Seborrheic dermatitis (SD) is a common skin condition seen frequently in clinical practice. The use of varying terms such as sebopsoriasis, seborrheic dermatitis, seborrheic eczema, dandruff, and pityriasis capitis reflects the complex nature of this condition. Despite its frequency, much controversy remains regarding the pathogenesis of SD. This controversy extends to its classification in the spectrum of cutaneous diseases, having being classified as a form of dermatitis, a fungal disease, or an inflammatory disease, closely related with psoriasis. Some have postulated that SD is caused by Malassezia yeasts, based on the observation of their presence in affected skin and the therapeutic response to antifungal agents. Others have proposed that Malassezia is incidental to a primary inflammatory dermatosis that resulted in increased cell turnover, scaling, and inflammation in the epidermis, similar to psoriasis. The presence of host susceptibility factors, permitting the transition of M furfur to its pathogenic form, may be associated with immune response and inflammation. Metabolites produced by Malassezia species, including oleic acid, malssezin, and indole-3-carbaldehyde, have been implicated. SD also has been traditionally considered to be a form of dermatitis based on the presence of Malassezia in healthy skin, the absence the pathogenic mycelial form of Malassezia yeasts in SD, and its chronic course. As a result, proposed treatments vary, ranging from topical corticosteroids to topical antifungals and antimicrobial peptides.
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