Child and Adult Seborrheic Dermatitis: A Narrative Review of the Current Treatment Landscape

Abstract

Introduction

Seborrheic dermatitis (SD) is a common, chronic inflammatory skin condition affecting sebaceous gland-rich areas of the skin. The multifactorial etiology of SD involves sebocyte activity, skin microbiome dysbiosis, and immune factors. Various treatment options exist for management of SD.

Methods

A PubMed search conducted on November 1, 2024 using the terms “seborrheic dermatitis” and “treatment” (restricted to 2019–2024) yielded 389 results, from which relevant papers and additional references were included in this review.

Discussion

Topical antifungals, topical corticosteroids, and topical calcineurin inhibitors are first-line treatments for SD; however, long-term use of each of these may be limited by varying side effects. Roflumilast foam is a newly approved topical with potential to become a first-line treatment. Myriad systemic treatments exist as second- and third-line treatments for cases of moderate-to-severe and/or recalcitrant SD. Procedural interventions of varying efficacy exist.

Conclusions

The treatment of SD requires an individualized approach, utilizing a range of topical, systemic, and procedural interventions. The advent of new treatments like roflumilast foam offers novel, well-tolerated, and safer options than what has been available in the past.

Key Summary Points

Topical treatments are the center of seborrheic dermatitis (SD) treatment, with topical antifungals and topical anti-inflammatory agents regarded as first-line therapies.

Roflumilast 0.3% foam, a newly FDA-approved SD treatment, has shown rapid improvement in SD symptoms, suitability for diverse skin and hair types, and minimal side effects, thereby positioning itself as a potential first-line agent.

The addition of systemic agents, including oral antifungals and low-dose isotretinoin, to an SD treatment regimen may be warranted in moderate-to-severe and recalcitrant cases.

Lasers, non-laser light, and injection treatments have shown some efficacy in SD treatment, but their adoption is minimal because of widely available higher level of efficacy evidence topical and oral treatments.

While treatment algorithms exist to guide SD treatment, the availability of professional society guidelines and labeled SD-specific treatments is limited.

Introduction

Seborrheic dermatitis (SD) is a chronic inflammatory dermatosis characterized by erythema, scaling, and pruritus on sebaceous gland-rich skin surfaces including the scalp, face, chest, and upper back. SD most commonly affects adults, particularly men, with a global prevalence of 1–5% [1, 2]. While the pathogenesis of SD remains unclear, its etiology is likely multifactorial, postulated to involve an interaction between sebocyte activity, dysbiosis of the skin microbiome with pathologic contributions from Malassezia yeast and Staphylococcus epidermidis overgrowth, genetic susceptibility, and an altered immune response [1–4]. Predisposing factors such as immunosuppression, neurologic comorbid conditions, and stress can exacerbate symptoms [2, 5].

Treatment of SD aims to control symptoms and minimize disease flares, with approaches tailored to the severity and location of lesions as well as patient-specific factors, such as age and comorbidities. Topical therapies—including topical antifungals (TAFs), topical corticosteroids (TCSs), topical calcineurin inhibitors (TCIs), and over the counter (OTC) antifungal shampoos—are commonly used for cases with a limited extent of disease. Recent treatment advances, most notably US Food and Drug Administration (FDA) approval of the phosphodiesterase 4 inhibitor (PDE4i) roflumilast foam, offer promising alternatives as potential first-line treatments. For more severe, refractory cases, systemic treatments may be necessary [2, 6, 7].

This review explores the current treatment landscape for SD, examining both established and emerging therapies, while considering the unique challenges posed by the condition’s diverse presentations across different patient populations. Treatment recommendations are outlined in Table 1.

Table 1.

