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Basic Information

Author: Fred F. Ferri, MD

Definition

Lichen planus (LP) refers to an idiopathic pruritic, papulosquamous disease with characteristic histopathologic and clinical features, manifesting with a papular skin eruption characteristically found over the flexor surfaces of the extremities, genitalia, and mucous membranes.

Synonyms

  • Lichen
  • Lichen planus et atrophicus
  • LP
ICD-10CM CODES
L43Lichen planus
L43.0Hypertrophic lichen planus
L43.1Bullous lichen planus
L43.9Lichen planus, unspecified
L43.8Other lichen planus
Epidemiology & Demographics
Incidence:

1/100 new patients seen in dermatology clinics in the U.S. is diagnosed with LP.

Prevalence:

440 cases/100,000 persons

Predominant Sex:

Found equally between males and females (1:1)

Predominant Age:

Usually found in people between the ages of 30 and 60 yr

Risk Factors:

  • Associated with other autoimmune disorders (e.g., primary biliary cirrhosis, myasthenia gravis, ulcerative colitis, diabetes)
  • Associated with hepatitis C infection
  • Drug-induced form affects any area of the body surface (e.g., β-blocker, methyldopa, penicillamine, quinidine, NSAIDs, ACE inhibitors, sulfonylurea agents)
Physical Findings & Clinical Presentation

LP often manifests with pruritic, flat-topped violaceous papules, but the clinical presentation varies depending on the area involved. Classically, lesions are described with the six "P"s: Purple, pruritic, planar, polygonal, papule, and plaque. In some patients, fine white lines are visible across the surface of the lesions, known as Wickham striae.

History:

  • Usually starts on an extremity and may remain localized or spread to involve other areas over a 1- to 4-mo period
  • Pruritic

Physical findings:

  • Anatomic distribution:
    1. 1.Flexor surface of wrists, forearms, shins, and upper thighs
    2. 2.Neck and back area
    3. 3.Nails (5% to 10% of patients)
    4. 4.Scalp (lichen planopilaris)
    5. 5.Oral mucosa, buccal mucosa, tongue, gingiva, and lips; oral LP can cause extensive desquamative gingivitis
    6. 6.Vulva (Fig. E1), penis (Fig. E2)

Figure E1 Lichen planus of the vulva with a white, lacelike pattern and erythema.

(From Crum CP et al: Diagnostic gynecologic and obstetric pathology, ed 3, Philadelphia, 2018, Elsevier.)

Figure E2 Lichen planus of the penis.

(From Swartz MH et al: Textbook of physical diagnosis: history and examination, ed 8, Philadelphia, 2020, Elsevier.)

Genital mucosa:

  • Lesion configuration:
    1. 1.Linear
    2. 2.Annular (more common)
    3. 3.Reticular pattern noted on oral mucosa and genital area
  • Lesion morphology:
    1. 1.Papules most common presentation (flat, smooth, shiny) (Fig. E3)
    2. 2.Hypertrophic
    3. 3.Follicular
    4. 4.Vesicular
  • Color:
    1. 1.Dark red, bluish red, purplish-violaceous color is noted in cutaneous LP (Fig. E4).
    2. 2.Individual lesions characteristically have white lines visible (Wickham striae) (Fig. E5).
    3. 3.Oral and genital LP has a reticular network of white lines that may be raised or annular in appearance (Fig. E6).
  • Scalp lesions may result in alopecia.
  • The plaques of LP may be hypertrophic but show the characteristic violaceous coloration and intense hyperpigmentation (Fig. E7).

Figure E3 Flat-topped, purple, polygonal papules of lichen planus.

(From Kliegman RM et al: Nelson textbook of pediatrics, ed 22, Philadelphia, 2025, Elsevier.)

Figure E4 Shiny, flat-topped, polygonal, violaceous papules of lichen planus.

Note the Wickham striae (linear, whitish-gray streaks) on the surface.

(From Paller AS, Mancini AJ: Hurwitz clinical pediatric dermatology: a textbook of skin disorders of childhood and adolescence, ed 5, Philadelphia, 2016, Elsevier.)

Figure E5 A and B, Lichen planus.

Note the fine, reticulated white scales.

(From Swartz MH et al: Textbook of physical diagnosis, history and examination, ed 8, Philadelphia, 2020, Elsevier.)

Figure E6 Oral lichen planus.

Wickham striae on the buccal mucosa.

