Lichen planus

Meet the patient

A 52-year-old woman has three months of intensely itchy, purple, shiny bumps on her flexor wrists and ankles that cropped up exactly along the scratch marks she cannot stop making. Each papule carries a lacework of fine white lines, her buccal mucosa burns, and two fingernails are ridging and splitting.^[1][2]

Two questions sit under every lichen planus stem: is this classical LP or a named variant? (morphology and site decide) and which sites carry malignant or scarring risk I cannot miss? (mouth, genitalia, nail, scalp). Hold those two and the rest of the page slots into place.^[1]

One disease, one interface, many faces

LP is not a family of separate eruptions — it is a single autoimmune attack on the basal layer, read through whatever skin or mucosa it lands on. The fundamental lesion is a violaceous, flat-topped, polygonal papule that may coalesce into plaques, and the disease is classified by site and morphology rather than by any severity score.^[1]

It touches roughly 0.5 to 2 percent of people worldwide, peaks between 30 and 60 years, and runs a chronic relapsing course — classical cutaneous disease often fading within one to two years, while oral, genital, nail and follicular forms persist far longer.^[2]

Etymology for viva gold: lichen is Latin for 'tree moss' — the papules were said to resemble the crusty moss on tree bark — and planus simply means 'flat'. Two dead metaphors, one living disease that still looks exactly as its name describes.^[2]

The 6 P's — the cluster rule that earns the morphology marks

Do not recite morphology as a list. Cluster it, and the marks stay. The classical cutaneous papule is:^[1]

1. Pruritic — often intensely, and the itch usually precedes rash patient remembers.
2. Purple — a violaceous hue no common papulosquamous rival shares.
3. Polygonal — angular and sharp-edged, never round.
4. Planar — flat-topped, a surface you can plane a fingernail across.
5. Papules and Plaques — 2 to 10 mm, coalescing into larger plaques.^[1][2]

The sixth P is the one juniors drop — Place: the sites examiners test are the flexor wrists and forearms, ankles, lumbar back and genitalia, plus the easy-to-miss penile, perifollicular, palmoplantar and mucosal skin.^[1]

Wickham, Koebner and the colour purple — three signs that close the call

Three bedside signs settle lichen planus before the biopsy returns.^[1]

• Wickham striae — fine white reticular lines over the surface of the papule, the clinical face of wedge-shaped hypergranulosis and the closest thing LP has to a pathognomonic sign.
• Koebner phenomenon — new papules arising in lines of trauma, scratch and surgical scars; our patient's wrist lesions tracking her scratch marks are textbook.
• The violaceous hue — purple-red, never the salmon-pink of psoriasis or the brown of tinea.^[1][2]

The classic trap: psoriasis and eczema Koebnerise too, so Koebner alone never diagnoses LP. It is the combination of purple polygonal papules, Wickham striae and Koebner that closes the call — then reach for the dermatoscope.^[1]

Dermoscopy turns Wickham striae into pearly white or grey reticular lines on a violaceous background, with dotted or linear vessels at the rim — a pattern that cleanly separates LP from psoriasis (regular dotted vessels) and eczema (yellow scale, irregular vessels).^[6]

Which site? — the variants face-off

Classical cutaneous LP is only about half of what you will meet; the rest are named variants, and the site usually names the risk. Every variant shares the interface histology but wears a different clinical face, so learn each by where it sits and what it threatens.^[1][2]

^{[1] [2]}

The discriminator line beneath the table: striae mean LP, erosion means surveil for cancer, pterygium means permanent, perifollicular means scarring.^[1]

^{[1] [18]}

Two variants hide their own danger. Hypertrophic plaques on the shins can spawn squamous cell carcinoma inside a chronic lesion, so biopsy any ulcerated or verrucous nodule that will not settle; and annular LP on the penis mimics tinea, granuloma annulare and porokeratosis until dermoscopy shows the Wickham-edged rim.^[1][6]

Hepatitis C — the association examiners always probe

LP and hepatitis C travel together, and the link is bidirectional. A 2023 meta-analysis found HCV seropositivity roughly four times more frequent in LP patients, and LP more frequent in HCV-positive patients — strongest across Mediterranean, Middle-Eastern and Asian populations.^[7]

For oral LP specifically the signal is even cleaner: meta-analyses show a marked rise in the odds of HCV infection in oral LP, and the older 2010 review first established the same association.^[8][14]

The practical rule: offer hepatitis C serology to every patient with oral or genital LP, and to anyone from a high-prevalence region — however classical the skin lesions look. Consider hepatitis B and HIV alongside it per local protocol.^[1][7]

