New Insights into the Etiopathogenesis of Seborrheic Dermatitis

Abstract

1 Abstract Seborrheic dermatitis represents a chronic, widespread skin disease that is considered a multi-factorial disorder influenced, in part, by Malassezia spp.opportunistic activities as well as by various endogenous and exogenous factors. This review sys-tematizes the recent scientific achievements in the field of insufficiently elucidated etiology and pathogenesis of seborrheic dermatitis. Seborrheic dermatitis is initially described by P. G. Unna in 1887 and the association with Malassezia yeasts is accepted up to the middle of the 20th century, when the observed increased epider-mal cell turnover gradually prompts researchers to characterize this condition as being intrinsic to the skin[1, 2]. Seborrheic dermatitis is common dermatological problem that affects the seborrheic areas of the body. It is considered the same basic condition like dandruff sharing many features and respond-ing to similar treatments, differing only in locality and severity. Current use of varying terms for seborrheic dermatitis such as sebopsoriasis, seborrheic eczema, dandruff, and pityriasis capitis reflects the complex nature of this common skin pathology [3]. Much controversy remains regarding the pathogenesis of sebor-rheic dermatitis and its classification in the spectrum of cutaneous diseases as a form of dermatitis, a fungal disease, or an inflam-matory disease, closely related with psoriasis. The prevalence of seborrheic dermatitis peaks when sebaceous gland activity is high, during the first three months of life (infan-tile seborrheic dermatitis), during puberty and when sebum ex-cretion is reduced after the age of 50 years [2]. Because of smaller sebum production, seborrheic dermatitis flares occur more often in spring than in summer. Disease flare could be associated with altered population dynamics affected not only by variations in se-baceous gland activity but also by modifications in other nutrients supplied by sweat, such as essential amino acids like glycine and tryptophan. Glycine stimulates the fast growth of M. furfur and after its ex-haustion yeast cells employ tryptophan as a nitrogen source, in-creasing the production of indolic metabolites [4]. Such cycles of population growth, bioactive indole production, and subsequent deprivation of nutrients result in insufficiently masked antigens and ligands on the surface of the yeast cells leading to immune system activation.