Summary of topical and systemic treatments for seborrheic dermatitis

Treatment	Class	FDA-approved	Level of evidence	Recommended use	common potential side effects
Topicals (limited, focalized presentations)
Ketoconazole 2%	Antifungal	Yes	A [6]	1–2×/day for 2–4 weeks, then 1×/week	Skin dryness, pruritus, stinging, burning, tingling
Ciclopirox 1%	Antifungal	Yes	A [6]	2×/day for 4 weeks, then 1×/week	Skin dryness, pruritus, stinging, burning, tingling
Miconazole 2%	Antifungal	Yes	A [6]	1–2×/day	Skin dryness, pruritus, stinging, burning, tingling
Betamethasone valerate 0.12%	Corticosteroid	Yes	A [6, 15]	For the body; 1–2×/day for up to 3 weeks, then 2×/week	Skin atrophy, telangiectasias, hypertrichosis, perioral dermatitis (all with long-term use)
Clobetasol propionate 0.05%	Corticosteroid	No, off-label	A [6, 15]	For the body; 1–2×/day for up to 3 weeks, then 2×/week	Skin atrophy, telangiectasias, hypertrichosis, perioral dermatitis (all with long-term use)
Hydrocortisone 1%/2.5%	Corticosteroid	Yes	A [6, 15]	For the face; 1–2×/day for 7–10 days, then 2×/week	Skin atrophy, telangiectasias, hypertrichosis, perioral dermatitis (all with long-term use)
Pimecrolimus 1%	Calcineurin inhibitor	No, off-label	A [8, 15]	1–2×/day for up to 4 weeks	Application-site burning, erythema, irritation, or itching
Tacrolimus 0.1%	Calcineurin inhibitor	No, off-label	A [8, 15]	1×/day for 4 weeks, then 2×/week	Application-site burning, erythema, irritation, or itching
Roflumilast	Phosphodiesterase 4 inhibitor	Yes	A [26, 27]	1×/day	Nausea, diarrhea, application-site pain
Zinc pyrithione	Antifungal	Yes (combined with ketoconazole)	B [15]	2–3×/week for 2–4 weeks, then 1×/week or every other week	N/A
Selenium disulfide	Keratolytic, antifungal	Yes	C [6]	2–3×/week for 2–4 weeks, then 1×/week or every other week	Itching, irritation
Systemics (severe, recalcitrant presentations)
Itraconazole	Antifungal	No, off-label	A [15]	200 mg/day for 7 days, then 200 mg weekly for 2–11 months	Nausea, headache, drug–drug interactions
Fluconazole	Antifungal	No, off-label	B [48]	200 mg/weekly for 4 weeks OR 300 mg/week for 2 weeks	Elevated liver function tests, nausea
Terbinafine	Antifungal	No, off-label	A [8]	250 mg/day for 4–6 weeks	Taste disorders, tachycardia, insomnia, gastrointestinal symptoms, migraines, rash
Isotretinoin	Retinoid	No, off-label	B [7]	10–20 mg/day or every other day for 2–6 months	Cheilitis, nose bleeds, skin fragility, skin dryness, myalgias

Methods

A PubMed search was conducted on November 1, 2024 using the search terms “seborrheic dermatitis” and “treatment”. Publication dates were restricted to include 2019–2024. The search yielded 389 results, and relevant papers were included in this review. Additional publications cited in relevant papers were also included.

This article is based on previously conducted studies and does not contain any new studies performed by any of the authors with human participants nor animals.

Search Results

Topical Treatments

TAFs, TCSs, and TCIs are the mainstays of SD treatment, with the topical PDE4i roflumilast showing potential as a first-line therapy [2].

Topical Antifungals

Ketoconazole, ciclopirox olamine, and miconazole are TAFs FDA-approved for SD shown to be consistently effective in randomized controlled trials (RCTs), with level A evidence supporting their use [6, 8]. Ketoconazole 2% (shampoo, cream, gel, or foam), miconazole 2% (solution or cream), and ciclopirox (0.77% to 1–1.5% cream, lotion, shampoo, or gel) have shown comparable efficacy in improving erythema, scaling, and itch in head-to-head trials analyzed in a Cochrane review of 51 studies with a total of 9052 participants [5, 6, 9–11]. Recommendations for use beyond 5 weeks are limited, as almost all studies (45 of 51) included in the review did not last beyond that timeframe. TAFs may be used for SD on the scalp, face, ears, and chest [11, 12].

Ketoconazole, ciclopirox, and miconazole are well tolerated, and have been infrequently associated with application-site pruritus, dryness, stinging, burning, and tingling sensations, with one study citing their occurrence in 2–3% of patients with SD [7, 10, 11]. Incidences of allergic contact dermatitis have also been reported in less than 1% of patients treated with these agents, with irritation typically resolving after treatment discontinuation [10].

