Lichen Planus

Figure 3.10 A: Annular lichen planus (Courtesy of Dr. Paul Getz) B: Blaschkoid lichen planus (Courtesy of Dr. Iris K. Aronson) C: Oral lichen planus (Reprint from Norman R, ed. Diagnosis of Aging Skin Diseases. London: Springer; 2008)
Figure 3.10
A: Annular lichen planus
(Courtesy of Dr. Paul Getz)
B: Blaschkoid lichen planus
(Courtesy of Dr. Iris K.
Aronson
)
C: Oral lichen planus
(Reprint from Norman R, ed.
Diagnosis of Aging Skin
Diseases. London: Springer;
2008
)
Figure 3.11 A: Lichen planus, lips* B: Lichen planus, palmoplantar* C: Lichen planus, genital* *Courtesy of Dr. Paul Getz
Figure 3.11
A: Lichen planus, lips*
B: Lichen planus, palmoplantar*
C: Lichen planus, genital*
*Courtesy of Dr. Paul Getz
(Figures 3.10A–C, 3.11A–C, Table 3-4)
  • Pruritic papular disease of skin and mucous membranes
  • Due to cell-mediated autoimmune reaction toward basal layer keratinocytes; may be idiopathic, drug-related or infection-related (HCV)
  • 4P’s: papular, pruritic, polygonal, purple
  • Often lasts 1–2 years (except oral and hypertrophic forms, which typically have protracted courses)
  • Presents with intense pruritus and violaceous, smooth flat-topped papules and plaques with fine scale (Wickham’s striae) over flexor wrists, forearms, legs, presacrum and other areas, + Köebner phenomenon
  • No conclusive evidence to support association with autoimmune disease (per Bolognia); difficult to determine if true HLA association
  • Histology
    • Hyperkeratosis (without parakeratosis)
    • ↑ Granular layer
    • Partially effaced rete ridges with widened papillae (‘sawtooth’ appearance)
    • Vacuolar change of basal layer with colloid bodies
    • B and-like lymphocytic infiltrate at dermoepidermal junction
    • Dermal melanophages
  • Treatment: superpotent topical corticosteroids, topical calcineurin inhibitors, intralesional or systemic corticosteroid, phototherapy, methotrexate, acitretin, oral metronidazole (latter for erosive oral form)













   
 
Table 3-4 Types of Lichen Planus
 TypeDescription
 
Acute LP
Eruptive lichenoid papules with wide distribution, heals with hyperpigmentation; self-limited (typically resolves within 9 months)
 
Actinic LP
Photosensitive variant of LP with melasma-like appearance or lichenoid papules over face, neck and dorsal hands; typically in children and young adults with spring or summer onset (some consider entity as lichenoid form of polymorphous light eruption {PMLE})
 
Annular LP
 
Annular papules and plaques with central clearing (commonly over penis)
 
Atrophic LP
Lichenoid papules replaced with depressed atrophic areas typically over lower legs, ± residual hyperpigmentation; resembles lichen sclerosus clinically
 
Bullous LP
Vesicles and bullae arising within existing LP lesions (intense inflammatory reaction at dermoepidermal junction causes subepidermal bullae)
 
Drug-induced LP
Distribution typically generalized or sun-exposed sites; Wickham’s striae uncommon; ± eosinophils and parakeratosis on histology; medication typically taken for several months before eruption appears

{Common meds: β-blockers, captopril, penicillamine, HCTZ, antimalarials, furosemide, quinidine, NSAID, tetracycline, quinacrine, gold, sulfonylureas, hydroxyurea, methyldopa}
 
Erosive or
ulcerative LP
Painful, chronic, recalcitrant erosive lesions especially on oral mucosa and palmoplantar surface; small ↑ risk of SCC within longstanding lesions; erosive oral LP associated with liver disease (HCV)
 
Genital LP
Seen in up to 20% of LP patients; glans penis common site for men (annular lesions, small grouped papules, or larger plaques); vulvar LP commonly erosive and may coexist with gingival involvment (‘vulvovaginal gingival syndrome’)
 
Hypertrophic LP
Thick, hyperkeratotic intensely pruritic plaques commonly found over shins or dorsal feet; also known as LP verrucosus
 
Inverse LP
LP lesions in groin, axillae and inframammary regions
 
Linear LP
 
Linear groups of lichenoid papules following lines of Blaschko
 
Mucosal LP
Up to 50% patients with skin disease may have oral mucosal changes; ranges from reticular, atrophic, erosive, bullous, papular to pigmented; reticular type most common with lacy white hyperkeratosis on buccal mucosa, lips, tongue and gingiva; typically asymptomatic unless erosive; rarely may see esophageal, laryngeal or conjunctival involvement
 
Nail LP
10% of LP patients; may be isolated finding; typically lateral nail thinning, longitudinal ridging, dorsal pterygium, splitting, ± 20 nail dystrophy
 
LP/LE overlap
Clinical and histologic features of both lupus erythematosus (LE) and LP
 
Palmoplantar LP
Painful hyperkeratotic yellow to erythematous plaques on palms and soles (lateral borders and pressure points), ± ulceration, erosions; recalcitrant to therapy
 
LP Pemphigoides
Tense vesicles and bullae arise in normal, uninvolved skin; typically blisters occur weeks to months after appearance of typical LP lesions; overlap between bullous pemphigoid and LP; + IgG antibody to BP180 (NC16A)

{DIF: linear IgG/C3 at BMZ IIF: IgG at roof of blister (salt-split skin)}
 
LP Pigmentosus
Gray-brown macules in sun-exposed areas ± flexural folds in darker-skinned patients; similar to erythema dyschromicum perstans
 
Lichen planopilaris
Keratotic follicular papules with violaceous rim leading to cicatricial alopecia

{Graham-Little-Piccardi-Lasseur syndrome: typical skin/mucous membrane LP, scarring alopecia of scalp, nonscarring loss of pubic/axillary hairs}