Psoriasis affects approximately 6 to 9 million Americans. For most patients (approximately 75%), skin lesions usually present before the third decade of life. Various clinical presentations are observed, including annular, erythematous plaques on the extensor surfaces (psoriasis vulgaris), scattered, small erythematous papules (guttate psoriasis), extensive pustule formation on erythematous plaques (pustular psoriasis), generalized erythema (erythrodermic psoriasis), psoriasis of flexural skin (inverse psoriasis), scalp psoriasis, nail psoriasis, and psoriasis of the palms and soles. Environmental factors (trauma, infection, emotional stress, and medications) initiate or exacerbate psoriasis in patients with a genetic predisposition to the disease. The typical clinical disease course is characterized by chronicity. Rapid epidermal proliferation results in thickened skin and retention of the stratum corneum; the latter produces thick, adherent scale. Although removal of psoriatic scale may result in punctate bleeding, psoriasis is never characterized by extensive epidermal loss and ulceration. However, a secondary skin infection (eg, ecthyma gangrenosum, mucormycosis, or mycetoma) could produce skin necrosis and ulceration in a patient with psoriasis. Skin biopsy specimens from psoriatic skin are characterized by a uniformly thickened epidermis, dilated and congested dermal papillae, and infiltration of the epidermis by neutrophils. The lichenoid tissue reaction, in contrast, is characterized by a superficial, dermal, bandlike, lymphocytic infiltrate that obscures the basement membrane zone and is associated with necrosis of individual keratinocytes. A lichenoid tissue reaction is incompatible with a diagnosis of psoriasis.