Lichen planus (LP) is an acute or chronic inflammatory dermatosis involving skin and/or mucous

membranes, characterized by flat-topped (Latin planus, "flat"), pink to violaceous, shiny, pruritic
polygonal papules on the skin and milky white reticulated papules in the mouth. The features of
the lesions have been designated as the four P'spapule, purple, polygonal, pruritic.
Epidemiology and Etiology
Age of Onset
30 to 60 years.
Sex
Females > males.
Race
Hypertrophic LP more common in blacks.
Etiology
Idiopathic in most cases but it is evident that cell-mediated immunity plays a major role.
Majority of lymphocytes in the infiltrate are CD8
+
and CD45Ro
+
(memory) cells. Drugs, metals
(gold, mercury), or infection [hepatitis C virus (HCV)] result in alteration in cell-mediated
immunity. There could be HLA-associated genetic susceptibility that would explain a
predisposition in certain persons. Lichenoid lesions of chronic graft-versus-host disease (GVHD)
of skin are indistinguishable from those of LP.
History
Onset
Acute (days) or insidious (over weeks). Lesions last months to years, asymptomatic or pruritic;
sometimes severe pruritus. Mucous membrane lesions are painful, especially when ulcerated.
Physical Examination
Skin Lesions
Papules, flat-topped, 1 to 10 mm, sharply defined, shiny (Figs. 7-4 and 7-5). Violaceous, with
white lines (Wickham's striae) (Fig. 7-4), seen best with hand lens after application of mineral
oil. Polygonal or oval. Grouped (Figs. 7-4 and 7-5), linear (isomorphic phenomenon), annular, or
disseminated scattered discrete lesions when generalized (Fig. 7-6). In dark-skinned individuals,
postinflammatory hyperpigmentation is common.

Sites of Predilection
Wrists (flexor), lumbar region, shins (thicker, hyperkeratotic lesions), scalp, glans penis, mouth
Variants
Hypertrophic
Large thick plaques arise on the foot (Fig. 7-5A) and shins (Fig. 7-5B); more common in black
males. Although typical LP papule is smooth, hypertrophic lesions may become hyperkeratotic.
Follicular
Individual keratotic-follicular papules and plaques that lead to cicatricial alopecia. Spinous
follicular lesions, typical skin and mucous membrane LP, and cicatricial alopecia of the scalp are
called Graham Little syndrome. (See Section 29.)
Vesicular
Vesicular or bullous lesions may develop within LP patches or independent of them within
normal-appearing skin. There are direct immunofluorescence findings consistent with bullous
pemphigoid, and the sera of these patients contain bullous pemphigoid IgG autoantibodies (see
Section 6).
Actinicus
Papular LP lesions arise in sun-exposed sites, especially the dorsa of hands and arms.
Ulcerative
LP may lead to therapy-resistant ulcers, particularly on the soles, requiring skin grafting.
Mucous Membranes
Some 40 to 60% of individuals with LP have oropharyngeal involvement.
Reticular LP
Reticulate (netlike) pattern of lacy white hyperkeratosis on buccal mucosa (see Fig. 31-16), lips
(Fig. 7-7), tongue, gingiva; the most common pattern of oral LP.
Erosive or Ulcerative LP
Superficial erosion with/without overlying fibrin clot; occurs on tongue and buccal mucosa (see
Fig. 31-17); shiny red painful erosion of gingiva (desquamative gingivitis) (see Fig. 31-18) or
lips (Fig. 7-7). Carcinoma may very rarely develop in mouth lesions.
Genitalia
Papular (see Fig. 32-8), annular, or erosive lesions arise on penis (especially glans), scrotum,
labia majora, labia minora, vagina.
Hair and Nails
Scalp
Atrophic scalp skin with scarring alopecia.
Nails
Destruction of nail fold and nail bed with longitudinal splintering (see Fig. 30-10).
Lichen Planuslike Eruptions
Lichen planuslike eruptions closely mimic typical LP, both clinically and histologically. They
occur as a clinical manifestation of chronic GVHD; in dermatomyositis, and as cutaneous
manifestations of malignant lymphoma but may also develop as the result of therapy with certain
drugs and after industrial use of certain compounds
Table 7-1 Agents Inducing Lichen Planus and Lichenoid Reactions

Less-common Inducers
Common Inducers Commonly Prescribed Drugs Uncommonly Prescribed Drugs
Gold salts ACE inhibitors Methyldopa
Beta blockers Calcium channel blockers Antitubercular
Antimalarials Sulfonylurea hypoglycemic agents Sulfasalazine
Thiazide diuretics Nonsteroidal antiinflammatory drugs Heavy metals (arsenic, mercury)
Furosemide Ketoconazole Lithium
Spironolactone Tetracycline Iodides and radiocontrast media
Penicillamine Phenothiazine derivatives Antimony
Carbamazepine

Diagnosis and Differential Diagnosis
Clinical findings confirmed by histopathology.
Skin Lesions
Papular LP
Chronic cutaneous lupus erythematosus, psoriasis, pityriasis rosea, eczematous dermatitis,
lichenoid GVHD; superficial basal cell carcinoma, Bowen's disease (in situ squamous cell
carcinoma).
Hypertrophic LP
Psoriasis vulgaris, lichen simplex chronicus, prurigo nodularis, stasis dermatitis, Kaposi's
sarcoma.
Drug-Induced LP
See Table 7-1.
Mucous Membranes
Leukoplakia, pseudomembranous candidiasis (thrush), HIV-associated hairy leukoplakia, lupus
erythematosus, bite trauma, mucous patches of secondary syphilis, pemphigus vulgaris, bullous
pemphigoid.
Laboratory Examination
Dermatopathology
Inflammation with hyperkeratosis, increased granular layer, irregular acanthosis, liquefaction
degeneration of the basal cell layer, and bandlike mononuclear infiltrate that hugs the epidermis.
Degenerate keratinocytes (colloid, Civatte bodies) are found at the dermal-epidermal junction.
Direct immunofluorescence reveals heavy deposits of fibrin at the junction and IgM and, less
frequently, IgA, IgG, and C3 in the colloid bodies.
Course
Cutaneous LP usually persists for months, but in some cases, for years; hypertrophic LP on the
shins and oral LP often for decades. The incidence of oral cancer (squamous cell carcinoma) in
individuals with oral LP is increased by 5%; patients should be followed at regular intervals.
Management
Topical Therapy
Glucocorticoids
Topical glucocorticoids with occlusion for cutaneous lesions. Intralesional triamcinolone (3
mg/mL) is helpful for symptomatic cutaneous or oral mucosal lesions and lips.
Cyclosporine and Tacrolimus Solutions
Retention "mouthwash" for severely symptomatic oral LP.
Systemic Therapy
Cyclosporine
In very resistant and generalized cases, 5 mg/kg per day will induce rapid remission, quite often
not followed by recurrence.
Glucocorticoids
Oral prednisone is effective for individuals with symptomatic pruritus, painful erosions,
dysphagia, or cosmetic disfigurement. A short, tapered course is preferred: 70 mg initially,
tapered by 5 mg.
Systemic Retinoids (Acitretin)
1 mg/kg per day is helpful as adjunctive measure in severe (oral, hypertrophic) cases, but usually
additional topical treatment is required.
PUVA Photochemotherapy
In individuals with generalized LP or cases resistant to topical therapy.
Reports of Other Successful Treatment
Mycophenolate mofetil, heparin analogues (enoxaparin) in low doses have antiproliferative and
immunomodulatory properties; azathioprine.