Lichen planus and psoriasis are both chronic inflammatory conditions that primarily affect the skin. Though they can appear similar, they are distinct medical conditions with differentiating characteristics. Understanding these distinctions is important for accurate diagnosis and effective management.
Identifying Characteristics
Lichen planus presents as a rash of small, flat-topped, shiny bumps, often purple or reddish-purple. Papules are usually polygonal and can merge into larger plaques. A distinctive feature is Wickham’s striae: fine, white, lace-like lines visible on lesion surfaces, especially on mucous membranes (e.g., inner cheeks). Intense itching is a common symptom.
It commonly affects wrists, arms, lower back, and ankles; oral mucosa may show lacy white patches or painful sores. Nails may thin, ridge, split, or be lost, and scalp involvement can lead to hair loss.
Psoriasis manifests as thick, raised patches of discolored skin with silvery scales (plaques). On brown/black skin, patches may appear purple or dark brown with gray scales. Plaques result from accelerated skin cell turnover, building on the surface. Affected areas can be itchy or sore; severe cases may cause skin around joints to crack and bleed.
Plaques frequently appear on elbows, knees, scalp, and lower back, but can develop anywhere. Nails can be affected (pitting, discoloration, or separation from the nail bed). Many also develop psoriatic arthritis, causing joint pain, stiffness, and swelling in any joint (e.g., fingers, toes).
Contributing Factors
Lichen planus is an inflammatory condition involving an immune system response; its exact cause is often unknown. The immune system mistakenly attacks skin and mucous membrane cells. Triggers include hepatitis C virus. Certain medications (e.g., for high blood pressure, diabetes, heart conditions, malaria) can induce lichenoid reactions. Stress may contribute to onset or flare-up.
Psoriasis is a chronic autoimmune condition where the immune system malfunctions, causing rapid skin cell growth. Genetics play a significant role, with a strong familial predisposition; precise reasons for immune dysfunction are still being investigated. Specific genetic mutations are linked to psoriasis development, and risk increases if one or both parents have the condition.
Environmental factors and triggers can activate psoriasis in genetically predisposed individuals. Common triggers include infections (e.g., strep throat, preceding guttate psoriasis). Skin injury, severe sunburn, smoking, heavy alcohol consumption, and certain medications (e.g., lithium, blood pressure drugs) can exacerbate symptoms.
How They Are Diagnosed
Diagnosis involves clinical examination to assess lesion appearance and distribution. A thorough patient history, including symptoms or exposures, is crucial. When uncertain, a skin biopsy is often performed for definitive diagnosis.
Biopsy histopathology reveals characteristic features: “saw-tooth” epidermal hyperplasia, granular cell layer thickening, and a dense band of lymphocytes at the dermal-epidermal junction. Blood tests for hepatitis C may be recommended due to its viral association. Direct immunofluorescence studies, examining immune deposits in skin samples, can further support the diagnosis.
Psoriasis is often diagnosed based on distinct skin lesion appearance during clinical examination. Providers evaluate skin, scalp, and nails for characteristic plaques and scales. A skin biopsy is not always necessary for classic presentations, but may be performed to confirm diagnosis, determine specific type, or differentiate from similar conditions like eczema.
Histopathological findings include hyperkeratosis, parakeratosis, and increased skin cell proliferation, leading to epidermal thickening. Specific microscopic features, like Munro’s microabscesses (collections of neutrophils), further support a psoriasis diagnosis. These methods underscore the importance of professional medical evaluation for accurate identification.
Treatment Strategies
Treatment for lichen planus focuses on alleviating symptoms and managing the chronic condition. Topical corticosteroids are common first-line for localized lesions due to anti-inflammatory properties. For more widespread or severe cases, oral corticosteroids may be prescribed to reduce inflammation.
Phototherapy (narrowband UVB) is an effective treatment for generalized lichen planus. Other immune-modulating drugs (e.g., calcineurin inhibitors, retinoids, systemic immunosuppressants like methotrexate) may be considered for resistant or specific forms, including oral lichen planus. Treatment also involves avoiding triggers and addressing underlying conditions, such as hepatitis C.
Psoriasis management aims to slow rapid skin cell growth and reduce inflammation, often requiring chronic treatment. Topical treatments are the first approach for mild to moderate cases. These include corticosteroids (reducing inflammation and itching) and vitamin D analogs (slowing skin cell production). Calcineurin inhibitors are also used, particularly for sensitive areas.
For moderate to severe psoriasis, phototherapy (UVB light) slows skin cell production. Systemic medications (e.g., methotrexate or cyclosporine) suppress the immune response throughout the body. Biologic drugs, targeting specific immune system parts, are advanced treatment options for severe cases. These varied strategies highlight the tailored approach required for each condition based on its unique pathology.