(From Paller AS, Mancini AJ: Hurwitz clinical pediatric dermatology: a textbook of skin disorders of childhood and adolescence, ed 5, Philadelphia, 2016, Elsevier.)

Figure E7 Lichen planus.

The plaques of lichen planus may be hypertrophic but show the characteristic violaceous coloration and intense hyperpigmentation.

(From Paller AS, Mancini AJ: Hurwitz clinical pediatric dermatology: a textbook of skin disorders of childhood and adolescence, ed 5, Philadelphia, 2016, Elsevier.)

Etiology

LP is characterized by an immunologic reaction mediated by CD8+ T cells. These cells induce keratinocytes to undergo apoptosis. Although the inflammatory reaction is believed to be autoimmune, the antigen targeted by these effector T lymphocytes is unknown.

Diagnosis

Differential Diagnosis

  • Drug eruption, psoriasis, Bowen disease, leukoplakia, candidiasis, lupus rash, secondary syphilis, seborrheic dermatitis, chronic graft-versus-host disease
  • Table E1 summarizes key features of LP variants

TABLE E1 Key Features of LP Variants

Acute (exanthematous) LPRapid onset of disseminated lesions; heals with PIH; rapidly self-resolves (3-9 mo)
Actinic LP (LP subtropicus)Most common in Middle Eastern and Indian patients (also Africans); young adults or children; onset in spring or summer on sun-exposed sites (face, forehead > dorsal UE, neck, intertriginous sites); comprised of discoid papules/plaques (hyperpigmented focus with hypopigmented rim) or melasmalike patches (less common)
Annular LPUsually asymptomatic; annular plaques with raised violaceous-white edge with central clearing; resembles GA but is scaly; axilla is most common site, followed by penis
Atrophic LPEnlarging small violaceous, annular plaques with centrally depressed/atrophic, hyperpigmented area; clinically resembles early morphea or LS&A legs most common site
Bullous LPBlisters develop on longstanding LP lesions due to extensive epidermal damage (expanded Max-Joseph spaces)
Drug-induced LP (lichenoid drug eruption)
  • In comparison with idiopathic LP: patients typically 10 yr older (mid 60s); often spares "classic LP sites"; lesions more generalized and more eczematous or psoriasiform than classic morphology; Wickham striae absent; frequently photodistributed (esp. HCTZ)-various drugs have spectrum of activity in UVB range; spares mucous membranes; histology: like LP but frequently has parakeratosis, deeper infiltrate, eosinophils, apoptotic keratinocytes in higher levels of epidermis; average latency period of 12 mo after initial medication exposure; delayed resolution (months)
  • Culprits: ACE inhibitors, antimalarials, β-blockers, gold, lithium, mercury amalgam, allopurinol, anticonvulsants, antiretrovirals, NSAIDs, penicillamine, carbamazepine, diltiazem, thiazide diuretics, quinidine, TNF-α inhibitors
Genital LP
  • Men: annular LP on glans penis
  • Women: vulvar LP is most commonly erosive and 70% have concomitant vaginal involvement; often a/w oral involvement ("vulvovaginal-gingival syndrome:" protracted course with scarring, chronic pain, dyspareunia, and nail involvement)
Hypertrophic LP (aka "LP verrucosus")Extremely pruritic, thick, scaly plaques; most commonly on dorsal feet/shins, wrists; symmetric; lasts longer (avg. duration 6 yr); may multiple keratoacanthomas or follicular-based SCCs; biopsy may show many eosinophils
Inverse LPAxilla > inguinal and inframammary folds > antecubital and popliteal fossae; poorly defined hyperpigmentation usually present (thus may overlap with LP pigmentosus)
Linear LPRefers to lesions that appear spontaneously (not due to koebnerization) in a Blaschkoid distribution; favors younger patients (20-30 yo); likely due to somatic mosaicism
Oral LPOver half of patients with cutaneous LP have oral involvement
Reticular LP: most common; lacy white raised linear lines; usually asymptomatic; most commonly on bilateral buccal mucosa > gingivae > tongue > lips
Atrophic, erosive, and bullous oral LP: more painful, F > M; must check for esophageal and genital involvement; may progress to SCC (1%-2%)
Nail LPSeen in 10% of LP patients; usually affects several nails; classic findings = longitudinal ridging, lateral thinning, fissuring, and dorsal pterygium; kids lack these other nail findings but may present as 20-nail dystrophy (rare in adults)
LP/LE overlapAcral sites with bullae, ulceration, nail loss, and pain; overlapping features of lupus and LP seen clinically and on H&E/DIF
Palmoplantar LPCommonly ulcerative (esp. on soles); occurs in 30-40 yo age group; extremely painful and recalcitrant to therapy; usually with typical LP elsewhere
LP pemphigoidesVesicobullous lesions occur anywhere on skin (most commonly on uninvolved skin) due to circulating IgG antibodies against BPAG2 (180-kD antigen, type XVII collagen); occurs weeks to months after onset of LP; pathogenesis: LP damages epidermis exposes hidden antigens that are recognized by T cells
LP pigmentosusSkin types 3 and 4; brown or slate gray macules on sun-exposed face, neck, and flexures; lacks preceding erythema and minimally pruritic; evolves into reticulate hyperpigmented patches; classic LP lesions in only 20%; occurs later in life (30-40 yo) than ashy dermatosis (childhood to late 20s); discussed further in Section 3.26
Lichen planopilaris (LPP; follicular LP)Perifollicular hyperkeratosis with narrow violaceous rim on scalp (> other hair-bearing areas) scarring hair loss; frontal fibrosing alopecia: variant in elderly women along the frontal hairline
Graham-Little-Piccardi-Lasseur syndromeVariant of LPP; classic triad = nonscarring pubic and axillary hair loss w/ disseminated spiny follicular papules (KP-like), cutaneous or mucosal LP, and scarring alopecia on scalp

