Lichen Planus

Lichen planus (LP) is a chronic, T-cell-mediated inflammatory disease that can involve the skin, oral and genital mucosa, nails, and hair-bearing scalp, alone or in combination.^[1] Cytotoxic CD8+ T cells, activated against an unidentified antigenic change on basal keratinocytes, mount a band-like attack along the dermo-epidermal junction that destroys the basal cell layer and produces the disease's signature "saw-tooth" histology.^[1] Cutaneous LP affects roughly 0.2-1% of adults worldwide, while oral LP is more common still, affecting an estimated 1-4% of the population - mucosal disease frequently outlasts skin disease by years.^[1] A modest female predominance (about 1.5:1) and a peak incidence between 30 and 60 years are typical; up to 10% of patients have an affected first-degree relative, and incidence is reported higher in patients of African American, Indian, and Arab descent.^[1]

The classic cutaneous lesion is captured by the mnemonic the "6 P's" - purple, polygonal, planar (flat-topped), pruritic papules and plaques - but LP's actual clinical range is far broader, spanning hypertrophic, atrophic, bullous, actinic, inverse, and pigmented cutaneous variants; reticular, erosive, atrophic, papular, plaque-like, and bullous oral disease; vulvar, vaginal, and penile involvement; a scarring, permanently hair-destroying scalp variant (lichen planopilaris); and a nail dystrophy that can end in irreversible pterygium formation.^[1] Three threads run through this entire chapter. First, LP has a genuine, well-quantified association with hepatitis C infection, with a pooled odds ratio around 4.5 for HCV seropositivity in LP patients.^[2] Second, a recognized list of medications produces a near-identical "lichenoid" eruption that must be actively distinguished from idiopathic LP, since the fix is simply identifying and stopping the drug.^[1] Third, erosive oral (and, less often, genital) LP carries a small but real malignant transformation risk - on the order of 1% in the best pooled estimates - that turns this disease from a purely symptomatic problem into one needing lifelong surveillance.^[3]

Classic cutaneous lichen planus on the anterior shin - violaceous, flat-topped, polygonal papules, a favoured site alongside the flexor wrists and lower back. (Warfieldian, Wikimedia Commons, CC BY-SA 3.0)

Classic cutaneous lichen planus - the "6 P's"

The hallmark lesion is purple (violaceous; yellow-brown on palms and soles), polygonal, planar (flat-topped rather than dome-shaped), pruritic papules and plaques, classically a few millimetres wide and favouring the flexor wrists, dorsal hands, lower back, ankles, and shins.^[1] Close inspection or dermoscopy of an individual papule often reveals Wickham striae - a fine, lace-like network of white lines on the surface, sometimes bordered by red globules on dermoscopy - one of the most useful bedside clues to LP.^[1] New lesions frequently arise in sites of skin trauma or scratching, the Koebner (isomorphic) phenomenon, and established plaques often resolve into grey-brown post-inflammatory hyperpigmentation that can outlast the active disease by months to years.^[1]

Cutaneous variants

Oral lichen planus

Reticular oral lichen planus - lacy, white Wickham striae on the buccal mucosa, the most common and typically asymptomatic oral pattern. (Ian Furst, Wikimedia Commons, CC BY-SA 4.0)

Mucosal involvement affects over half of all LP patients and is frequently the sole presenting sign, with no skin disease at all.^[1] 6 recognized oral patterns exist, and more than 1 often coexists in the same patient:^[1]

• Reticular - the most common pattern: asymptomatic, lacy white Wickham striae, typically bilateral and symmetric on the buccal mucosa, sometimes extending to the tongue, gingiva, or lips. Easily mistaken for leukoplakia or chronic candidiasis if the classic lacy pattern is not specifically recognized.^[1]
• Erosive - painful, irregular erosions and ulcers, often ringed by radiating white striae, worsened by hot, spicy, or acidic food; the pattern most often responsible for symptoms driving patients to seek care, and the pattern carrying the highest malignant transformation risk.^[1][3]
• Atrophic - diffuse redness and thinning of the mucosa, often painful; when confined to the gingiva it produces desquamative gingivitis - diffuse red, peeling gingiva that is also a shared endpoint of pemphigus vulgaris and mucous membrane pemphigoid, so biopsy with direct immunofluorescence is often needed to tell these apart.^[1]
• Papular, plaque-like, and bullous - less common patterns; plaque-like lesions in particular can resemble leukoplakia clinically.^[1]

