Seborrheic Dermatitis 

Updated: Aug 13, 2019
Author: Marc Zachary Handler, MD; Chief Editor: William D James, MD 

Overview

Practice Essentials

Seborrheic dermatitis is a papulosquamous disorder patterned on the sebum-rich areas of the scalp, face, and trunk (see the image below). In addition to sebum, this dermatitis is linked to Malassezia,[1] immunologic abnormalities, and activation of complement. Its severity ranges from mild dandruff to exfoliative erythroderma.

Seborrheic dermatitis may affect any hair-bearing Seborrheic dermatitis may affect any hair-bearing area, and the chest is frequently involved. Courtesy of Wilford Hall Medical Center Dermatology Teaching slides.

Signs and symptoms

History findings in seborrheic dermatitis may include the following:

  • Intermittent, active phases manifesting with burning, scaling, and itching, alternating with inactive periods; activity is increased in winter and early spring, with remissions commonly occurring in summer.

  • In active phases, potential secondary infection in intertriginous areas

  • Candidal overgrowth

  • Generalized seborrheic erythroderma (rare)

Physical findings may include the following:

  • Scalp appearance ranging from mild, patchy scaling to widespread, thick, adherent crusts; plaques are rare; lesions may spread from the scalp onto the forehead, the posterior part of the neck, and the postauricular skin

  • Seborrheic skin lesions manifesting as scaling over red, inflamed skin; hypopigmentation (in dark-skinned individuals); oozing and crusting; blepharitis (occurring independently)

  • Lesion distribution following the oily and hair-bearing areas of the head and the neck; extension to submental skin can occur

  • Either of two distinct truncal patterns: (1) annular or geographic petaloid scaling or (2) pityriasiform variety (rare)

Malassezia organisms are probably not the cause of seborrheic dermatitis but a cofactor linked to a T-cell depression, increased sebum levels, and an activation of the alternative complement pathway. Various medications may also flare or induce seborrheic dermatitis.[2, 3]

See Clinical Presentation for more detail.

Diagnosis

The diagnosis of seborrheic dermatitis is usually made on clinical grounds, based on a history of waxing and waning severity and by the distribution of involvement upon examination.

A skin biopsy may be needed in persons with exfoliative erythroderma, and a fungal culture can be used to rule out tinea capitis, though tinea capitis is rare in adults. Dermatopathologic findings of seborrheic dermatitis are nonspecific and typically include the following:

  • Hyperkeratosis

  • Acanthosis

  • Accentuated rete ridges

  • Focal spongiosis

  • Parakeratosis

See Workup for more detail.

Management

Early treatment of flares is encouraged. Behavior modification techniques in reducing excoriations are especially helpful with scalp involvement.

Pharmacologic agents that may be used include the following:

  • Topical corticosteroids (discouraged except for short-term use and at risk for tachyphylaxis when used as monotherapy)

  • For skin involvement, ketoconazole, naftifine, or ciclopirox creams and gels[4, 5, 6] ; alternatively, calcineurin inhibitors (ie, pimecrolimus, tacrolimus),[7, 8, 9] sulfur or sulfonamide combinations, or propylene glycol[10, 11, 12, 13, 14]

  • For acute flares, class IV or lower corticosteroid creams, lotions, or solutions

  • For severe or unresponsive lesions, systemic fluconazole[15]

Treatment of dandruff may involve the following:

  • More frequent shampooing or longer lathering

  • Discontinuance of hair spray or hair pomades

  • Use of shampoos containing salicylic acid, tar, selenium, sulfur, or zinc[16, 17] ; selenium sulfide (2.5%), ketoconazole, and ciclopirox shampoos may help by reducing Malassezia yeast scalp reservoirs[18, 19, 20] ; an alternative to a shampoo with zinc is a conditioner rinse with zinc, 0.01% fluocinolone, and acetonide topical oil

  • Overnight application of tar, bath oil, or Baker’s P&S solution; Derma-Smoothe F/S oil is especially helpful for widespread plaques

See Treatment and Medication for more detail.

