Seborrhoeic Dermatitis (SD) is a very common chronic and/or relapsing inflammatory skin disorder, whose pathobiology remains poorly understood.Yeast of the genus Malassezia has long been regarded as the central predisposing factor, based on the observations that high counts of Malassezia are closely associated with SD and antifungal treatment tends to clear symptoms. However, strong challenges to this notion remain. A causal relationship and the exact role of Malassezia in SD pathobiology have not been firmly established.Additionally, a Malassezia aetiology cannot easily explain the effective treatment of SD symptoms with weak topical steroids, nor the much-discussed relationship of SD to dandruff on the one hand, and psoriasis on the other.

The incidence of SD notably peaks in three age groups, in infancy between 2 weeks and 12 months of age, during adolescence, and between age 30 and 60 years during adulthood. This observation, together with the fact that SD occurs only in seborrhoeic areas, already raise the question whether these incidence peaks correlate with defined environmental, microbial and/or hormonal (eg androgen) changes in the skin milieu. In infants, SD presents as “cradle cap”—yellowish, greasy and crusty skin on the scalp—that is usually self-resolving. In adolescents and adults, SD often presents as yellow, greasy scales with erythematous skin in seborrhoeic areas such as the scalp, face (eyebrows, nasolabial folds, above the upper lip)ears, retro-auricular area and the upper chest. In addition to skin inflammation, SD can be associated with pruritus

Current treatment options1 usually manage SD signs and symptoms effectively, but do not provide a cure, so the natural course of the disease is chronic with recurrent episodes of flare-ups. Triggering events include stress, cold and dry weather.Given the long-standing SD paradigm that excessive Malassezia presence/proliferation in conjunction with local skin irritation and inflammation play a key role in SD, treatment is centred on the topical application of antifungals and anti-inflammatory agents.

Antifungals such as ketoconazole have fungistatic properties that limit Malassezia growth and, as the still-living fungi are shed from the skin surface during epidermal turnover, lead to reduction of fungal counts. Topical steroids and immunomodulators reduce the production and action of pro-inflammatory cytokines (ie IL-1α, IL-6, IL-8 and TNFα) not only from keratinocytes, but also from neutrophils, and thus mitigate the onset/propagation of skin inflammation.27 Furthermore, some miscellaneous therapies (eg lithium gluconate, metronidazole) that have also been advocated as second- or third-line therapy of SD may exert their anti-inflammatory action via IL-10 and TLR2-4 in keratinocytes, and inhibition of free radical species respectively, Isotretinoin has also been suggested as alternative SD therapy, presumably via its impact on promoting keratinocyte differentiation.

Perhaps because SD generally responds well to treatment and is not commonly associated with severe comorbidities—with the notable exception of HIV infection and other states of severe immunosuppression—systematic research efforts devoted to SD have been rather unsatisfactory compared with other inflammatory dermatoses such as atopic dermatitis (AD) and psoriasis.The conceptual advance in recent years towards understanding SD pathobiology has been incremental, and a fully plausible SD pathobiology concept is still missing. Instead, the discussion on SD continues to be dominated by the role of Malassezia yeast, just as it has been for decades, likely because this is the easiest to measure, manage and manipulate. Here, we argue that this needs to change.

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Anabell Rose

Editorial Assistant

Hair Therapy & Transplantation