see also:

• scalp and hair conditions
• dermatology

• seborrheic dermatitis (SD) a common condition characterised by dry, flaky or greasy skin especially around scalp and areas with sebum glands
• it is a common cause of dandruff
• SD has a predominantly bimodal distribution, with a peak during infancy (2-12 months of age) and another peak in early adulthood.

• sebaceous glands secrete lipids onto the skin surface
  • greatest concentration on the face, followed by the back and the chest; none on the palms, soles and back of the feet
  • sebaceous gland activity is stimulated by androgens and adrenal corticosteroids
  • high sebum activity has a direct correlation with SD and acne, and an inverse relationship with atopic eczema (AD)
  • skin surface lipid film is composed of both sebocyte and keratinocyte derived lipids
    • keratinocyte lipids are incorporated within the layers of the stratum corneum, while sebocyte lipids are secreted onto the skin surface
    • squalene is present only in sebum lipids and is used as a marker to differentiate sebaceous from keratinocyte lipids
• certain bacteria may also contribute to the pathogenesis of SD by their ability to hydrolyse sebum and supply nutrients that promote the growth of Malassezia
  • Staphylococcus species and M. restricta were associated with an increased incidence of scalp disease
  • Propionobacterium species and M. globosa were associated with a normal scalp
  • the balance of M. restricta with other bacterial and fungal organisms was found to be important in the development of SD
• the Malassezia fungus (a lipophilic budding yeast) colonizes areas that are covered with lipids
• lipase is secreted by Malassezia, resulting in the generation of free fatty acids (FFA) and lipid peroxides that activate the inflammatory response
  • Malassezia uses saturated fatty acids, leaving behind irritating unsaturated fatty acids such as oleic acids which are believed to be the main trigger for SD
  • if oleic acid is applied topically, patients with SD experience more extensive skin desquamation than non-SD subjects
• the immune system then generates cytokines, such as IL-1α, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12 and TNF-α.
• this stimulates keratinocyte proliferation and differentiation.
• this results in skin barrier disruption with resulting clinically evident erythema, pruritus and scaling ¹⁾
  • the quantity of yeasts directly correlates with the severity of disease in those predisposed to SD
  • M. restricta and M. globosa are likely the most virulent subspecies, producing large quantities of irritating oleic acids, leading to IL-8 and IL-17 activation
    • virulence factors include:
      • high cell wall lipid content, which provides mechanical stability, promotes resistance to osmosis and also protects it from phagocytosis
      • increased expression of lipase genes
    • on the scalp and forehead, M. restricta is the most common while M. globosa is the most common species found on the chest and back - this is due to to different lipid content at different body sites
    • M. globosa seems to be more common in individuals younger than 14 years, and M. sympodialis seems to be more common in older subjects.
    • adults between 21-30 have been shown to have the highest positive culture rate, with the chest having the highest and the thighs having the lowest positive culture rates of all evaluated body parts
  • IL-17 and IL-4 might play a big role in pathogenesis but needs further research
  • The complex interplay of Malassezia, keratinocytes and the immune response against an altered lipid composition in the skin plays a crucial role in SD pathogenesis.
• in HIV / AIDS, SD is thought to be secondary to a combination of immune dysregulation and disruption in skin microbiota with unhindered Malassezia proliferation.
• in Parkinson's disease, SD is most likely secondary to parasympathetic hyperactivity with increased sebum production as well as facial immobility which leads to sebum accumulation

• whilst SD is often familial, no clear genetic predisposition has been established
• SD, and SD-like syndromes, share genetic mutations that appear to impair the ability of the immune system to restrict Malassezia growth, partially due to complement system dysfunction
• 11 gene mutations or protein deficiencies have been identified that can induce SD or an SD-like rash - most play a role in either the immune response or epidermal differentiation
  • mutations associated with impaired cutaneous immunity:
    • ACT1
      • ACT1 mutation leads to defects in cutaneous immunity by abolishing IL-17, leading to an SD-like inflammation in response to cutaneous fungi
    • C5
      • C5 complement defects can present with diarrhoea, recurrent infections, generalized SD and wasting in infants, better known as Leiner's disease.
    • IKBKG
      • IKBKG encodes nuclear factor kB essential modulator (NEMO) which is essential for NK-kB signalling. This pathway plays a vital role in the regulation of the innate and adaptive immunity, cytokine production, infection, and inflammation
    • STK4
      • STK4 mutation leads to CD4 lymphopenia, low serum C4 level and various combined immunodeficiencies
    • Biotinidase
      • mutation leads to enzyme deficiency which results in decreased free biotin for cellular use
  • mutations associated with epidermal differentiation
    • ZNF750 mutation resulted in a defected zinc finger transcription factor. It is a key regulator for keratinocyte terminal differentiation

• the incidence is higher among human immunodeficiency virus (HIV)-infected immunocompromised patients ranging from 30% to 83%
• lymphoma
• bone marrow suppression

• male gender - increased androgen activity
  • androgens affect sebaceous gland activity and lipid composition in a way that promotes Malassezia growth
• individual lipid composition
• immune status
• neuropsychiatric factors (including Parkinson's disease (PD) and other neuropsychiatric diseases)
• high environmental humidity and heat
• stress
• poor skin and hair care practices
• certain medications such as antineoplastic agents and epidermal growth factor receptor (EGFR) inhibitors
• diet is controversial but SD seems greater in Western diets compared to fruit dominant diets
• other neurological conditions such as stroke (CVA)
• frequent use of cosmetics in women