Studies of topical terbinafine 1% cream, clotrimazole 1% cream, and sertaconazole 2% cream have shown their off-label efficacy in the treatment of SD. While one trial showed topical terbinafine’s comparable efficacy to ketoconazole for facial SD, terbinafine still only has level C evidence for use [7, 8, 11]. Both clotrimazole and sertaconazole were observed to have similar efficacy to hydrocortisone 1% in head-to-head trials, though a comparative trial demonstrated sertaconazole’s superiority for treating extensive facial SD in comparison to clotrimazole [7, 11].

Strains of Malassezia species resistant to azoles have been identified, prompting the need for alternative treatment options [13, 14].

Topical Corticosteroids

TCSs are cornerstones of SD treatment given their anti-inflammatory, immunosuppressive, and antiproliferative properties. Level A evidence supports their use in improving SD symptoms and inducing SD clearance [6, 8, 15].

TCSs of varying strengths and potencies can be used on- and off-label for SD, including clobetasol 0.05% (shampoo, solution, lotion), fluocinolone 0.01% (shampoo, solution, cream, oil), betamethasone valerate 0.12% (foam), betamethasone valerate 0.1% (cream, lotion), betamethasone dipropionate 0.05% (lotion) for SD on the scalp and/or body and desonide 0.05% (cream, foam, gel, lotion, ointment), hydrocortisone 2.5% (cream, ointment), and hydrocortisone 1% (cream, ointment) for eyelid and face SD (FSD) [5, 7, 8, 12, 16, 17].

Recommended dosing regimens vary with steroid potency and application site. TCSs can be used once to twice daily for 2–4 weeks for body and scalp SD (SSD); however, use may be limited to 10–14 days with subsequent twice-weekly maintenance application. Abbreviated regimens of TCSs for FSD involve once- to twice-daily application for 5–10 days [5, 8].

If TAF monotherapy fails to elicit improvement, TCSs are alternative first-line agents that may be used concomitantly [1, 7]. TCSs were determined to be as effective for SD as topical azole antifungals in a Cochrane review of 36 RCTs with 2706 participants, while TCSs and TCIs were deemed to offer similar short-term efficacy [18].

Most studies of TCSs in SD have only lasted 4 weeks, as their long-term use is limited by potential skin atrophy, telangiectasias, hypertrichosis, and perioral dermatitis [6, 7].

Topical Calcineurin Inhibitors

While the TCIs pimecrolimus (1% cream) and tacrolimus (0.1% ointment) may not have FDA approval for SD, level A evidence supports their use [8, 15]. TCIs boast anti-inflammatory effects through decreased production of pro-inflammatory cytokines [19]. The safer short-term use of TCIs compared to TCSs makes them especially useful on sensitive skin areas, including the face, neck, and eyelids, although they are still efficacious on the scalp and chest [7, 12, 16, 19, 20].

Pimecrolimus and tacrolimus have revealed comparable, if not superior, efficacy to TCSs and antifungals for SD. Regimens may include pimecrolimus once to twice daily for up to 4 weeks and tacrolimus twice daily for 4 weeks, followed by twice-weekly applications thereafter for the face and body. Of note, however, some studies only recommend application of TCIs until SD resolution, which typically occurs in less than 4 weeks [2, 5, 19–22]. In one study, SD symptom relief from pimecrolimus was observed to be longer lasting than that of betamethasone valerate 0.1% cream [17].

Pimecrolimus is often preferred over tacrolimus owing to its greater cosmetic profile [7]. As hypopigmentation is common in skin of color patients with SD, treatment with pimecrolimus may improve both SD symptoms and SD-associated hypopigmentation. TCIs are also favorable in older patients, circumventing side effects of long-term TCS use [4, 23].

While some physicians remain concerned about risk of malignancy with long-term TCI use that originated from early studies of orally administered pimecrolimus in monkeys at doses exceeding that of topical pimecrolimus, there has not been a documented association in humans to date. Common side effects of TCIs include burning, erythema, irritation, or itching at the application site. Clinical studies have described application-site burning sensations in 10–37% of pimecrolimus users and in 14–18% of tacrolimus users, while tingling occurred in 6–7% of participants using tacrolimus. For both treatments, symptoms subsided or improved within the initial few days of treatment [2, 7, 17, 24].