Background

Seborrheic dermatitis is a papulosquamous disorder patterned on the sebum-rich areas of the scalp, face, and trunk. When localized to the scalp, it is commonly referred to as dandruff. In addition to sebum, this dermatitis is linked to Malassezia,[1] immunologic abnormalities, and activation of complement. It is commonly aggravated by changes in humidity, changes in seasons, trauma (eg, scratching), or emotional stress. The severity varies from mild dandruff to exfoliative erythroderma. Seborrheic dermatitis may worsen in Parkinson disease and in AIDS.[21, 22]  Increased perspiration in Parkinson disease may be the link to seborrheic dermatitis.

Pathophysiology

Seborrheic dermatitis is associated with normal levels of Malassezia but an abnormal immune response. Helper T cells, phytohemagglutinin and concanavalin stimulation, and antibody titers are depressed compared with those of control subjects. Zani et al report that even with antifungal treatments, there was no reduction in levels of Malassezia.[23] The contribution of Malassezia species to seborrheic dermatitis may come from its lipase activity—releasing inflammatory free fatty acids—and from its ability to activate the alternative complement pathway.[24]

Etiology of Seborrheic Dermatitis

The exact pathophysiology remains unclear. Malassezia organisms are probably not the cause but are a cofactor linked to a T-cell depression, increased sebum levels, and an activation of the alternative complement pathway. Persons prone to this dermatitis also may have a skin-barrier dysfunction.[25, 26]

Because seborrheic dermatitis is uncommon in preadolescent children, and tinea capitis is uncommon after adolescence, dandruff in a child is more likely to represent a fungal infection. A fungal culture should be completed for confirmation.

Various medications may flare or induce seborrheic dermatitis. These medications include auranofin, aurothioglucose, buspirone, chlorpromazine, cimetidine, ethionamide, fluorouracil, gold, griseofulvin, haloperidol, interferon alfa, lithium, methoxsalen, methyldopa, phenothiazines, psoralens, stanozolol, thiothixene, and trioxsalen.[2, 3]

Epidemiology

The prevalence rate of seborrheic dermatitis is 3-5%, with a worldwide distribution. In the United States alone, $300 million is spent annually on dandruff over-the-counter treatments.[27] Dandruff, the mildest form of this dermatitis, is probably far more common and is present in an estimated 15-20% of the population.

Race

Seborrheic dermatitis occurs in persons of all races.

Sex

Seborrheic dermatitis is slightly worse in males than in females.

Age

The usual onset occurs with puberty. It peaks at age 40 years and is less severe, but present, among older people. In infants, it occurs as cradle cap or, uncommonly, as a flexural eruption or erythroderma.[28]

 

Presentation

History

Intermittent, active phases of seborrheic dermatitis manifest with burning, scaling, and itching, alternating with inactive periods. Activity is increased in winter and early spring, with remissions commonly occurring in summer.

Active phases of seborrheic dermatitis may be complicated by secondary infection in the intertriginous areas.

Candidal overgrowth is common in infantile napkin dermatitis. Such children may have a diaper dermatitis variant of seborrheic dermatitis or psoriasis.

Generalized seborrheic erythroderma is rare. It occurs more often in association with AIDS,[21, 22] congestive heart failure, Parkinson disease, and immunosuppression in premature infants.

Physical Examination

The scalp appearance of seborrheic dermatitis varies from mild, patchy scaling to widespread, thick, adherent crusts. Plaques are rare. From the scalp, seborrheic dermatitis can spread onto the forehead, the posterior part of the neck, and the postauricular skin, as in psoriasis. Note the images below.

Seborrheic dermatitis affecting the scalp line and Seborrheic dermatitis affecting the scalp line and the eyebrows with red skin and scaling. Courtesy of Wilford Hall Medical Center Dermatology slide files.
Seborrheic dermatitis may affect any hair-bearing Seborrheic dermatitis may affect any hair-bearing area, and the chest is frequently involved. Courtesy of Wilford Hall Medical Center Dermatology Teaching slides.

Seborrheic dermatitis skin lesions manifest as branny or greasy scaling over red, inflamed skin. Hypopigmentation is seen in dark-skinned individuals. Infectious eczematoid dermatitis, with oozing and crusting, suggests secondary infection. A seborrheic blepharitis may occur independently.

Distribution follows the oily and hair-bearing areas of the head and the neck, such as the scalp, the forehead, the eyebrows, the lash line, the nasolabial folds, the beard, and the postauricular skin. An extension to submental skin can occur. Presternal or interscapular involvement is more common than nonscaling intertrigo of the umbilicus, axillae, inframammary and inguinal folds, perineum, or anogenital crease, which also may be present.

