Erosive genital or oesophageal disease can produce adhesions, narrowing, dyspareunia, urinary symptoms, dysphagia and nutritional harm, requiring multidisciplinary monitoring and practical prevention of scarring.

05

Long-lasting dyspigmentation

Resolved cutaneous disease can leave darker or lighter marks without scarring. Distinguish inactive pigment from raised, itchy or erosive activity before continuing potent treatment.

Monitoring and follow-up

  • Reassess cutaneous treatment within the prescribed corticosteroid course, comparing papule thickness, itch and new lesions rather than expecting residual grey-brown pigment to disappear quickly.
  • Monitor scalp and nails closely for expansion of perifollicular inflammation, loss of follicular openings, pterygium and new structural damage; expedite treatment if progression continues.
  • Provide regular oral or genital review for persistent erosive disease, with self-reporting instructions for non-healing ulcer, lump, induration, bleeding, swallowing change or worsening stenosis.
  • For systemic treatment, follow the selected medicine's blood, infection, pregnancy and adverse-effect protocol and identify one team responsible for results and repeat prescriptions.
  • Assess pain, nutrition, sexual and urinary function, sleep, distress and treatment practicality; use professional interpreters and trauma-informed examination where needed.

Special situations

Pale striae survive colour variation

In deeply pigmented skin, a papule may appear brown rather than purple, while fine Wickham striae remain a valuable surface clue under good lighting.

Flat pigment is not failure

Successful control can leave grey-brown macules for months. Continuing very potent steroid after elevation, scale and itch resolve adds toxicity without accelerating pigment clearance.

Site determines prognosis

A few scalp follicles or one rapidly changing nail can have more irreversible consequence than many transient wrist papules, so extent alone cannot set urgency.

Lichenoid is descriptive

A pathology report of lichenoid interface inflammation has a differential. Medication, lupus, graft-versus-host disease and contact patterns must still be reconciled clinically.

Consent includes anatomy

Mucosal examination should be explained in advance, limited to what is clinically needed, and performed with explicit permission, privacy and a chaperone offer.

Common pitfalls

  1. 01

    Treating residual hyperpigmentation with repeated very potent corticosteroid after active papules have flattened.

  2. 02

    Examining only ordinary skin and missing scarring scalp, nail, oral or genital disease.

  3. 03

    Calling a persistent oral ulcer lichen planus without palpation, documentation and timely biopsy assessment.

  4. 04

    Stopping an essential suspected culprit medicine abruptly without evaluating latency, indication and alternatives with its prescriber.

  5. 05

    Placing a direct-immunofluorescence specimen in formalin instead of the required transport medium.

  6. 06

    Using systemic retinoid without the complete long post-treatment pregnancy-prevention programme.

Practice

Two practice questions

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Question 1 of 2
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DermatologyOriginal SBA

Scalp activity and urgency

A patient with lichen planus develops scalp burning, perifollicular scale and patches where follicular openings are disappearing. What is the best next step?

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Sources and review status5 sources · checked 27 Aug 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

  • British Association of Dermatologists: lichen planus
  • British Association of Dermatologists: oral lichen planus
  • Dermovate ointment Summary of Product Characteristics
  • Acitretin capsules Summary of Product Characteristics
  • MHRA: safe use of emollient skin creams