Topical Phosphodiesterase Inhibitors

Roflumilast 0.3% foam is a potent PDE4i recently approved for treating SD in patients ages 9 and older. Remarkably, topical roflumilast is the first FDA-approved drug for SD in the past two decades and functions through suppression of proinflammatory cytokines implicated in SD [25, 26]. In clinical trials, roflumilast was well tolerated and achieved significant improvements in itch, scaling, and erythema. Itch improvements occurred within 48 h of first application, and half of patients achieved clinical SD clearance within 8 weeks. Roflumilast is safe for application on all body surfaces, with relevant treatment-emergent adverse events (AEs) in a phase III trial of 457 patients including nausea (1.6%), diarrhea (0.6%), and application-site pain (0.3%). While significant improvements in dyspigmentation were observed with roflumilast treatment, new dyspigmentation did occur, although uncommonly, in 7 out of the 457 patients [26, 27]. Additionally, the foam formulation of roflumilast is suitable for a diverse range of skin and hair types [28].

Crisaborole, another PDE4i, has shown efficacy for off-label SD management. In a study of 30 patients, twice-daily use for 4 weeks led to clinical and subjective improvement. Unspecified AEs were reported in 2% of study participants; however, common AEs of crisaborole include burning/stinging, erythema, and pruritus. With the advent of roflumilast and its potential for first-line treatment, crisaborole is a second-line topical PDE4i for SD [29].

Metronidazole

Metronidazole 0.75% gel has shown superiority compared to placebo for treating facial SD in multiple trials. While level B evidence supports its recommended twice daily use for 4 weeks, metronidazole is not clinically utilized given the abundance of alternative treatment options [7, 8].

Case Reports of Prescription Topical Treatments

Ruxolitinib 1.5% cream, approved for AD and vitiligo, successfully treated recalcitrant facial SD with concomitant rosacea in one case with twice-daily application for 2 weeks and elicited almost complete resolution in another case of treatment-refractory SD with every other day application for 4 weeks [30, 31]. Ruxolitinib for SD treatment is currently undergoing further evaluation in clinical trials [32].

Tapinarof is an aryl hydrocarbon receptor agonist with notable anti-inflammatory and skin barrier-modifying effects that is FDA-approved for plaque psoriasis, with one case report demonstrating its efficacy in treating recalcitrant, extensive SD [33].

Ivermectin 1% cream, an anti-parasitic and anti-inflammatory topical approved for rosacea, showed success in a case series of eight patients for treatment of limited SD [34].

Over the Counter Topical Treatments

Level A evidence supports the efficacy of lithium gluconate 8% (ointment, gel) for facial SD; however, topical lithium salts (gluconate and succinate) are currently only available in Europe [7, 35].

Antifungal shampoos with selenium disulfide (1% OTC, 2.5% prescription) and zinc pyrithione (1% OTC) are effective for managing SD on the scalp and beyond, with their popularity related to their accessibility and affordability. While selenium disulfide functions to rebalance the skin microbiome and reduce adherent flakes as a keratolytic, zinc pyrithione employs an antifungal mode of action [7]. Danish guidelines detail the level B evidence supporting the use of selenium disulfide and zinc pyrithione as alternatives to topical ketoconazole; however, evidence remains limited [15]. A recent study of 64 patients with moderate-to-severe SSD observed that selenium disulfide 1% shampoo is as effective as ketoconazole 2% shampoo, with selenium disulfide eliciting superior cosmetic outcomes [36]. Regimens vary; however, an emphasis on initial management with 2–3 applications weekly for 2–4 weeks followed by weekly to biweekly maintenance applications are recommended [5–7, 15]. These shampoos are unlikely to maintain SD remission as monotherapy, with one study of 400 patients using selenium disulfide and zinc pyrithione shampoos citing a 50% relapse in less than 1 month after discontinuing thrice-weekly use [37]. Selenium disulfide may cause scalp itching and irritation and can be malodorous, while zinc pyrithione is well tolerated and odorless [38–40].

The use of coal tar 4% shampoo on the scalp once to twice weekly has been used for SSD given its antifungal, anti-inflammatory, keratolytic, and sebum-reducing properties. However, safety concerns have been posed—most notably skin atrophy, telangiectasias, hyperpigmentation, and an increased risk of squamous cell carcinoma with long-term use [7].