Two distinct truncal patterns of seborrheic dermatitis can occasionally occur. An annular or geographic petaloid scaling is the most common. A rare pityriasiform variety can be seen on the trunk and the neck, with peripheral scaling around ovoid patches, mimicking pityriasis rosea. Note the image below.

African Americans and persons from other darker-sk African Americans and persons from other darker-skinned races are susceptible to annular seborrheic dermatitis, also called petaloid seborrheic dermatitis or seborrhea petaloides. Sarcoidosis, secondary syphilis, and even discoid lupus may be in the differential in such cases. Courtesy of Jeffrey J. Meffert, MD.
 

DDx

 

Workup

Laboratory Studies

A clinical diagnosis of seborrheic dermatitis is usually made based on a history of waxing and waning severity and by the distribution of involvement upon examination.

Procedures

A skin biopsy may be needed in persons with exfoliative erythroderma, and a fungal culture can be used to rule out tinea capitis, although tinea capitis in the adult is rare.

Histologic Findings

Dermatopathologic findings of seborrheic dermatitis are nonspecific, but they may present in an acute or chronic stage.[27] In the acute stage, inflammation is noted perifollicularly and perivascularly. Spongiosis and psoriasiform hyperplasia is often seen, as well as the classic finding, "shoulder” parakeratosis, with parakeratosis around the follicular opening. Neutrophils are often seen in the crust at the margins. Chronic seborrheic dermatitis may appear similar to psoriasis, but psoriasis is distinguished by regular acanthosis, thinned rete ridges, exocytosis, parakeratosis, and an absence of spongiosis. Neutrophils may be seen in both diseases.[27]

 

Treatment

Medical Care

Early treatment of flares is encouraged. Behavior modification techniques in reducing excoriations are especially helpful with scalp involvement.

Low-potency topical corticosteroids, such as hydrocortisone, desonide, and mometasone furoate, have shown to be efficacious on the face.[30] Topical steroids have been associated with the development of telangiectasias and thinning of the skin.[30] Although the levels of Malassezia yeast does not correlate with the severity of seborrheic dermatitis, antifungal therapies are first-line therapies.[23] Ketoconazole, naftifine, or ciclopirox creams and gels are effective therapies.[4, 5, 6] Alternatives include calcineurin inhibitors (ie, pimecrolimus, tacrolimus),[7, 8, 9] sulfur or sulfonamide combinations, or propylene glycol.[10, 11, 12, 13, 14, 31] Class IV or lower corticosteroid creams, lotions, or solutions can be used for acute flares.[32] Tea tree oil has been reported to benefit the condition.[33, 34] Systemic fluconazole may help if seborrheic dermatitis is severe or unresponsive.[15] Combination therapy has been recommended.[35]

Dandruff responds to more frequent shampooing or a longer period of lathering. Use of hair spray or hair pomades should be stopped. Shampoos containing salicylic acid, tar, selenium, sulfur, or zinc are effective and may be used in an alternating schedule.[16, 17]  An alternative to a shampoo with zinc is a conditioner rinse with zinc, 0.01% fluocinolone, and acetonide topical oil. Overnight occlusion of tar, bath oil, or Baker's P&S solution may help to soften thick scalp plaques. Derma-Smoothe F/S oil is especially helpful when widespread scalp plaques are present. Selenium sulfide (2.5%), ketoconazole, and ciclopirox shampoos may help by reducing Malassezia yeast scalp reservoirs.[18, 19, 20] Shampoos may be used on truncal lesions or in beards but may cause inflammation in the intertriginous or facial areas.

Systemic low-dose isotretinoin taken by mouth has been reported to benefit severe seborrheic dermatitis.[36] Metronidazole 1% gel has been evaluated, with inconclusive results for the treatment of seborrheic dermatitis of the face.[37, 38] Some suggest using a nonsteroidal cream such as pimecrolimus; patients have reported improvement of up to 80%.[32, 39] Bikowski recommends azelaic acid.[40] Seborrheic blepharitis may respond to gentle cleaning of eyelashes with baby shampoo and cotton applicators. The use of ketoconazole cream in this anatomical region is controversial.