Not every purple papule is LP — the drug-eruption trap

Before you commit to idiopathic LP, take a drug history. Lichenoid drug eruptions mimic LP clinically but are driven by a medication, often run a photodistributed pattern, and classically show eosinophils and parakeratosis on a biopsy that true LP does not.^[2]

The repeat-offender list to recite in a viva: antimalarials, beta-blockers, ACE inhibitors, NSAIDs, methyldopa, penicillamine, gold, lithium, TNF-alpha inhibitors and immune checkpoint inhibitors.^[2]

What juniors write versus what gets marks: "lichen planus" earns a prescription; "lichenoid drug eruption — withdraw the agent" earns the patient getting better. Read the drug list and biopsy before reaching for immunosuppression.^[1][2]

Why it happens — basal keratinocytes under T-cell attack

LP is a cell-mediated autoimmune attack on basal keratinocytes at the dermo-epidermal junction. Something — a modified self-peptide, a viral antigen such as HCV, or a drug hapten — is presented to CD8-positive cytotoxic T-cells, which home to the basal layer and kill keratinocytes through granzyme B, perforin and the Fas-Fas-ligand pathway.^[1]

Death of the basal layer produces the signature vacuolar interface change, and a cytokine loop of TNF-alpha, IFN-gamma, IL-6, IL-17 and IL-23 amplifies recruitment — which is why the infiltrate settles into a dense band and why wedge-shaped hypergranulosis, and with it Wickham striae, appear.^[1][2]

Read the biopsy — the histology that closes the case

A 4-mm punch biopsy of an active lesion closes atypical cases and separates LP from its drug-induced and lupus mimics. Reproduce the triad examiners quote:^[1]

• Sawtooth rete ridges — the dermo-epidermal junction turns jagged and pointed.
• Band-like lymphocytic infiltrate — a dense dermal lymphocytic sheet hugging the epidermis.
• Civatte, or colloid, bodies — apoptotic basal cells dropped into the papillary dermis.^[1][2]

Add wedge-shaped hypergranulosis and compact orthokeratosis and the picture is complete — and wedge-shaped hypergranulosis is exactly what you are seeing at the bedside as Wickham striae.^[1]

Direct immunofluorescence is not needed for classical LP, but earns its place when an erosion could be pemphigus, pemphigoid or lupus: LP shows shaggy fibrinogen and cytoid bodies with no linear deposit, pemphigoid shows linear IgG and C3 at the basement membrane, and lupus shows granular IgG and C3.^[1]

The biopsy discriminator that wins marks: a lichenoid drug eruption layers eosinophils and parakeratosis, and often a deeper perivascular infiltrate, onto the LP pattern — hunt for them before you label the disease idiopathic.^[1][2]

The mimics — discriminators, not lists

Differentials earn marks by discriminator, not by enumeration. Run them by the site in front of you.^[1]

^{[1] [2] [5] [11]}

The erosive mouth is a cancer-risk for life

Erosive oral LP is an oral potentially malignant disorder, and the surveillance commitment is lifelong. The WHO sorts oral LP into reticular, erosive, atrophic, plaque-like, papular and bullous patterns — reticular lacy Wickham striae on the buccal mucosa is the commonest and the benign end, while erosive disease is the painful, high-morbidity end that carries the malignant risk.^[1][9]

The cumulative risk of oral squamous cell carcinoma is low but real, and the patients who transform are the ones with persistent ulceration, induration, a new plaque, bleeding, reduced tongue mobility or cervical lymphadenopathy.^[9]

The non-negotiable plan: surveillance every 3 to 6 months, biopsy any suspicious area, and drive smoking and alcohol cessation at every visit. Missing a cancer inside an erosive LP is the preventable harm this disease kills with.^[1][9]

Pterygium is permanent — nail and scalp LP scar

Two LP sites leave irreversible damage if you wait: the nail matrix and the hair follicle. Treat both early, because you cannot regrow what has scarred.^[5][11]

Nail LP shows longitudinal ridging, fissuring, thinning, onycholysis and trachyonychia — and dorsal pterygium, the proximal nail fold fusing onto the nail plate, is the sign that says the matrix has scarred. Pterygium does not reverse; isolated nail LP occurs in up to 10 percent of patients, and around half of nail LP patients also have skin, mucosal or scalp disease.^[5]

Lichen planopilaris gives perifollicular violaceous erythema and scale at the scalp margin with progressive scarring alopecia, while frontal fibrosing alopecia is its postmenopausal cousin — a band-like frontotemporal recession with eyebrow loss. The goal is to halt disease activity, not to regrow hair, because follicular destruction is permanent.^[11]

The treatment ladder — topical, light, then systemic

Start topical, add light, and reserve systemics for widespread, erosive, hypertrophic, nail or follicular disease. The ladder is the same whatever the site; what changes is which rung you reach for first.^[1]

