Lichen Planus

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).

• Hepatitis C Infection: Patients with HCV have a significantly increased risk, especially for oral LP.
• Certain Medications: Drugs like beta-blockers, ACE inhibitors, and NSAIDs can cause lichenoid drug eruptions.
• Genetics: Certain HLA associations (HLA-B7, HLA-DR1, HLA-DR10) suggest genetic susceptibility.

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.

Characteristic Clinical Presentation

• Intense Pruritus: Severe itching of the skin lesions, out of proportion to the rash size.
• Oral Pain and Burning: In erosive oral LP, eating spicy or acidic foods causes significant pain.
• Nail Dystrophy: Longitudinal ridging, splitting, and rarely, complete loss of the nail plate (pterygium formation).

Physical Examination Signs

• Violaceous, flat-topped polygonal papules on the flexor surfaces of the wrists and ankles
• Wickham Striae: Fine white reticular lines on the surface of papules or the buccal mucosa
• Koebner Phenomenon: New lesions developing along lines of skin trauma or scratching

• Squamous Cell Carcinoma (SCC): Erosive oral and vulvovaginal LP carry a 1-3% lifetime risk of malignant transformation into SCC.
• Post-inflammatory Hyperpigmentation: Dark brown macules remaining after active lesions resolve, especially in darker skin types.

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.

Differential Diagnosis

• Psoriasis
• Lichenoid Drug Eruption
• Graft-Versus-Host Disease (GVHD)
• Leukoplakia (for oral lesions)

Laboratory Tests & Biomarkers

• Hepatitis C Antibody and RNA: Positive in up to 16% of patients, particularly in Southern Europe and Japan
• Direct Immunofluorescence (DIF): Shaggy band of fibrinogen along the basement membrane zone, with IgM/IgA/IgG/C3 in Civatte bodies

Imaging Modalities & Findings

• None: Not indicated for diagnosis.

• Acute Cutaneous
  Rapid onset of widespread, highly pruritic papules; usually resolves in 1-2 years.
• Hypertrophic LP
  Thick, hyperkeratotic plaques typically on the shins; highly pruritic and chronic.
• Erosive Oral/Mucosal LP
  Painful ulcerations on mucosal surfaces (mouth, genitals); highly recalcitrant and chronic.

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.

Recommended Lifestyle Changes

• Avoid scratching to prevent the Koebner phenomenon; keep nails trimmed.
• For oral LP, avoid spicy, acidic, or hard/rough foods (like chips) that can traumatize the mucosa.
• Use a soft-bristled toothbrush and mild toothpaste.

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.