Combination shampoos with non-steroidal anti-inflammatory and antioxidative agents (glycyrrhetinic acid, bisabolol, cannabidiol), antifungal agents (piroctone olamine, lactoferrin, naftifine hydrochloride), keratolytics (lipohydroxy acid, salicylic acid) and combinations of zinc pyrithione, various plant extracts, and luliconazole and hydroxy acid derivatives with copper tripeptides have all shown potential in treating SSD; however, additional evidence is warranted [6, 41–43].

Investigations into the influence of the gut–skin axis, prebiotics, and probiotics on SD have been inconsistent. Research on the role of biotin, nicotinamide, zinc, vitamin E, and vitamin D in decreasing SD risk points to their potential to modulate inflammation and skin barrier function, though their therapeutic impact as supplements for SD remains uncertain [7, 44].

Studies have shown the efficacy of topical recombinant human thymosin beta-4, a topical cream continuing glutathione, and a shampoo with an active ingredient derived from fatty acids for treatment of SSD and FSD; however, none of these formulations are commercially available at this time [45–47]. For FSD, botanical treatments including aloe vera, tea tree oil, and Quassia amara extract have some clinical evidence for their use [35]. Additional treatments include topical nicotinamide applied daily for 12 weeks and Promiseb^®, a combination nonsteroidal cream with multiple active ingredients that has been shown to be comparable to topical desonide [7].

Systemic Treatments

The addition of systemic oral agents to an SD treatment regimen is reserved for worsening, extensive, and recalcitrant presentations.

Oral Antifungals

The off-label use of oral antifungals (OAFs), including terbinafine, itraconazole, fluconazole, and pramiconazole, can be considered for extensive, intractable, and/or multifocal SD [16, 48]. Studies supporting oral treatment with terbinafine and itraconazole for SD have warranted their level A and B evidence for use, respectively [8].

Treatment with terbinafine 250 mg once daily for 4–6 weeks may be used for moderate-to-severe SD, showing success in a study of 174 patients in treating hairline, chest, and/or interscapular SD [5, 7, 8, 48, 49]. Two RCTs of terbinafine for SD reported no serious AEs, while an open trial reported 1% of 661 patients discontinued treatment secondary to gastrointestinal complaints and 5% of patients experienced mild, transient AEs [48]. Reported AEs of terbinafine include taste disorders, tachycardia, insomnia, gastrointestinal symptoms, migraines, and rash.

Regimens of itraconazole 200 mg once daily for 7 days followed by pulse therapy for 2–11 months and fluconazole pulse regimens of 200 mg once weekly for 4 weeks or 300 mg once weekly for 2 weeks have shown efficacy [48]. Notably, itraconazole and fluconazole’s fewer adverse effects are secondary to their weaker binding of human CYP when compared to ketoconazole [50]. Itraconazole has an acceptable safety profile with common AEs including nausea, headache, and drug–drug interactions. An RCT of 68 subjects taking itraconazole found no derangements in serum complete blood counts nor liver function tests (LFTs) neither during nor at the completion of the study [7, 51]. When used for less than 4 weeks and/or for pulse regimens in SD for patients without pre-existing liver disease, LFT monitoring is not indicated [52]. Reported AEs of fluconazole include elevated LFTs and nausea; thus, LFT monitoring may be indicated [7].

Pramiconazole has been shown to be effective with a single 200-mg dose for SD treatment, with reported AEs including diarrhea and gastrointestinal symptoms [7, 48].

While the efficacy of orally administered ketoconazole for SD has been demonstrated (although with SD recurrence upon discontinuation), it is not recommended for use because of its poor safety profile [7, 48].

Isotretinoin

Low-dose isotretinoin (10–20 mg every 1–2 days for 2–6 months) has been shown to improve refractory SD [5]. In one study of 48 subjects treated with isotretinoin 10–20 mg daily for 2–6 months, improvements in pruritus, erythema, and scaling were observed. A reported 11.1% of patients relapsed within 3 months of treatment cessation, and no serious AEs led to treatment discontinuation [53]. In a case of recalcitrant SD, a patient achieved and maintained SD clearance for 1 year without relapse with continuous use of isotretinoin 20 mg daily and topical ketoconazole [48].

