Seborrheic dermatitis and hair loss
Seborrheic dermatitis and hair loss

SEBORRHEIC DERMATITIS AND HAIR LOSS

Seborrheic dermatitis is a common inflammatory condition of the skin.  On the scalp, the condition presents as lesions of oily scaling with mild to severe skin inflammation due to hyperkeratinisation and infection.  The lesions appear as mild shedding of the skin to crusts completely fixed to the scalp.  The excess of keratinised skin can lead to blocking or capping of the hair follicle and

Seborrheic dermatitis is caused by an altered relationship between commensal bacteria on the skin, increased sebum production, deteriorated skin barrier function and an increased keratin turnover rate leading to thickened scales on the scalp.

Therapy for flare ups of seborrheic dermatitis consist of antifungal agents, low-potency corticosteroids, immunomodulators, nutritional supplements and alternative non-medical topical formulations.  Seborrheic dermatitis usually resolves after conventional treatment but may re-appear even after successful therapeutic treatment if underlying causes, such as zinc deficiency, are not resolved or if the treatment period is not sufficient.

FOLLICULAR HYPERKERATINISATION AND RETENTION HYPERKERATOSIS IN SEBORRHEIC DERMATITIS

When the skin is exposed to repeated injury, such as inflammatory events due to infection, it will usually elicit an increased proliferative rate of skin cells.  The skin cells will also produce more keratin in response to assault, thus increasing the thickness of the outer layer of the skin.  Defective keratin production leads to irregular aggregates of intermediate filaments, which then leads to impaired barrier function.  The skin then reacts with compensatory hyperproliferation, this leads to hyperkeratinisation and retention hyperkeratosis.

Hyperkeratinisation (the abnormal and rapid shedding of skin cells) can be considered as one if the most crucial events in the development of seborrheic dermatitis.  Retention hyperkeratosis occurs when skin cells of the hair follicle remain adhered to the skin so they cannot shed normally.  This abnormal skin shedding begins under the skin, around 8 weeks before the condition is visible on the skin.  Keratin cells affected by seborrheic dermatitis have an increased number of desmosomes that connect cell membranes together with intermediate filaments known as tonofilaments resulting in a thicker and more cohesive tonofilament.

HORMONES LINKED WITH SEBORRHEIC DERMATITIS ANDROGENS

Sebaceous glands secrete sebum, which coats the hair shaft and the skin.  Sebum reduces water loss from the scalp, protects the skin from UV radiation and aids in the transport of fat-soluble antioxidants to the skin surface.  Sebum production is under hormonal control and sebaceous glands are regulated by androgens, retinoids and growth factors.

Sebaceous glands can independently convert weak androgens such as dehydroepiandrosterone sulphate into testosterone and dihydrotestosterone.  Androgen receptors in the pilosebaceous unit respond to testosterone and the more potent dihydrotestosterone (DHT).  Generally, a high level of DHT will increase activity of the sebaceous gland leading to an increase amount of sebum on the scalp.

SEBORRHEIC DERMATITIS AND THE MALASSEZIA SPECIES

The current accepted theory on the pathogenesis of the disease is irritation of the skin due to the secretion of fatty acids from the Malassezia species.  The Malassezia species makes up a normal part of the scalp flora and is present in other regions of the body that are abundant in sebum.

In 1952, Leone linked Malassezia species with various other dermatologic complaints [1].  The participation of this fungus with seborrheic dermatitis was suggested by the fact that the condition variably responds to antifungal treatment.

The potential manifestation of seborrheic dermatitis depends on the immunological profile of the patient.  The exact physiopathology of seborrheic dermatitis is yet to be completely determined; however, a reaction to the Malassezia species on the skin is a necessary for the disease to progress.  In 1989, researchers failed to find any difference in the amount of Malassezia species between individuals with seborrheic dermatitis and healthy controls, or between affected areas and non-affected areas [2].  These findings suggest other mechanisms are associated with the reaction to the fungus and they may not be related to the amount of Malassezia present.

To prove that Malassezia species contributed to the skin inflammation seen in seborrheic dermatitis, Plotkin and De Angelis demonstrated the production of lipase (an enzyme that breaks down fat) caused an inflammatory response when left on the skin surface [3,4].  The development of seborrheic dermatitis depends on three factors:  the production of sebum, the metabolism of Malassezia and the immunocompetence of the individual to resist bacterial infection [5].

Malassezia hydrolyses triglycerides in sebum into unsaturated acids, such as oleic acid and arachidonic acid by lipase.  These metabolites stimulate keratin cell abnormalities resulting in disruption of the skin cell barrier.

THE IMMUNE AND ANTIOXIDANT RESPONSE IN SEBORRHEIC DERMATITIS

Immunity to fungal infection is primarily determined by the hosts’ cell mediated immune response, any deficiencies in any part of the cell mediated response will increase susceptibility to infection in the presence of fungus.

Bergbrant determined the quantity of Malassezia species in the skin was not the determining factor for the inflammatory reaction seen in seborrheic dermatitis, but rather the amount of lipid in the skin surface and the immune response of the individual.  The relationship between the season, stress and reduced T-cell function was also observed [6].

The main complicating factor that determines the severity of seborrheic dermatitis is secondary bacterial infection, which increases inflammation, discomfort and T cell activity.  Memory T cells are activated by inflammation and confer rapid protection by killing infected cells.  Memory T cells remain even after infection has been eliminated and controlled.  Upon re-exposure to the specific invading offender, memory T cells become effector cells that can respond quickly.  This explains the chronic relapsing experienced by patients with seborrheic dermatitis.