A localized oral lichenoid lesion in direct topographic contact with a dental amalgam restoration suggests a contact reaction to mercury or another dental metal rather than idiopathic OLP - patch testing and, if positive, amalgam replacement can be diagnostic and curative for this specific presentation (see Assessment and Diagnosis).^[1]

Genital lichen planus

On the glans penis, LP classically forms an annular ring of papules around the glans; white reticular streaks and, less often, erosive disease also occur.^[1] Vulvar disease ranges from asymptomatic lacy white streaks to painful, persistent erosions and ulcers, and - particularly with the erosive subtype - can progress to genuinely disabling scarring: labial fusion, resorption of the labia minora, clitoral hood adhesions, and introital stenosis narrowing the vaginal opening. Concurrent vaginal involvement produces a painful desquamative vaginitis that can itself prevent intercourse.^[1] The combination of erosive vulvovaginal LP, erosive oral LP, and (often) gingival involvement defines the vulvovaginal-gingival syndrome, a severe, scarring, difficult-to-treat presentation with a reported association to the HLA-DQB1*02:01 allele.^[1] Because scarring is progressive and only partially reversible once established, genital LP - especially the erosive pattern - deserves early, adequately potent treatment rather than a "wait and see" approach (see Red Flags and Choose Initial Treatment).

Nail lichen planus

Affects roughly 10% of LP patients, usually several nails at once, and can occur with or without skin/mucosal disease.^[1] The typical sequence is nail-plate thinning, longitudinal ridging and fissuring, then scarring of the nail matrix producing a pterygium - permanent adhesion of the proximal nail fold to the nail bed - progressing in severe, untreated cases to a rough, sandpaper-like texture (trachonychia) or complete, irreversible nail loss (anonychia).^[1] When all 20 nails are affected with no skin or mucosal disease elsewhere, this is termed 20-nail dystrophy, a pattern seen more often in children.^[1] Because pterygium formation is not reversible once it has occurred, nail LP - like lichen planopilaris below - is a genuine "treat early" situation rather than one where a watch-and-wait approach is low-risk.

Lichen planopilaris and other hair-bearing scalp involvement

Lichen planopilaris (LPP) presents as tiny, red, spiny follicular papules with perifollicular erythema and scale, extending into smooth, shiny, permanently bald patches punctuated by isolated surviving hairs ("lonely hairs") - a scarring alopecia in which lost hair follicles do not regrow.^[1] Frontal fibrosing alopecia is a distinct clinical pattern of LPP - a band of scarring hair loss along the frontal and temporal hairline, often with eyebrow loss, seen predominantly in postmenopausal women.^[1] Graham-Little-Piccardi-Lasseur syndrome is a rare familial variant combining scalp LPP, typical cutaneous/mucosal LP elsewhere, and non-scarring loss of axillary and pubic hair with follicular papules.^[1] Pseudopelade of Brocq describes late-stage, "burnt-out" scarring alopecia patches - sometimes an LPP end-stage, sometimes idiopathic - classically likened to "footprints in the snow."

Esophageal lichen planus

An underrecognized site, predominantly in women, that can cause dysphagia, odynophagia, and esophageal strictures, and - like erosive oral and genital disease - carries a risk of malignant transformation to squamous cell carcinoma.^[1] Consider it specifically in an LP patient (especially one with erosive oral disease) reporting new or worsening swallowing difficulty (see Red Flags).

