Lichen planus

Lichen planus 

Updated: 12/18/2023

© Jun Wang, MD, PhD

General features
  • Likely immune disorder
  • More common in 30-60
  • May be confined to oral mucosa
  • Usually regressin 6 to 18 months
Pathogenesis
  • Cell-mediated (CD8+ T cells) immune response to antigens at basal cells or dermoepidermal junction, with unknown triggering factors
  • May be associated with immunity disorders, such as ulcerative colitis, dermatomyositis, etc, and certain infections, such as hepatitis C
  • Stressful events may play a role in the onset or exacerbation
Clinical features
Follicular: Lichenplanopilaris, hair follicles centered
Hypertrophic: Extremely pruritic, more common on extensor surfaces of lower extremities
Vesicular/bullous
Pathological features
  • Lichenoid inflammation: Band like chronic inflammatory infiltrate (T cells and macrophages) that destroys the dermoepidermal junction
  • Hyperkeratosis and acanthosis with prominent granular cell layer
  • Sawtoothing of rete pegs
  • Civatte bodies (apoptotic basal cells, PAS+)
  • Artifactual cleft formation at dermal epidermal junction
  • Occasional subepidermal bullae (Bullous lichen planus)
Immunofluorescence studies
Diagnosis
  • Commonly based on clinical findings
  • Biopsy (deep enough to include dermoepidermal junction) if uncertain
Management
  • Individualized treatment
  • Steroids, tropical or systemic, metronidazole, retinoids, etc.
  • UV-B radiation or psoralen with UV-A radiation for widespread cases
  • Usually self-limited  

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