THERAPIES FOR TREATING SEBORRHEIC DERMATITIS

Since this chronic inflammatory disease occurs in response to the presence of Malassezia species on the scalp, the amount of lipid on the skin, nutritional deficiencies and secondary bacterial infection.  The objective of treatment consists of reducing the oiliness on the scalp, controlling inflammation and reducing the potential aggravation of a secondary bacterial infection.

Various types of therapeutic agents and medication are used to combat seborrheic dermatitis.  Due to the chronic and relapsing nature of the disease, it is important the patient remain compliant with treatment even if the condition appears to resolve before the treatment period has elapsed.

Anti-inflammatory agents | Conventional treatment for adult seborrheic dermatitis often starts with topical steroids or a calcineurin inhibitor.  These topical therapies can be administered as a shampoo, topical steroid solutions, lotions applied to the scalp or creams applied to the skin.  Adults with the condition will typically use topical steroids once or twice daily in addition to a medicated shampoo.  These conventional treatments have fungicidal and anti-inflammatory properties.  Topical corticosteroids result in rapid improvement in symptoms of seborrheic dermatitis; however, relapses are frequent.   Corticosteroids can only be used for short periods as side effects will occur with prolonged use.  Calcineurin inhibitors exert an effect equal to low potency corticosteroids, are well tolerated and induce a more prolonged remission than corticosteroids.

Keratolytics | Keratolytics based on salicylic acid and sometimes sulphur, help with the softening and removal of the scalps adhered to the hair and scalp.  More traditional methods for treating seborrheic dermatitis have keratolytic but not specific antifungal properties.  Popular keratolytic that are widely used to treat seborrheic dermatitis include salicylic acid, tar and zinc pyrithione shampoos.  Zinc pyrithione is a non-specific keratolytic with antifungal properties.

Antifungals | Antifungals work by targeting Malassezia directly.  When treatment stops, and the normal flora is restored, the condition will appear again.  Antifungals do not generally deal with any secondary bacterial infection that may be aggravating the condition.

Laser therapy | Combination treatments with lasers (e.g., pulsed-dye laser, 755-nm alexandrite laser, 810-nm diode laser, 1064-nm Nd:YAG laser) and microdermabrasion are non-invasive techniques currently under approval for different hyperkeratotic diseases.

Nutritional therapies | Most of the mechanisms involved in seborrheic dermatitis are related to the function of zinc.  Zinc in the skin acts as a natural bactericide reducing the potential for secondary bacterial infection that worsens the condition.  Zinc has antifungal properties, regulates cell replication, immune activity and wound repair.  Zinc improves immune activity by preserving natural killer cell function and has anti-inflammatory effects.  A 2019 study showed patients with seborrheic dermatitis had significantly lower levels of zinc than healthy controls [7].

Low levels of zinc lead to metabolic alterations that reduce sulphur availability, enzyme function, B-complex vitamin capacity and affect iron use in the body.  Patients with seborrheic will need to address the secondary nutritional deficiencies that may be present for long term disease remission.

Topical therapies | The hair follicle is an ideal delivery route for topical agents.  Topical formulations that incorporate red clover and caffeine can help in the management of seborrheic dermatitis.  Red clover contains phytoestrogens that help to modulate skin physiology, targeting skin cells, sebaceous glands and improving immune responses.  Caffeine is a powerful antioxidant that acts in several ways to improve symptoms of inflammation.  Caffeine plays a supportive role in cell death preventing inflammatory triggers to cell injury or infection.

THE FINAL WORD

Seborrheic dermatitis affects up to 5% of the general population.  While it is slightly more common in men, women tend to have more aggravated and severe symptoms.  This condition can flare up after puberty and remain as a chronic condition throughout life.  To reduce the severity and risk of disease relapse, several therapies can be used to control the disease.  With proper and sustained long-term management, seborrheic dermatitis can be treated successfully.

REFERENCES

  1. Inamadar AC PA. The genus Malassezia and human disease. Indian J Dermatol Venereol Leprol. 2003;69:265-70.
  2. McGinley KJ, Leyden JJ, Marples RR, Kligman AM. Quantitative microbiology of the scalp in non-dandruff, dandruff, and seborrheic dermatitis. J Invest Dermatol. 1975;64:401-5.
  3. Plotkin LI, Squiquera L, Mathov I, Galimberti R, Leoni J. Characterization of the lipase activity of Malassezia furfur. J Med Vet Mycol. 1996;34:43-8.
  4. DeAngelis YM, Saunders CW, Johnstone KR, Reeder NL, Coleman CG, Kaczvinsky JR Jr, et al. Isolation and expression of a Malassezia globosa lipase gene, LIP1. J Invest Dermatol. 2007;127:2138-46.
  5. Dawson TL Jr. Malassezia globosa and restricta: breakthrough understanding of the etiology and treatment of dandruff and seborrheicdermatitis through whole-genome analysis. J Investig Dermatol Symp Proc. 2007;12:15-9.
  6. Bergbrant IM, Faergemann J. Seborrhoeic dermatitis and Pityrosporum ovale: a cultural and immunological study. Acta Derm Venereol. 1989;69:332-5.
  7. Karabay, E.A. and Cerman, A.A., 2019. Serum zinc levels in seborrheic dermatitis: a case-control study. Turkish journal of medical sciences49(5), pp.1503-1508.