• Age 30-60 years is the typical window at onset; LP is uncommon in children (under 5% of all cases), though 20-nail dystrophy and actinic LP are both disproportionately pediatric presentations.^[1]
• Female sex - a modest overall predominance (about 1.5:1); frontal fibrosing alopecia in particular is overwhelmingly a disease of postmenopausal women.^[1]
• Family history - up to 10% of patients have an affected first-degree relative, suggesting a genetic contribution.^[1]
• Hepatitis C infection - a genuine, well-quantified bidirectional association. A 2023 systematic review/meta-analysis found LP patients have significantly higher odds of being HCV-seropositive than controls (pooled odds ratio 4.48, 95% CI 3.48-5.77), with global HCV prevalence of 9.42% among LP patients overall and LP prevalence of 7.05% among HCV-positive patients; the association was stronger for cutaneous LP (odds ratio 5.95) than for oral LP (odds ratio 3.49), and stronger still in Mediterranean-basin countries.^[2] HCV-positive status independently raises the odds of malignant transformation in oral lichenoid disease as well (see Assessment and Diagnosis).^[3]
• Dental metal contact allergy (mercury from amalgam restorations, less often other metals) - relevant specifically to an oral lichenoid lesion in direct contact with a restoration, and confirmed by patch testing (see Assessment and Diagnosis).^[1]
• Graft-versus-host disease - chronic cutaneous and oral GVHD can produce lichenoid lesions that are histologically and clinically similar to idiopathic LP; always consider this in a patient with a history of allogeneic hematopoietic stem cell transplant.^[1]
• An emerging, still-developing literature has reported LP flares temporally associated with COVID-19 infection and, less often, COVID-19 vaccination; causality is not established, and this should not change routine vaccination counselling.^[1]

Drug-induced lichenoid reactions - a critical mimic

A recognized list of medications can trigger an eruption that looks and, on biopsy, largely behaves like idiopathic LP - a lichenoid drug eruption. Distribution is often more photodistributed and symmetric/generalized than idiopathic LP, Wickham striae are typically absent, and the latency from starting the drug to eruption can run from several months to over a year, which is exactly why the connection is so often missed.^[1] A thorough medication review is a genuinely essential part of assessing any new LP presentation.

Diagnostic approach

A classic cutaneous presentation - violaceous, flat-topped, polygonal, pruritic papules with Wickham striae in a typical distribution - can often be diagnosed clinically.^[1] Biopsy is genuinely useful, and often necessary, whenever the presentation is atypical, mucosal-only or scalp-only (where LP and lupus erythematosus can look very similar), before starting a systemic immunosuppressant, or whenever malignant transformation is a concern (see Red Flags).^[1]

Histopathology

The classic findings are hyperkeratosis without parakeratosis, wedge-shaped hypergranulosis, irregular "saw-tooth" rete ridges, liquefactive degeneration of the basal cell layer, a dense, band-like lymphocytic infiltrate hugging the dermo-epidermal junction, and colloid (Civatte) bodies - apoptotic keratinocytes - in the lower epidermis and upper dermis.^[1] Eosinophils are typically absent in idiopathic LP; their presence should raise suspicion for a drug-induced lichenoid reaction instead.^[1]

Direct immunofluorescence and dermoscopy

Direct immunofluorescence (DIF) is not needed routinely but is genuinely useful when the differential includes lupus erythematosus (particularly scalp-only or mucosal-only disease) or an immunobullous disease (bullous LP vs. lichen planus pemphigoides, or desquamative gingivitis vs. pemphigus/mucous membrane pemphigoid) - DIF in LP characteristically shows colloid bodies staining for IgM (and, less consistently, IgG, IgA, and C3) and "shaggy" fibrinogen deposition along the basement membrane zone.^[1] Dermoscopy of a cutaneous or mucosal lesion shows Wickham striae as a network of white lines, sometimes with red globules or dots at the periphery reflecting the underlying vascular pattern - a fast, non-invasive way to support the diagnosis at the bedside.^[1]

Patch testing for suspected dental-metal contact reaction

For an oral lichenoid lesion in direct topographic contact with a dental amalgam restoration, patch testing for mercury and other dental metals helps distinguish a genuine contact reaction from idiopathic OLP; if positive and the lesion has not responded to standard therapy, replacing the amalgam restoration with a composite material (coordinated with dentistry) can be diagnostic and, in confirmed cases, curative.^[1]

Distinguishing idiopathic LP from a drug-induced lichenoid reaction

Favour a drug cause when the eruption is more photodistributed or symmetric/generalized than typical idiopathic LP, Wickham striae are absent, onset followed a new medication by several months to over a year, and/or eosinophils are seen on biopsy.^[1] The diagnosis is ultimately confirmed by response to withdrawal - lesions gradually resolve once the culprit drug is stopped, though this can take weeks to several months, so counsel patients accordingly rather than expecting rapid clearing.^[1]