 

Medication

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Antifungals

Class Summary

The mechanism of action may involve alteration of RNA and DNA metabolism or an intracellular accumulation of peroxide that is toxic to fungal cells.

Ketoconazole topical

Ketoconazole topical is available as ketoconazole cream 2% (Nizoral), ketoconazole foam (Extina), ketoconazole shampoo 2% (Nizoral 2%; prescription only in United States), and ketoconazole shampoo 1% (Nizoral A-D Shampoo; over-the-counter in United States). It is an imidazole broad-spectrum antifungal agent. It inhibits the synthesis of ergosterol, causing cellular components to leak, resulting in fungal cell death.

Corticosteroids

Class Summary

Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. They also modify the body's immune response to diverse stimuli.

Betamethasone topical (Valisone)

Betamethasone is a medium-strength topical corticosteroid for body areas. It decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability. Betamethasone affects the production of lymphokines and has inhibitory effects on Langerhans cells.

Desonide

Desonide is used for inflammatory dermatoses responsive to steroids. It decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability.

Keratolytics

Class Summary

Keratolytics cause cornified epithelium to swell, soften, macerate, and then desquamate.

Coal tar shampoo (DHS Tar, MG217, Theraplex T, Psoriasin); Scytera foam

Coal tar shampoo inhibits deregulated epidermal proliferation and dermal infiltration; it is antipruritic and antibacterial.

Immunosuppressants

Class Summary

Immunosuppressants exert anti-inflammatory affects by inhibiting T-lymphocyte activation. They are safer than topical steroids for prolonged use or in skin folds.

Tacrolimus ointment (Protopic)

Tacrolimus ointment is a nonsteroidal anti-inflammatory agent. It should not cause steroid-type skin atrophy. It is currently indicated only for atopic dermatitis in immunocompetent patients aged 2 years and older.

Pimecrolimus (Elidel cream 1%)

Pimecrolimus is a nonsteroidal anti-inflammatory agent. It should not cause steroid-type skin atrophy. It is currently indicated only for atopic dermatitis in immunocompetent patients aged 2 years and older. Use cream sparingly to avoid maceration in skin folds.

 

Questions & Answers

Overview

What is seborrheic dermatitis?

What are the signs and symptoms of seborrheic dermatitis?

Which physical findings suggest seborrheic dermatitis?

What causes seborrheic dermatitis?

How is seborrheic dermatitis diagnosed?

Which drugs may be used to treat seborrheic dermatitis?

What are the treatment options for seborrheic dermatitis dandruff?

What is seborrheic dermatitis?

What is the pathophysiology of seborrheic dermatitis?

What is the pathophysiology of seborrheic dermatitis?

When is a fungal culture indicated in the diagnosis of seborrheic dermatitis?

Which medications may induce seborrheic dermatitis?

What is the prevalence of seborrheic dermatitis?

What are the racial predilections of seborrheic dermatitis?

How does the prevalence of seborrheic dermatitis vary by sex?

How does the prevalence of seborrheic dermatitis vary by age?

Presentation

What are the signs and symptoms of seborrheic dermatitis?

Which physical findings are characteristic of seborrheic dermatitis?

What is the manifestation of seborrheic dermatitis skin lesions?

What is the distribution of seborrheic dermatitis?

Which physical findings are characteristic of a truncal pattern in seborrheic dermatitis?

DDX

Which conditions should be included in the differential diagnoses of seborrheic dermatitis?

What are the differential diagnoses for Seborrheic Dermatitis?

Workup

How is seborrheic dermatitis diagnosed?

What is the role of skin biopsy in the workup of seborrheic dermatitis?

Which histologic findings suggest seborrheic dermatitis?

Treatment

What is the role of behavior modification in the management of seborrheic dermatitis?

Which drugs are used for the treatment of seborrheic dermatitis?

How is seborrheic dermatitis dandruff treated?

What is the efficacy of medical treatment for seborrheic dermatitis?

Medications

Which medications in the drug class Antifungals are used in the treatment of Seborrheic Dermatitis?

Which medications in the drug class Corticosteroids are used in the treatment of Seborrheic Dermatitis?

Which medications in the drug class Keratolytics are used in the treatment of Seborrheic Dermatitis?

Which medications in the drug class Immunosuppressants are used in the treatment of Seborrheic Dermatitis?