Apremilast

Apremilast, an oral PDE4i approved for psoriasis and psoriatic arthritis, functions by the same mechanism as its topical counterparts to treat inflammatory dermatoses. A case series of patients with recalcitrant SD on the scalp, face, ears, and chest showed significant disease improvement after 3 months of oral treatment with off-label apremilast 30 mg twice daily; one patient reported nausea [54]. While it was reported that one patient required tacrolimus for maintenance therapy, the study did not specify a time course during which they evaluated for relapse.

Prednisone

Use of prednisone at 0.5 mg/kg/day for 15 days followed by a gradual taper successfully treated one case of severe, recalcitrant SD. Relapse was prevented with tapering, followed by maintenance therapy with TCSs and TAFs [48].

Biologics

One case series cites the use of ustekinumab, a biologic targeting interleukin (IL)-12 and IL-23, for chronic, refractory SD in six patients. The authors reported near to complete clearance of SD after 3–5 doses in 5/6 patients, with clearance maintained after treatment cessation for varying durations (6–38 weeks) and 3/6 subjects requiring topical maintenance regimens. No AEs were reported [55].

Additional Oral Treatments

Recent studies have shown the efficacy of various herbal medicines and traditional Chinese medicine in treating SD [56–59]. In one study, a low-dose oral homeopathic medication containing potassium bromide, sodium bromide, nickel sulfate, and sodium chloride showed significantly improved chronic dandruff after 10 weeks [7].

Procedural Treatments

Multiple procedure-based treatments have been explored for SD with varying efficacy and uptake.

Injections

Botulinum neurotoxin injections for scalp and facial SD are posited to reduce sebaceous gland activity. While one trial of 20 patients showed no significant improvement in SD severity after 150 units of toxin, other clinical studies suggest its potential in reducing sebum production [60].

QR678/QR678 Neo^®, an injectable polypeptide for hair growth, showed efficacy in a pilot study of 40 patients with SSD, improving erythema, pruritus, and flaking with sustained benefits at 1-year follow-up. While scalp discomfort and pruritus were reported, the treatment’s anti-inflammatory and antifungal properties warrant further investigation [60, 61].

Light

Phototherapy, including ultraviolet B (UVB) light, intense pulsed light (IPL), light-emitting diode (LED) therapy, and photodynamic therapy (PDT), may be efficacious for treating SD by targeting inflammation, Malassezia growth, and sebaceous gland activity. Narrow-band UVB, a treatment with level C evidence, improved severe scalp, chest, and face SD in a study of 18 patients treated three times weekly for at least 8 weeks, though 11 patients relapsed within 21 days [8, 60]. IPL combined with supramolecular salicylic acid significantly reduced SD lesions in 45 subjects treated every 4 weeks for three total sessions in another study. LED therapy reduced pruritus, scaling, and sebum production and improved skin appearance and texture in one patient with recalcitrant facial SD [60, 62–64]. Indole-3-acetic acid (IAA) PDT with 520-nm green light significantly reduce pruritus, burning, erythema, tightness, scaling, and sebum secretion after three weekly sessions in a study of 23 subjects with FSD, with results maintained for 3 weeks post-treatment [60, 65].

Lasers

In a study of 34 subjects, combining tacrolimus with 1064-nm Nd:YAG laser therapy reduced seborrhea more than in the tacrolimus alone group, while both groups saw reductions in erythema, scaling, and affected areas of SD. Additionally, the laser group exhibited decreased Malassezia levels and improved skin texture. The 1450-nm and 1726-nm diode Nd:YAG lasers show potential in targeting sebum production, and pulsed dye lasers can be leveraged to reduce follicular inflammation in patients with SD [60, 66].

Cryotherapy

Precision cryotherapy, which targets specific anatomic regions with temperatures between − 20 and 10 °C, was found to be safe and effective for SSD in a study of 24 subjects. After three treatments at 2-week intervals, patients reported significant improvements in itch and erythema by week 8 [60, 67].

Other Procedure-Based Treatments

A study of 72 patients with facial SD treated every 2 weeks with a transdermal liquid jet of vitamin B₆, glycyrrhizin, metronidazole, and hyaluronic acid showed significant improvements in erythema and skin hydration after three or more treatments [68].