Hepatitis C screening

Given the well-documented bidirectional association, arrange HCV screening for newly diagnosed LP patients, particularly with erosive or widespread disease or in a higher HCV-prevalence population/region - screening both identifies a treatable infection and flags a patient at somewhat higher malignant-transformation risk if oral disease is present.^[2][3]

Differential diagnosis

• Control pruritus (cutaneous LP) or pain (erosive oral, genital, and ulcerative disease), which are frequently the dominant drivers of quality-of-life impact and treatment-seeking.
• Induce remission of active lesions and reduce time to resolution, while accepting that post-inflammatory hyperpigmentation can persist long after active disease has cleared.
• Prevent irreversible structural complications specifically where they are time-sensitive: permanent scarring alopecia in lichen planopilaris, nail matrix scarring/pterygium formation, and genital scarring/adhesions - all reasons to treat promptly rather than deferring in these particular presentations.
• Identify and, where feasible, discontinue a causative medication in suspected drug-induced lichenoid disease, rather than treating it as idiopathic LP indefinitely.
• Screen for and, where positive, coordinate management of hepatitis C infection, given the well-documented bidirectional association.
• Maintain lifelong malignant-transformation surveillance for erosive oral (and genital) disease - a genuine, ongoing treatment goal in its own right, not a one-time box to check at diagnosis.
• Minimize treatment-related morbidity, particularly from prolonged high-potency topical or systemic corticosteroid use, which carries real risks - including adrenal suppression from "just a topical steroid" applied in the mouth - that are easy to underestimate.
• Support nutrition, oral hygiene, and psychosocial wellbeing through what is frequently a chronic, relapsing-remitting, and visibly disfiguring or painful disease course.

Skin and mucosal care

• Use gentle, fragrance-free cleansers and regular emollients on affected skin; avoid harsh soaps, hot water, and vigorous scrubbing, all of which can Koebnerize new lesions.^[1]
• Avoid unnecessary skin trauma, tight clothing over active plaques, and picking or scratching, given the Koebner phenomenon.
• For oral disease: a soft-bristled toothbrush, gentle oral hygiene technique, and avoidance of spicy, acidic, very hot, or coarse/crunchy foods, alcohol, and tobacco during flares of erosive disease.^[1]

Photoprotection - critical, and different by variant

Routine sun protection (broad-spectrum sunscreen, protective clothing, shade-seeking) is reasonable general advice, but it is a genuine treatment requirement - not just good practice - for actinic LP and LP pigmentosus, both of which are directly triggered or worsened by ultraviolet exposure; phototherapy, which is a legitimate treatment for other cutaneous LP, should specifically be avoided in these 2 variants for exactly this reason (see Common Errors to Avoid).^[1]

Dental and periodontal care

Maintain regular dental hygiene and periodontal care in patients with oral LP - untreated periodontal disease and dental plaque can independently aggravate gingival LP. Coordinate with dentistry for patch testing and possible amalgam replacement when a lesion is directly apposed to a metal restoration and standard OLP therapy has not helped (see Assessment and Diagnosis).^[1]

Smoking and alcohol cessation

Counsel smoking and alcohol cessation specifically in patients with erosive oral LP - both are independently associated with a higher odds of malignant transformation (smoking approximately 1.8-fold, alcohol approximately 3.3-fold, in pooled analysis) on top of their well-established, unrelated risks for oral cancer generally.^[3]

Genital and sexual health counselling

For genital LP, counsel on gentle hygiene, avoidance of irritant soaps/wipes, and the use of a bland emollient or barrier ointment before intercourse where dyspareunia from erosive disease or early scarring is a concern; involve a pelvic floor physiotherapist or sex therapist where relevant to quality of life, and coordinate early with gynecology or urology if adhesions or stenosis are developing (see Red Flags).

Nutrition and hydration support

For painful erosive oral disease significant enough to limit intake, consider a temporary softer/blended diet and nutritional supplementation while pharmacologic treatment takes effect, rather than allowing dehydration or weight loss to go unaddressed.