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom
Avoid scratching and use emollient for itch, while warning that product residue on fabric and hair increases fire severity even when dry.
  • Scalp inflammation with perifollicular scale and loss of follicular openings can cause permanent scarring alopecia and warrants expedited dermatology review.
  • Rapid nail thinning, pterygium or destruction may become irreversible, so progressive nail-unit disease needs early specialist treatment.
  • Painful vulvovaginal erosion, discharge, narrowing or adhesions, or penile scarring and phimosis requires specialist genital examination with consent and appropriate multidisciplinary care.
  • Odynophagia, dysphagia, weight loss or food impaction can indicate oesophageal involvement or malignancy and needs prompt upper-gastrointestinal assessment.
    • Distinguish lichen planus from pemphigoid, pemphigus or lupus in erosive or bullous presentations.
    Interpretation and limitations
    Take a separate correctly handled perilesional specimen following laboratory instructions; formalin destroys the immunoreactants needed for this test.
  • 05
    Targeted hepatitis and infection testing
    Why
    Investigate relevant epidemiological risk or prepare for systemic immunosuppression without indiscriminate screening.
    Interpretation and limitations
    Obtain consent and explain implications. A positive result changes medical assessment but does not prove it caused the eruption, and negative testing does not exclude lichen planus.
  • 06
    Baseline systemic-treatment panel
    Why
    Check blood count, renal and liver function, pregnancy status, infection and agent-specific risks before specialist systemic therapy.
    Interpretation and limitations
    The exact panel follows the selected off-label medicine. Abnormalities may contraindicate treatment or need another specialty, not simply a smaller empirical dose.
    • Perifollicular inflammation with hair loss or rapidly progressive nail matrix change.
    +
    1. 1Arrange expedited dermatology assessment, document symptoms and photograph with consent, and exclude fungal or other scarring mimics where relevant.
    2. 2Use specialist-selected potent topical or intralesional corticosteroid and systemic anti-inflammatory therapy according to site, extent and progression; explain that the goal is to preserve remaining structures.
    3. 3Monitor activity at follicular margins and new nail growth, because destroyed follicles or matrix do not recover simply because inflammation later settles.
    03Mucosal diseaseControl erosion and prevent stenosisPainful oral, genital or oesophageal symptoms or scarring.+
    1. 1Examine with explicit consent, offer a chaperone, document nutrition, sexual and urinary function, and involve oral medicine, gynaecology, urology or gastroenterology according to anatomy.
    2. 2Use specialist site-specific topical corticosteroid or calcineurin-inhibitor treatment, explaining off-label status and how to apply it safely to mucosa.
    3. 3Biopsy persistent focal ulceration, induration, bleeding or growth and arrange continuing surveillance for severe erosive disease.
    04EscalationWidespread or refractory inflammationEscalationExtensive cutaneous disease, severe symptoms, scarring progression or failure of appropriate topical therapy.+
    1. 1Reconfirm diagnosis and medicine timeline, assess infection and pregnancy risk, and collect baseline bloods before systemic treatment.
    2. 2Dermatology may use a short oral corticosteroid course, narrowband UVB, acitretin, methotrexate or another immunomodulator according to phenotype and comorbidity; many uses are off-label.
    3. 3Set a response target and toxicity schedule before starting, and ensure any oral or genital cancer-surveillance plan has a named owner.
    Key medicines and prescribing safety3 treatments · regimens, roles and cautions+
    Licensed very potent topical corticosteroid for short-term resistant lichen planus on appropriate non-sensitive skin under clinical supervision.

    Clobetasol propionate 0.05% ointment

    Apply thinly to resistant cutaneous lichen planus once or twice daily for the shortest effective course, stopping or stepping down by 4 weeks; maximum 50 g weekly.

    Avoid face, flexures, genital mucosa, untreated infection, large areas and unplanned occlusion; prolonged exposure causes atrophy and systemic absorption, and persistent lesions need diagnostic review.

    Reduces dryness and scratching that can provoke Koebner lesions, but does not suppress scarring scalp, nail or mucosal inflammation.

    Emollient or soap substitute

    Apply generously as often as needed to dry or itchy intact skin, smoothing rather than rubbing and separating from active topical medicine by about 20 to 30 minutes.

    Oily residue on clothes, bedding and hair increases fire severity even when dry; avoid smoking and naked flames, wash fabrics frequently and manage slip risk.

    Licensed in the selected SmPC for severe refractory lichen ruber planus of skin and mucosa, after site-specific assessment and safer measures.

    Acitretin for severe refractory lichen planus

    Specialist SmPC guidance starts 25 or 30 mg orally once daily for 2 to 4 weeks, then adjusts individually to response and tolerability up to a maximum 75 mg daily.

    Highly teratogenic: specialist pregnancy prevention and testing continue for 3 years after stopping where pregnancy is possible; monitor liver, lipids and mucocutaneous toxicity and avoid tetracyclines.