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Seborrheic Dermatitis Management in 2026

Clinical Summary

Seborrheic Dermatitis: TH17/TH1 Pathways and Emerging Topical Therapies

  • Pathogenesis update (seborrheic dermatitis): Tape-stripping data (Mount Sinai) show TH17/TH1 cytokine predominance with Malassezia species (globosa, restricta, furfur) as triggers; shifts focus from microbiome-only to immune + barrier dysfunction.

  • Emerging therapies: Roflumilast (topical PDE4 inhibitor, FDA-approved) and other PDE4 agents reduce inflammatory cytokines; topical JAK inhibitors (e.g., ruxolitinib 1.5% cream) and microbiome-restoring therapies are under study; early reports include exosome-based therapy.

  • Treatment strategy: For refractory disease, use combination therapy—short-term topical corticosteroids for flares, then maintenance with nonsteroidals (PDE4 inhibitors, calcineurin inhibitors; emerging JAK/microbiome therapies).

Reviewed by Riya Gandhi, MA, Associate Editor of Immunology Group

Dr Brad Glick discusses how evolving insights into microbiome and immune pathways—particularly TH17- and TH1-driven inflammation—are reshaping the understanding and treatment of seborrheic dermatitis. Learn about emerging therapies including PDE4 inhibitors, topical JAK inhibitors, and microbiome-based treatments, along with practical strategies for managing recurrent flares and tailoring non-steroidal regimens to improve long-term outcomes and adherence.

Transcript

My name is Dr Brad Glick and I'm a board-certified dermatologist and I practice in South Florida.

How have recent insights into the immune and microbiome pathways of seborrheic dermatitis influenced treatment strategies in your practice?

Dr Glick: The microbiome and some of the targeted nature and our understanding of seborrheic dermatitis really has come from some recent work done at Mount Sinai School of Medicine in New York by Dr Emma Guttman and Dr Ben Unger. They did some tape stripping analyses looking at individuals with mild, moderate and severe seborrheic dermatitis and compared them to matched healthy controls. And actually, what they found in this tape stripping analysis is that there are categories and families of inflammatory cytokines, like TH17 and TH1 inflammatory cytokines, that appear to be the predominant targets for individuals who have this condition, perhaps less so for Th2 inflammatory cytokines. But this information and this data, this very well-run study, is critical because our understanding of seborrheic dermatitis has been very different previously. We previously thought that it was really only perhaps the microbiome that was impacted by an organism that we know as Melassezia. And more recently, not only do we know that there are various Malassezia species that are implicated in seborrheic dermatitis, such as globosa and restrictor, in addition to Malassezia furfur. Those are probably triggering phenomena in a scenario where an inflammatory burden is created by this host of inflammatory cytokines, most predominantly Th17 cytokines, responsible for the inflammatory changes, barrier dysfunction, and clinical findings that we see in patients with seborrheic dermatitis.

What new or emerging topical therapies show the most promise for improving outcomes and adherence in chronic cases?

Dr Glick: There are a host of new and emerging therapies for treating our patients with seborrheic dermatitis. Most of them are topical therapies, and I think that we rarely will utilize systemic therapies for seborrheic dermatitis. It is, after all, an outside-in or even inside out phenomena, much like we see in atopic dermatitis, but really limited to specific areas like the scalp and the face, chest, and the butterfly region of the upper back. These new and emergent therapies are inclusive of a category that we're familiar with already, approved originally in the space of plaque psoriasis, and that is roflumilast, which is a PDE4 inhibitor. And there are other PDE4 inhibitors that are emerging for the treatment of seborrheic dermatitis. And as we all know, there is upregulation of intracellular cyclic AMP, which results in downregulation of peripheral inflammatory cytokines in seborrheic dermatitis, much like we have in other conditions like plaque psoriasis and even atopic dermatitis. And we know that a product like roflumilast is approved across three spaces, including seborrheic dermatitis, plaque psoriasis, and atopic dermatitis, across a number of different age groups. Other areas of interest and targeted therapies, specifically topical therapies, would include the use of topical JAK inhibitors. So Janus kinase inhibitors like ruxolitinib cream, 1.5%, which we know is FDA approved to treat mild to moderate atopic dermatitis. But nevertheless, it appears that it may have a role in treating seborrheic dermatitis very much by some of the commentaries that I made previously about the fact that we've learned more that inflammatory cytokines, in addition to the changes that we know occur in seborrheic dermatitis from the microbiome, are responsible for the inflammatory changes that we see in seborrheic dermatitis. So it makes sense that genus kinase inhibitors, particularly the topical agents, might be a benefit in the setting of seborrheic dermatitis. And it appears that there are some small studies being done right now, as we speak in that particular area. Some of the other emerging therapies, which are kind of unique, are those that impact the microbiome. We know certainly in conditions like seborrheic dermatitis and atopic dermatitis that there is an impairment of the barrier. There's an inability for our normal commensals to behave properly. And restoring those appropriate commensals to the skin barrier are potential targeted therapy for treating our patients with seborrheic dermatitis. And so microbiome topical therapies will become available at some point. And most of them are being studied in the setting of atopic dermatitis, so we'll stay tuned in that regard. Finally, there was a recent report of the use of exosomes, believe it or not, for the treatment of patients with seborrheic dermatitis. And this was one case that was reported in the Journal of the American Academy of Dermatology, but nevertheless, that may as well show prominence as with all of our topical therapies for treating our patients with seborrheic dermatitis, restoring that microbiome, improving the skin barrier, and downregulating what we now know of those key inflammatory cytokines such as TH17 and TH1, and less so Th2 inflammatory cytokines in the management of seborrheic dermatitis.

How do you approach customizing treatment regimens for patients, particularly those with recurrent flares or sensitivities to traditional therapies?

Dr Glick: When we have challenges for patients that are flaring and breaking through traditional therapies, and to mention the traditional therapies for treating seborrheic dermatitis have largely been azole antimycotic therapies, antifungal agents, other forms, ciclopirox olamine and other olamines and piroctone antifungal therapeutics, but also those individuals that are failing more traditional therapies such as the use of those antifungals and even topical corticosteroids are really appropriate candidate for the use of our newer generation non-steroidal therapies. And of course, we know we have one that is FDA approved for seborrheic dermatitis. It is available in a 0.3% foam and it can be used in the scalp and actually also approved for treating patients with plaque psoriasis that can be used in the scalp and the body. So there's an opportunity here for individuals that are flaring to be able to use these newer generation therapies like non-steroidal therapies. Now, I must say with the advent of non-steroidal therapies, with the previous use that I have performed on my patients previously, such as with topical calcineurin inhibitors, we still need to go, even if it's retrospectively thinking, and use topical corticosteroids short term for recovering our patients who have flares of seborrheic dermatitis. But I think really the better answer is the use of combination therapy, topical corticosteroids for getting patients through flares, maintenance therapies with possibly topical calcineurin inhibitors or newer generation PDE4 inhibitors, and where emerging therapies are concerned, possibly more long-term use of topical anti-inflammatory therapies such as JAK inhibitors, other PDE4 inhibitors, perhaps topical therapies that restore the microbiome as well.

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