Psychosocial support and expectation-setting

• Explain the expected natural history up front: cutaneous LP often resolves within 1-2 years even without treatment, though post-inflammatory hyperpigmentation can persist much longer; mucosal (oral/genital) disease and lichen planopilaris are typically more chronic, relapsing-remitting conditions that can persist for a decade or more.^[1]
• Be explicit that hair loss in established lichen planopilaris and nail-matrix scarring in advanced nail LP are permanent - this shapes both the urgency of early treatment and realistic goals once scarring has occurred.^[1]
• For visible or genital disease, acknowledge the real psychosocial and intimacy impact directly rather than focusing only on lesion counts, and offer camouflage makeup counselling or a mental health/sexual health referral where appropriate.
• Reinforce that LP is not contagious - a common and reasonable patient concern worth addressing explicitly, especially with visible facial or genital lesions.

Pregnancy

Breastfeeding

Topical corticosteroids at any potency are generally compatible with breastfeeding; wash the area before the next feed if applied near the breast/nipple. Avoid acitretin, methotrexate, and mycophenolate mofetil as above. A short oral prednisone course is also generally compatible.

Children

LP is uncommon in children (under 5% of cases) but when it occurs, 20-nail dystrophy and actinic LP are both disproportionately represented.^[1] Children have a higher body-surface-area-to-weight ratio and thinner skin, increasing systemic absorption from topical corticosteroids - favour the lowest effective potency and shortest effective course, and dose systemic agents (methotrexate 0.25 mg/kg/week, and others) by weight per the current product monograph.^[1]

Darker skin tones

Post-inflammatory hyperpigmentation is common after LP of any type and can persist for months to years after the active lesion itself has resolved - counsel on this expected course explicitly so it is not mistaken for ongoing active disease or treatment failure. LP pigmentosus and actinic LP are both reported more often in patients with darker skin tones and in Middle Eastern/North African/South Asian populations specifically.^[1]

Hepatitis C-positive patients

Coordinate LP management with the patient's hepatology/infectious disease team managing HCV treatment; treating the underlying HCV infection does not reliably clear coexisting LP, so continue LP-directed therapy in parallel rather than assuming antiviral treatment alone will resolve the skin/mucosal disease. HCV-positive status is also an independent risk factor for malignant transformation in oral lichenoid disease, reinforcing the case for surveillance in this group (see Monitoring and Follow-Up).^[3]

Renal impairment

Cyclosporine is nephrotoxic in its own right and needs particularly careful renal and blood-pressure monitoring in any degree of pre-existing renal impairment; adjust or avoid methotrexate with reduced eGFR per current Canadian labelling conventions used throughout this content library (avoid below 50 mL/min/1.73 m²).

Hepatic impairment

Acitretin, methotrexate, and azathioprine all carry hepatotoxicity risk and need closer monitoring, or an alternative agent, in significant hepatic impairment; mycophenolate mofetil's comparatively lower hepatotoxicity profile can make it a preferable alternative in this situation.

1. Confirm genuine adherence and correct application/dosing before labelling a topical or oral regimen a failure - both topical technique and, for oral disease, avoidance of aggravating foods/alcohol/tobacco are common, fixable gaps.
2. Reconsider the diagnosis: rule out a missed drug-induced lichenoid reaction (structured medication review), a dental-metal contact reaction for a localized oral lesion, or an alternative/overlapping diagnosis (lupus erythematosus, an immunobullous disease) via biopsy with direct immunofluorescence if not already done.
3. Localized cutaneous disease not controlled by an adequate trial of superpotent topical corticosteroid: add intralesional triamcinolone to resistant lesions before moving to systemic therapy.
4. Widespread cutaneous disease inadequately controlled by an oral corticosteroid taper: escalate to phototherapy (NB-UVB or PUVA, if not already tried and not actinic/pigmentosus LP) or a 2nd-line systemic agent (acitretin, methotrexate, sulfasalazine, or isotretinoin).
5. Oral LP not improving after an adequate 6-week trial of high-potency topical corticosteroid or topical tacrolimus: try the alternative topical agent if not already used, then escalate to an oral corticosteroid course, then to cyclosporine, azathioprine, mycophenolate mofetil, or methotrexate.
6. Genital LP with ongoing erosive disease or early scarring despite adequate topical therapy: escalate to systemic therapy and involve gynecology/urology proactively rather than waiting for adhesions to become established.
7. Lichen planopilaris with persistent active inflammation despite topical/intralesional corticosteroid and hydroxychloroquine: escalate to mycophenolate mofetil, methotrexate, or cyclosporine - do not continue an ineffective regimen while active, irreversible follicle loss continues.
8. Multiple standard systemic options genuinely exhausted: consider referral to a specialist dermatology or oral medicine centre for case-by-case consideration of biologics (TNF-alpha inhibitors have case-level evidence) or emerging options, recognizing the evidence base here is limited to case reports/series.