Treatment Considerations

Patient Demographics

OTC shampoos and solution-based topicals can be drying or irritating, especially on heat- or chemical-treated hair, leading to damage [69]. Drying products like ketoconazole shampoo should be used cautiously in populations with fragile hair, and counseling should clearly detail topical application focused on the scalp to avoid hair damage. Additionally, when choosing TAF formulations, one study of SD treatments showed black patients favored ointments and oils while Caucasian patients preferred foams, gels, and sprays [23].

Managing SD in older adults requires consideration of chronic health conditions, limited mobility, and potential cognitive decline. First-line options include OTC and prescription antifungal shampoos, which are effective with few side effects, though they may be less potent than other treatments. TCSs provide stronger relief but require careful monitoring, and systemic treatments like isotretinoin or oral corticosteroids warrant extra caution in patients with polypharmacy [4].

Diet

Dietary factors may influence SD, but evidence is mixed. A case–control study of 267 patients, including 59 with SD, found higher SD prevalence linked to consumption of simple carbohydrates, while patients with SD consumed more non-acidic fruits, vegetables, and nuts [70]. Certain foods, like citrus and leafy greens, have had varied effects, sometimes improving and other times worsening SD symptoms. These findings contrast with larger studies, which suggest a fruit-based diet may reduce SD risk in women, while a Western diet increases risk for all patients [6, 44].

Hair Care Practices

Treatment for SD should consider washing frequency, as less frequent washing can make treatment more challenging. While one study found that while both ketoconazole 2% foam (leave-in treatment) and shampoo (requiring washing) were effective, foam users reported higher satisfaction, likely owing to better penetration and longer contact time among those who wash less frequently [23]. Experts recommend that patients avoid covering their hair for extended periods, if possible, as this can disrupt the scalp microbiome and exacerbate SSD. Some recommend refraining from using oily hair products that act as occlusive agents. To prevent SD worsening, counseling on hair washing every 2 weeks and avoiding scalp oils or pomades is warranted. As it has been shown that hair extensions may irritate the scalp and contribute to SD, natural hairstyles may also help manage SD [6, 23].

Conclusions

The myriad presentations and pathophysiologic drivers of SD lend themselves to a wide arsenal of treatment strategies. SD treatment requires a tailored approach based on individual patients and their needs, including condition severity and lesional distribution. Initial treatment should focus on healthy skin care practices, and treatment plans should address both the underlying disease as well as secondary features.

Treatment for limited disease may employ OTC antifungal shampoos or first-line prescription treatments, including FDA-approved TAFs and TCSs, off-label TCIs, and/or topical roflumilast. With increased uptake of topical roflumilast, the drug may climb its way to the top of the SD treatment ladder. Refractory cases may require OAFs or low-dose isotretinoin. Varying combinations of treatments can leverage anti-inflammatory, anti-fungal, and keratolytic modalities. Maintenance regimens may involve TAFs, with adjunctive use of keratolytics [6, 35] (Fig. 1). Although the potential for side effects with long-term use of certain agents remains a consideration, the broad array of available treatments ensures that patients can find an effective and tolerable regimen. Additionally, considerations such as patient demographics, diet, and hair care practices play an important role in optimizing treatment outcomes.

Fig. 1.

Recommended treatment algorithm for management of seborrheic dermatitis

Ongoing investigations should aim to identify additional treatments, like roflumilast, that may be used on all affected body surfaces for prolonged periods with minimal or no AE risk with the aim of controlling, or even possibly eliminating, this chronic condition. Through thoughtful treatment strategies, healthcare professionals can better manage symptoms and improve the quality of life for patients with SD.

Author Contributions

Manuscript concept: Savanna I Vidal, Nikita Menta and Lawrence Green. Manuscript drafting: Savanna I Vidal, Nikita Menta and Lawrence Green. Figure/table creation: Savanna I Vidal and Nikita Menta and Manuscript review: Lawrence Green.

Funding

No funding nor sponsorship was received for this study nor publication of this article.

Declarations

Conflict of Interest

Savanna I Vidals work is funded through an independent research grant from Galderma. Nikita Mentas work is funded through independent research grants from Incyte and Johnson & Johnson. Lawrence Green is an investigator, speaker or advisor to Amgen, Arcutis, BMS, Dermavant/Organaon, Incyte, Janssen, Pfizer, UCB, OrthoDerm, Vyne, and Takeda.

Ethical Approval

This article is based on previously conducted studies and does not contain any new studies performed by any of the authors with human participants nor animals.