New Insights into the Etiopathogenesis of Seborrheic Dermatitis

Abstract

Seborrheic dermatitis represents a chronic, widespread skin disease that is considered a multifactorial disorder influenced, in part, by Malassezia spp.opportunistic activities as well as by various endogenous and exogenous factors. This review systematizes the recent scientific achievements in the field of insufficiently elucidated etiology and pathogenesis of seborrheic dermatitis. IntroductionSeborrheic 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 epidermal 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 responding 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 seborrheic dermatitis and its classification in the spectrum of cutaneous diseases as a form of dermatitis, a fungal disease, or an inflammatory disease, closely related with psoriasis.The prevalence of seborrheic dermatitis peaks when sebaceous gland activity is high, during the first three months of life (infantile seborrheic dermatitis), during puberty and when sebum excretion 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 sebaceous 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 exhaustion yeast cells employ tryptophan as a nitrogen source, increasing 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.Seborrheic dermatitis occurs on the scalp as well as on face, retroauricular area, and the upper chest, causing flaking, scaling, inflammation, pruritus, and, sometimes, marked erythema [5]. Flaking is usually white-to-yellowish, and may be oily or dry. Various intrinsic and environmental factors, such as sebaceous secretions, skin surface fungal colonization, individual susceptibility, and interactions between these factors play a pathogenetic role in seborrheic dermatitis. Etiology of Seborrheic DermatitisThere are three principal factors that play a role in the etiology of seborrheic dermatitis [6]: sebaceous gland secretion, alteration in col...

Relationship between diet and seborrheic dermatitis

“…However, sebaceous glands are the main source of lipids of skin surface [6]. Therefore, sebaceous secretions are considered to play a pathogenetic role in seborrheic dermatitis [8]. Sebaceous glands provide lipid substrates for the Malassezia growth.…”

“…Sebaceous gland secretions metabolise to irritating unsaturated fatty acids by Malassezia [4]. The prevelance of the disease is directly correlated with increased sebaceous gland activity [8]. Predilection sites are sebaceous gland rich areas like face, ears, scalp and the upper trunk [6].…”

Thiol-Disulfide Homeostasis in Skin Diseases

“…Seborrheic dermatitis is a relapsing skin condition that affects the seborrheic areas of the body. The activity of the sebaceous glands, the cutaneous microflora, and the susceptibility of the host are related to the pathogenesis of seborrheic dermatitis [ 69 ]. Predisposing factors include male gender, stress, climate change and obesity [ 70 , 71 ].…”

“…promote a chronic inflammatory process. As the inflammatory process spreads, the proliferation and differentiation of keratinocytes are altered, resulting in the disruption of the skin barrier [ 69 ]. The hyperproliferative theory in the pathogenesis of seborrheic dermatitis has been recently discussed [ 72 ].…”

New Approaches to the Treatment of Patients With Seborrheic Deermatitis

“…is supposed to be the main cause of SD, however, the amount of these lipophilic microorganisms is often within normal limits on the skin of patients [1,2]. Genetic predisposition, hormonal status change, gastrointestinal tract and the nervous system diseases, dysfunction of the epidermal barrier may provoke the disease [3,4].…”