^{[1] [3] [4] [10]}

Choosing the systemic agent by phenotype — each drug earns its niche, and the retinoids and antimetabolites are all teratogenic, so contraceptive counselling is mandatory before the first prescription.^[1]

^{[1] [3] [12] [10]}

Oral LP deserves its own sentence. Topical clobetasol propionate 0.05% gel or fluocinonide 0.05% gel is the cornerstone for symptomatic disease, with topical tacrolimus 0.1% as the steroid-sparing alternative for erosive and refractory cases; watch for candidal superinfection with prolonged topical steroid use.^[4][13]

Nail LP leans on steroid injections into the nail apparatus — a retrospective series of isolated nail LP reported moderate-to-good improvement in most patients after repeated intramatricial and intramuscular triamcinolone acetonide sessions — with oral retinoids for progressive disease; the review names intralesional or intramuscular corticosteroid injections and oral retinoids as the treatment mainstays, and the risk of permanent disfigurement is exactly why early diagnosis and prompt treatment matter before pterygium and anonychia set in.^[5][15]

Scalp LP — lichen planopilaris and frontal fibrosing alopecia. In the network meta-analysis, topical clobetasol plus hydroxychloroquine with N-acetylcysteine came out on top, while methotrexate and cyclosporine did worse than hydroxychloroquine; pioglitazone and mycophenolate mofetil belong only after inadequate response to better-supported agents. For FFA, 5-alpha-reductase inhibitors, intralesional steroids and hydroxychloroquine carry the highest level of evidence. The aim is to stop activity early, because follicles that have died do not regrow.^[11][16]

The high-yield numbers

^{[1] [2] [7] [9]}

Cutaneous disease usually resolves within one to two years but often leaves post-inflammatory hyperpigmentation, especially in skin of colour; oral, genital, nail and follicular forms persist longer and set the follow-up rhythm — limited cutaneous LP at 4-8 weeks, erosive oral LP at 3-6 monthly surveillance, nail LP at 4-6 weekly initially, and lichen planopilaris quarterly.^[1][9]

Pregnancy, children and the elderly

Special populations bend the ladder, not the diagnosis. In pregnancy, favour topical corticosteroids and calcineurin inhibitors at the lowest potency for the shortest time, and avoid acitretin, methotrexate and mycophenolate — acitretin stays teratogenic for three years after stopping.^[1]

In children, oral LP and nail disease occur but drug reactions and contact allergens must be excluded first; use lower-potency topical steroids and watch growth if systemics are needed. In the elderly, drug-induced lichenoid eruptions and polypharmacy dominate, potent steroids atrophy thin skin, so prefer calcineurin inhibitors on the face and folds and monitor bone, glucose and blood pressure if systemic steroids are required.^[1][2]

The mantra

Topical first, light next, systemic last — but the erosive mouth is a cancer-risk for life, and the pterygium nail is permanent. Say it as one breath on the ward round and you have the whole disease in a sentence.^[1]

Ward-round test

A patient has itchy purple polygonal papules on the wrists with white surface lines — what are the lines, and what do they mean histologically?ShowHide

The lines are Wickham striae, fine white reticular markings over the papule surface, and histologically they correspond to wedge-shaped hypergranulosis. They are the closest thing LP has to a pathognomonic sign.^[1][6]

An erosive oral LP patient returns with a new indurated ulcer on the buccal mucosa — what do you do, and why?ShowHide

Biopsy it the same clinic visit. Erosive oral LP is an oral potentially malignant disorder, and a new indurated ulcer, plaque, bleeding or reduced tongue mobility raises squamous cell carcinoma until proven otherwise — the disease is surveilled every 3-6 months precisely to catch this.^[1][9]

A 70-year-old develops widespread purple papules two months after starting a new blood-pressure tablet — what is the diagnosis, and how does the biopsy differ from idiopathic LP?ShowHide

Think lichenoid drug eruption, with beta-blockers and ACE inhibitors high on the list. Biopsy shows the LP pattern plus eosinophils and parakeratosis, often with a deeper perivascular infiltrate; the move is to withdraw the drug, not to start immunosuppression.^[1][2]

A postmenopausal woman has a receding frontotemporal hairline and loss of eyebrows — name the variant, one evidence-backed systemic, and the goal of treatment.ShowHide

This is frontal fibrosing alopecia, a variant of lichen planopilaris within the same lichenoid spectrum. Hydroxychloroquine is one of the systemics with the best evidence in FFA, alongside 5-alpha-reductase inhibitors and intralesional steroids, and the goal is to halt disease activity, not regrow hair — follicular destruction is permanent.^[11][16][17]

References18ShowHide

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