Lichen Planus
An itchy, purplish skin rash with flat-topped bumps, often accompanied by white, lacy patches in the mouth, driven by an autoimmune reaction.
Emergency Management: Rarely presents as an emergency. Severe esophageal involvement can cause strictures leading to complete food impaction requiring urgent endoscopy.
Lichen Planus is a chronic, inflammatory, T-cell mediated autoimmune disease that affects the skin, mucous membranes, nails, and scalp. It is characterized by intensely pruritic, violaceous, flat-topped papules and plaques.
Detailed Overview
LP manifests with the classic '6 Ps': planar, purple, polygonal, pruritic, papules, and plaques. Mucosal involvement, particularly oral lichen planus, presents with reticular white lines (Wickham striae) and can be erosive and painful. It is often associated with Hepatitis C infection. The clinical course can be self-limiting for cutaneous forms (resolving in 1-2 years), but mucosal LP is typically chronic.
Epidemiology & Demographics
Affects approximately 1% of the general population. Most commonly seen in adults aged 30 to 60. There is no strong gender predilection for cutaneous LP, but oral LP is twice as common in women.
Etiological Mechanism
Considered an idiopathic cell-mediated immune response targeting basal keratinocytes. It is strongly linked to Hepatitis C virus (HCV) infection, and certain medications can trigger lichenoid drug eruptions.
Primary Causes
Primary trigger is unknown (idiopathic). Secondary causes include HCV infection, contact allergens (dental amalgams), and medications (ACE inhibitors, thiazides, antimalarials).
An unknown antigen (possibly viral or drug-induced) on basal keratinocytes activates CD8+ cytotoxic T cells. These T cells migrate to the dermo-epidermal junction and induce apoptosis of the basal cells. This leads to characteristic histological findings: dense band-like lymphocytic infiltrate in the upper dermis, 'saw-tooth' rete ridges, and colloid (Civatte) bodies representing apoptotic keratinocytes.
Diagnostic Criteria & Guidelines
Primarily clinical diagnosis based on the 6 Ps and Wickham striae. Confirmation requires a 4 mm punch biopsy showing hyperkeratosis, wedge-shaped hypergranulosis, saw-tooth rete ridges, and a band-like lymphocytic infiltrate at the dermoepidermal junction.
For Cutaneous LP: High-potency topical corticosteroids (e.g., Clobetasol propionate 0.05% ointment BID for 2-4 weeks). For Oral LP: High-potency topical corticosteroids in an adhesive base (e.g., Fluocinonide 0.05% gel applied TID).
Second-Line & Adjunctive Therapy
For widespread/refractory cutaneous LP: Oral Prednisone (0.5-1 mg/kg/day tapered over 2-6 weeks) or Narrowband UVB phototherapy. For recalcitrant oral LP: Oral Acitretin 25 mg/day or Topical Calcineurin inhibitors (Tacrolimus 0.1% ointment).
Surgical & Procedural Management
Laser excision or cryotherapy for painful, isolated, hypertrophic lesions. Excision of suspicious oral lesions to rule out SCC.
Patient Counseling & Advice
Inform the patient that cutaneous LP usually resolves spontaneously within 1-2 years, but leaves hyperpigmentation. Stress that mucosal LP is a chronic, relapsing condition requiring long-term surveillance for oral cancer.
Follow-Up & Monitoring Schedule
Biannual dental/dermatology exams for patients with oral/genital LP to screen for malignant transformation to squamous cell carcinoma.
Preventive Strategies
No primary prevention exists. Avoidance of known triggers (suspect drugs, dental amalgams in allergic individuals) can prevent exacerbations.
Cutaneous LP has a good prognosis, clearing in 68% of patients within 1 year. Hypertrophic and mucosal LP are chronic, persistent, and difficult to treat, often lasting for decades.