Seborrheic dermatitis guide: causes, scalp vs. face, and effective treatments

Seborrheic dermatitis is one of the most common skin conditions — affecting 3–5% of the general population and up to 83% of HIV-positive individuals. It is chronic, relapsing, and manageable but not curable. Here is the complete evidence-based guide.

What causes seborrheic dermatitis

Malassezia — the central role

Malassezia is a genus of lipophilic yeasts that normally colonize human skin as part of the microbiome. In seborrheic dermatitis, Malassezia (primarily M. globosa and M. restricta) overgrows in sebaceous-rich areas and triggers inflammation through:

Lipolysis of sebum triglycerides — Malassezia secretes lipases that cleave sebum into free fatty acids (FFAs). Oleic acid and arachidonic acid — produced by this lipolysis — are the specific FFAs that directly penetrate the stratum corneum and trigger inflammation
Free fatty acid-driven inflammation — oleic acid disrupts the lipid bilayer of the stratum corneum → increased permeability → keratinocyte activation → cytokine release (IL-1α, IL-8, TNF-α)
Immune activation — Malassezia cell wall components activate toll-like receptors → innate immune cascade

Why only some people get seborrheic dermatitis: Sebaceous gland activity and Malassezia colonization levels are similar across individuals. The differentiating factor is the immune response — seborrheic dermatitis patients have an exaggerated inflammatory response to the same Malassezia products that non-affected individuals tolerate. This explains the dramatically higher prevalence in immunocompromised individuals.

Why sebaceous-rich areas

Malassezia requires sebum-derived lipids for survival (it cannot synthesize certain long-chain fatty acids). The areas of highest sebaceous density — scalp, face (nasolabial folds, eyebrows, glabella, beard area), central chest, and back — are where it thrives. This explains the characteristic distribution of seborrheic dermatitis.

Contributing factors

Sebum production: Higher sebum output provides more substrate for Malassezia. Seborrheic dermatitis peaks in infancy (cradle cap — high maternal hormone-driven sebaceous activity), in adolescence (androgen-driven sebum surge), and in adult males (higher lifetime sebum production).

Immune state: Any immunodeficiency dramatically increases severity — HIV, organ transplant, Parkinson's disease (neurogenic inflammation), and malignancy all associate with severe seborrheic dermatitis. Neurological conditions may increase sebaceous activity via autonomic dysfunction.

Stress: Stress increases sebum production via corticotropin-releasing hormone (CRH) acting on sebocytes; also impairs immune regulation. Seborrheic dermatitis reliably flares with stress.

Season: Worse in winter (low humidity, reduced UV — UV has mild antifungal activity; cold drives indoor heating that reduces ambient humidity).

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Scalp seborrheic dermatitis (dandruff)

"Dandruff" is mild-moderate scalp seborrheic dermatitis — accelerated scalp cell turnover (turnover cycle reduced from ~28 days to ~7 days) producing visible flakes with or without scalp erythema and pruritus.

Distinguishing from scalp psoriasis:
Seborrheic: yellowish, greasy, loose flakes; scalp erythema without sharp borders
Psoriasis: thicker, silvery-white, adherent plaques; sharper borders; may extend beyond the hairline onto the forehead (psoriatic "headband" pattern)

Scalp treatment options

Zinc pyrithione (ZPT) 1–2%: Antifungal and antibacterial; disrupts fungal membrane transport. Available OTC in most antidandruff shampoos. Use 2–3× per week; leave on the scalp 3–5 minutes before rinsing. Effective maintenance treatment.

Ketoconazole 2% shampoo: Azole antifungal — inhibits ergosterol synthesis in Malassezia cell membrane. Most evidence-based antidandruff treatment; head-to-head studies show superiority to ZPT for moderate-severe disease. Use 2× weekly for 4 weeks to treat; once weekly for maintenance.

Selenium sulfide 1–2.5%: Cytostatic and antifungal; reduces scalp cell turnover rate. Effective for moderate-severe dandruff; some cosmetic concerns (discoloration risk on colored or chemically treated hair).