ACE, Angiotensin-converting enzyme; DIF, direct immunofluorescence; GA, geographic atrophy; H&E, hematoxylin and eosin staining; HCTZ, hydrochlorothiazide; IgG, immunoglobulin G; KP, keratosis pilaris; LE, lupus erythematosus; LP, Lichen planus; LPP, lichen planopilaris; LS&A, lichen sclerosus et atrophicus; NSAIDs, nonsteroidal antiinflammatory drugs; PIH, pregnancy-induced hypertension; SCC, squamous cell carcinoma; TNF, tumor necrosis factor; UE, upper extremity; UVB, ultraviolet B radiation.

From Alikhan A, Hocker TLH: Review of dermatology, ed 2, Philadelphia, 2024, Elsevier.

Workup

If the diagnosis is questionable, a skin biopsy is performed.

Laboratory Tests

  • Laboratory tests are not specific for the diagnosis of LP
  • Liver function tests
  • Serology for hepatitis B and C
  • Lipid panels screening is useful since increases in serum triglycerides and decreases in HDL (high-density lipoprotein) cholesterol are common in patients with LP
Imaging Studies

Imaging studies are not helpful in diagnosing LP.

Treatment

Nonpharmacologic Therapy

  • Avoid scratching.
  • Use mild soaps and emollients after bathing to prevent dryness.
General Rx
For Cutaneous Lp:

  • Topical steroids (e.g., triamcinolone acetonide 0.1%, fluocinonide 0.05%, clobetasol propionate 0.05% cream or ointment) with occlusion used twice daily
  • Acitretin 30 mg/day PO for 8 wk
  • Systemic prednisone 30 to 60 mg/day as a starting dose and tapered to 15 to 20 mg/day maintenance for 6 wk can be used for widespread lesions
  • Intradermal steroid triamcinolone acetonide 5 mg/ml can be tried for thick hyperkeratotic lesions
  • Hydroxyzine 25 mg PO q6h can be used for pruritus
  • Phototherapy: PUVA or narrow-band ultraviolet B therapy: 2 or 3 times per wk, for a total of 12 sessions (i.e., one cycle)
For Oral Lp:

  • Topical steroid fluocinonide in an adhesive base used six times/day for 9 wk
  • Topical calcineurin in steroid-unresponsive cases
  • Topical or systemic retinoids 0.1% retinoic acid in an adhesive base or gel
  • Etretinate 75 mg/day for 2 mo
Disposition

  • Spontaneous remissions of cutaneous LP occur in >65% of cases within the first year.
  • Spontaneous remission of oral LP usually occurs by 5 yr.
  • 10% to 20% of patients will have recurrence.
Referral

To dermatologist if diagnosis is unclear

Pearls & Considerations

Comments

  • LP can be remembered as purple, planar, pruritic, polygonal, papules, and plaques (six Ps).
  • Lesions can develop at the site of prior skin injury (Koebner phenomenon).
  • Although there is an increased risk of squamous cell carcinoma in chronic lesions of mucosal LP, transformation to skin cancer is uncommon.
Related Content

  • Lichen Planus (Patient Information)