Lichen planus (cutaneous)
LP; lichen ruber planus; lichen planopilaris (follicular); Lassueur-Graham-Little syndrome
Lichen planus is a chronic immune-mediated inflammatory dermatosis affecting skin, mucosae, hair and nails. The classical cutaneous form presents with pruritic violaceous flat-topped polygonal papules β the "5 Ps" β with delicate white Wickham striae on the surface. UK relevance to skin oncology: chronic hypertrophic lichen planus on the legs carries a recognised risk of cutaneous SCC development after years; oral and genital lichen planus carry a 1β3% SCC progression risk (see oral LP); lichen planus-like keratosis (BLK) is a benign solitary entity (different histology). Treatment is largely topical / intralesional / phototherapy; aggressive disease may need systemic immunosuppression.
Classical cutaneous LP β "5 Ps"
- Pruritic, Purple (violaceous), Polygonal, Papular, Planar (flat-topped).
- Surface β delicate Wickham striae (fine white reticulated lines visible with magnifying glass / mineral oil / dermoscopy).
- Common sites β flexor wrists, dorsal hands, ankles, lower back, oral and genital mucosae.
- KΓΆbner phenomenon β new lesions at sites of trauma.
- Onset usually 30β60 years; women slightly over-represented.
Variants
- Hypertrophic LP β thick verrucous plaques typically on shins / ankles; chronic; intensely pruritic; SCC risk over years.
- Linear LP β along Blaschko lines.
- Annular LP β particularly in genital and axillary areas.
- Bullous LP β vesicles / bullae within LP plaques.
- Lichen planopilaris (follicular LP) β scarring alopecia of scalp; perifollicular erythema and follicular hyperkeratosis; pseudopelade-like central scarring. Frontal fibrosing alopecia is a variant.
- Mucosal LP β oral (see oral LP) and genital (see lichen sclerosus overlap).
- Nail LP β longitudinal grooves, ridging, pterygium formation; permanent nail loss.
- Lichen planus pigmentosus β Fitzpatrick IVβVI; pigmented patches, particularly face.
SCC risk in chronic LP
- Hypertrophic LP on the legs β recognised SCC risk after decades of chronic disease.
- Oral LP β 1β3% lifetime SCC risk; erosive variant highest risk; see oral LP.
- Genital (erosive) LP β carries a recognised but lower and less well-quantified SCC risk; a distinct entity from lichen sclerosus, with which it can clinically overlap (their malignant risks should not be equated).
- Biopsy any new keratotic / ulcerated / non-healing area within chronic LP plaques.
- Annual surveillance of high-risk variants.
Diagnosis
- Skin biopsy:
- Hyperkeratosis without parakeratosis; wedge-shaped hypergranulosis.
- Sawtooth rete ridges.
- Band-like (lichenoid) lymphocytic infiltrate at the dermoepidermal junction.
- Apoptotic keratinocytes (Civatte bodies / colloid bodies).
- Pigment incontinence.
- Direct immunofluorescence β fibrinogen and IgM along dermoepidermal junction; supplementary.
- Hepatitis C serology β recognised association in some series; check in atypical / refractory cases.
- Drug history β lichenoid drug eruption (ACE inhibitors, beta-blockers, antimalarials, NSAIDs, ICI).
Management
- Localised disease β superpotent topical corticosteroid; topical tacrolimus.
- Generalised or hypertrophic β narrowband UVB or PUVA; intralesional triamcinolone for thick plaques.
- Refractory / severe β oral acitretin, methotrexate, oral steroids (short course), hydroxychloroquine, ciclosporin, mycophenolate.
- Mucosal LP β topical superpotent steroid in adhesive base, topical tacrolimus, intralesional steroid.
- Lichen planopilaris β topical / intralesional steroids, hydroxychloroquine, oral antimalarials, mycophenolate; preventive of further scarring rather than reversing scarring alopecia.
- Surveillance of high-risk variants for SCC; biopsy any change.
References
- Le Cleach L, Chosidow O. Lichen planus. N Engl J Med; 2012.
- Solomon LW. Chronic ulcerative lichen planus β current concepts. Periodontol 2000; 2008.
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