Ciclopirox 1% shampoo: Broad antifungal; chelates iron and manganese required for fungal metabolism. Prescription in many countries; strong evidence base for seborrheic dermatitis.

Coal tar 0.5–5%: Reduces scalp cell proliferation rate and has antifungal activity. Older, less cosmetically elegant; effective for refractory scalp SD. Not appropriate during pregnancy.

Salicylic acid 2–3%: Keratolytic — softens and removes scale. Not directly antifungal but improves penetration of antifungal actives when used in combination.

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Facial seborrheic dermatitis

Facial SD most commonly involves:
Eyebrows — scaling along the brow with underlying erythema
Nasolabial folds — greasy yellowish scale in the fold; may extend onto the adjacent cheek
Glabella (between the brows)
Beard and mustache area in men
Behind and inside the ears
Eyelids (seborrheic blepharitis) — scaling on the eyelid margins; associated with meibomian gland dysfunction and dry eye

Distinguishing facial SD from rosacea:
Seborrheic: scaling/flaking present; yellowish, greasy appearance; nasolabial and eyebrow distribution
Rosacea: flushing and persistent redness; telangiectasia; no scaling; central face but different pattern

Distinguishing from atopic/contact dermatitis:
Seborrheic: greasy scale; characteristic distribution (sebaceous areas)
Atopic: intense pruritus; dry rather than greasy scaling; flexural distribution
Contact: sharp border matching the contact area; patient history identifies the contactant

Facial treatment options

Ketoconazole 2% cream: Applied to affected areas once daily for 2–4 weeks; then twice weekly for maintenance. Most evidence-supported topical antifungal for facial SD.

Ciclopirox 0.77% cream/gel: Similar efficacy to ketoconazole; prescription.

Low-potency topical corticosteroids (short-term): Hydrocortisone 1% cream provides rapid anti-inflammatory relief for an acute flare. Use for 1–2 weeks maximum on the face — steroids do not treat the underlying Malassezia and long-term use causes skin atrophy, telangiectasia, and steroid-induced rosacea on the face.

Combination approach: Ketoconazole for the antifungal component + short-course hydrocortisone for acute inflammation — then taper to ketoconazole-only maintenance. This mirrors the clinical approach in guidelines.

Calcineurin inhibitors (tacrolimus 0.1%, pimecrolimus 1%): Evidence-based for facial SD — anti-inflammatory without steroid atrophy risk. Appropriate for long-term facial use where repeat steroid use would be problematic.

Zinc pyrithione-containing face products: Washing with ZPT-containing cleansers reduces Malassezia load on the face. Available in bar soaps and liquid washes; useful for mild facial SD maintenance.

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Seborrheic blepharitis

Scaling and inflammation of the eyelid margins — a common component of facial SD that is often treated separately:
Clean the eyelid margins daily with diluted baby shampoo or lid scrub wipes
Warm compresses applied to the eyelids for 10 minutes daily to liquefy meibomian secretions
Ophthalmology referral if there is corneal involvement or significant dry eye symptoms

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Maintenance strategy

Seborrheic dermatitis is chronic and relapsing — treatment controls symptoms but does not eliminate the underlying Malassezia colonization. Maintenance is more important than acute treatment:

Scalp: Continue ketoconazole or ZPT shampoo once weekly as maintenance after initial treatment — prevents relapse. Most patients need ongoing maintenance indefinitely.

Face: Ketoconazole cream applied twice weekly to affected areas; or ZPT-containing cleanser used as a face wash 2–3× weekly.

Trigger management: Stress reduction, gentle non-fragrant cleansers, avoiding comedogenic products in sebaceous-rich areas, maintaining consistent skincare routine.

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When to see a dermatologist

Seborrheic dermatitis not controlled with OTC ketoconazole or ZPT after 4–6 weeks
Widespread or severe facial or truncal involvement
Eyelid margin involvement with eye symptoms
Any suspicion of psoriasis (thick plaques, joint involvement)
Rapid onset or unusual severity in a previously unaffected adult — may warrant evaluation for immune status

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