Lichen planus is a chronic inflammatory skin disorder of unknown cause that affects less than 1% of the population. It is believed to be immune-mediated and involves CD8+ T cells attacking basal keratinocytes. Clinically, it presents with pruritic, purple, polygonal papules or plaques on the wrists, ankles, lower back and genitals. The diagnosis is made through skin biopsy demonstrating characteristic histopathological features. Topical corticosteroids are the mainstay of treatment, while phototherapy and systemic corticosteroids may be used for more severe or widespread disease.

1. Lichen planus
INTRODUCTION —
Uncommon disorder
Unknown cause
EPIDEMIOLOGY —
Prevalence- <1%
Age- 30-60 years
Gender – M=F
ETIOLOGY —
GENETICS- HLA B7, HLA B8, HLABw35
ENVIRONMENTAL
1) Hepatitis C virus —
2) Drugs — (LICHENOID DRUG ERUPTION)
Antihypertensives- ACE inhibitors, CCB, diuretics
Antimalarials- Chloroquine, Hydroxychloroquine
Gold salts
penicillamine
PATHOGENESIS
Not known.
An immune-mediated mechanism
CD8+ T cells, directed against basal keratinocytes
Upregulation of intercellular adhesion molecule-1 (ICAM-1) and cytokines associated with a
Th1 immune response,

2. CLINICAL FEATURES —
Cutaneous lichen planus
Pruritic
Purple (actually a slight violaceous hue)
Polygonal
Papules or plaques
Plane (flat topped)
“Wickham’s striae”- fine white lines on the surface, appreciated through oil or water.
Sites- ankles, flexor aspects of wrists, lower back
Koebner reaction
.
Variants —
●Hypertrophic lichen planus – intensely pruritic,
Flat-topped
Anterior lower legs.
Cutaneous squamous cell carcinoma
●Annular lichen planus – Annular plaques
Genitalia
●Bullous lichen planus – vesicles or bullae on existing cutaneous lesions
Because of intense inflammation
●Actinic lichen planus – photo distributed
Annular plaques with halo

3. Middle East, India, and east Africa
●Lichen planus pigmentosus gray-brown or dark brown macules
Sun-exposed or flexural areas
●Inverse lichen planus – intertriginous sites, such as the axillae, inguinal creases
●Atrophic lichen planus – violaceous, round or oval, atrophic plaques.
●Lichen planopilaris (follicular lichen planus) – follicular papules
Scalp
Graham little picardi syndrome-
follicular papules + cicatricial alopecia of scalp + non cicatricial alopecia of axillary or pubic
hair
Overlap syndromes —
●Lichen planus pemphigoides – overlapping features of lichen planus and bullous
pemphigoid.
bullae in sites of previously normal appearing skin.
DIF- linear deposition of IgG and C3 at the dermal-epidermal junction.
●Lichen planus-lupus erythematosus overlap syndrome –
skin lesions with clinical, histologic, and/or immunopathologic features of both diseases.

4. Other forms of lichen planus —
●Nail lichen planus – longitudinal ridging,
nail plate thinning,
longitudinal fissuring,
trachyonychia
erythema of the lunula
pterygium
●Lichen planopilaris – lichen planus of scalp scalp.
Patients present with areas of cicatricial hair loss with keratotic
follicular papules
●Oral lichen planus - lacelike Wickham's striae on the buccal mucosa
papular, atrophic, or erosive lesions
●Genital lichen planus – violaceous papules on the glans penis or vulva.
●Esophageal lichen planus – dysphagia or odynophagia
endoscopic findings include pseudomembranes, friable and
inflamed mucosa, submucosal papules, lacy white plaques,
erosions, strictures, and other abnormalities
●Otic lichen planus – external auditory canals and tympanic membranes.
erythema, induration, and stenosis of the external auditory canal;

5. otorrhea; and hearing
DIAGNOSIS —
The physical examination –
entire cutaneous surface
scalp
oral cavity
external genitalia.
Biopsy — HISTOPATHOLOGY —
●Hyperkeratosis without parakeratosis
●Vacuolization of the basal layer
●Civatte bodies (apoptotic keratinocytes) in the lower epidermis
●Wedge-shaped hypergranulosis, "saw-tooth" shaped rete ridges
●Small clefts at the dermal-epidermal junction (Max-Joseph spaces)
●Band-like lymphocytic infiltrate at the dermal-epidermal junction
●Eosinophilic colloid bodies (apoptotic keratinocytes) in the papillary dermis
●Pigment incontinence (most prominent in dark-skinned individuals)
Direct immunofluorescence -
in patients with bullous lesions to differentiate the condition from an autoimmune blistering
disease.
-colloid bodies in the papillary dermis that stain for complement and immunoglobulins
(especially IgM)
irregular fibrin deposition along the dermal-epidermal junction
Dermoscopy — Wickham’s striae
ADDITIONAL TESTING —

6. test for HCV infection
NATURAL HISTORY —
50% resolve in 1 year
80% resolve in 3 year
Almost all resolve in 5 year
TREATMENT —
Topical corticosteroids —
mainstay of treatment
trunk and extremities - high potency or super high potency topical corticosteroid cream or
ointment twice daily
intertriginous or facial skin- mid-potency or low-potency corticosteroid creams or ointments.
Intralesional corticosteroids —
hypertrophic lichen planus
triamcinolone acetonide in a concentration of 2.5 to 10 mg/mL.
maximum- 40 mg per treatment session.
repeated after four to six weeks.
Systemic glucocorticoids —
Generalized disease
short course of an oral glucocorticoid when acute control of cutaneous lichen planus is necessary
30 to 60 mg daily for four to six weeks followed by a taper of the dose to discontinuation over
the next four to six weeks
Phototherapy —
UVB and PUVA

7. Narrowband UVB is the most common modality used
Oral retinoids —
disease that cannot be managed with local corticosteroids or phototherapy.
High risk of side effects
Pregnancy category X
Other treatments —
Oral antihistamines – for pruritis
Thalidomide
Dapsone
Griseofulvin
HCQS
sulfasalzine