• Treating asymptomatic reticular oral LP with topical or systemic therapy "just in case," rather than monitoring it - the treatment's adverse-effect burden is not justified without symptoms.^[1]
• Using phototherapy for actinic LP or LP pigmentosus - both variants are directly triggered or worsened by ultraviolet exposure, so phototherapy is specifically the wrong treatment here even though it is a legitimate option for other cutaneous LP.^[1]
• Treating a longstanding hypertrophic, erosive oral, or erosive genital plaque as "just unresponsive LP" rather than biopsying a new ulcer, enlarging nodule, or indurated area to exclude malignant transformation.
• Missing a drug-induced lichenoid reaction by not performing a structured medication review, especially when the eruption is photodistributed, generalized, or lacks Wickham striae, or the patient recently started a recognized culprit medication.
• Treating "just a topical steroid in the mouth" as inherently risk-free - prolonged, frequent use carries a real, biochemically demonstrable risk of adrenal suppression.
• Deferring treatment of active lichen planopilaris or progressive nail LP with a watch-and-wait approach - unlike most cutaneous LP, the resulting scarring alopecia and nail pterygium are permanent once established.
• Missing early genital scarring (labial fusion, introital stenosis) because genital sites were not specifically examined in a patient presenting with cutaneous or oral LP - actively ask about and, with consent, examine genital involvement rather than waiting for the patient to raise it.
• Attributing new dysphagia in an LP patient to reflux or simple oral discomfort without considering esophageal LP.
• Assuming a worsening rash on hydroxychloroquine, an antimalarial also used to treat LP itself, must reflect undertreated disease rather than considering a hydroxychloroquine-induced lichenoid reaction.
• Not screening for hepatitis C in a newly diagnosed LP patient, particularly with erosive or widespread disease, given the well-documented bidirectional association.
• Prescribing acitretin without confirming pregnancy status and providing pregnancy-prevention counselling, given its prolonged teratogenic risk after discontinuation.
• Stopping a prolonged systemic or high-potency topical corticosteroid course abruptly rather than tapering, risking rebound flare and, for systemic courses, adrenal insufficiency.

How to use this table: Doses are adult doses and require patient-specific confirmation (renal/hepatic function, weight, allergy history). Pediatric dosing is weight-based per the current product monograph unless stated. Drug pricing is intentionally omitted. Select any drug name to open its complete Pharmasist Drug Database page.

Topical and Intralesional Corticosteroids

First-line for localized cutaneous, oral, and genital disease. Use an ointment base (not cream) on genital skin for better tolerability; use a lower-concentration gel formulation in the mouth.

Topical Calcineurin Inhibitors

A genuine first-line alternative to topical corticosteroids for oral and genital LP, particularly where prolonged steroid exposure is a concern; also used as a cutaneous adjunct.

Systemic Corticosteroid Induction

First-line for widespread/diffuse cutaneous LP and for severe, rapidly symptomatic erosive oral or genital disease needing faster control than topical therapy alone can provide.

Retinoids

Among the better trial-evidenced second-line systemic options for cutaneous LP, though absolute contraindication in pregnancy limits use in patients who could become pregnant.

Steroid-Sparing Immunosuppressive Agents

Used for refractory cutaneous, oral, or genital LP, and (hydroxychloroquine specifically) as first-choice therapy for lichen planopilaris.

Pruritus Adjunct

Symptomatic relief only for itchy cutaneous LP; does not substitute for adequately potent lesion-directed therapy.