Unraveling the Pathophysiology of Seborrheic Dermatitis

Welcome back to another Dermatology Times DermView series. In this episode titled, Unraveling the Pathophysiology of Seborrheic Dermatitis, Christopher Bunick MD, PhD, led the conversation about the following question:

What is our current understanding of the pathophysiology of SD? What role do immune dysregulation, colonization of Malassezia yeast, epidermal barrier and sebaceous gland dysfunctions play in SD?

Benjamin Ungar, MD covered the current understanding of seborrheic dermatitis (SD) that highlights a multifactorial pathophysiology driven by interactions between host immunity, skin microbiome, and barrier function. Immune dysregulation plays a central role, with exaggerated inflammatory responses contributing to erythema, scaling, and pruritus. Colonization by Malassezia yeast is a key trigger, as its metabolic byproducts can activate inflammatory pathways in susceptible individuals. Epidermal barrier dysfunction further amplifies disease activity by increasing transepidermal water loss and allowing greater penetration of irritants and microbial antigens. Sebaceous gland activity provides a lipid-rich environment that supports Malassezia growth, linking sebum production to disease distribution and severity. Together, these interconnected mechanisms help explain the chronic, relapsing nature of SD and inform more targeted, non-steroidal therapeutic approaches.

Throughout the conversation, the experts provide a comprehensive reflection on the field and the factors that may shape how clinicians approach care moving forward.

In the next episode, Differentiating Seborrheic Dermatitis: Immunologic and Clinical Insights, panelists will continue their discussion on and highlight distinguishing seborrheic dermatitis from other chronic inflammatory dermatoses such as atopic dermatitis and psoriasis, emphasizing key clinical and diagnostic features. It also explores emerging evidence on immune and barrier dysfunction—particularly Th17/Th22 cytokine pathways—and their implications for targeted treatment selection in SD.