Dandruff is caused by the rapid release of skin cells observed as skin flakes on the scalp and on the shoulder areas where flakes of skin have fallen to.

Dandruff is a condition characterized by flaking of skin (most commonly scalp skin) resulting from rapid turnover and release of skin cells.

Dandruff is Reliant on Three Factors:

• Sebum production
• Microbial metabolism (specifically Malassezia)
• Susceptibility of individual

Sebum Production

Sebaceous gland activity shows a strong association with most disorders that cause scalp flaking. Early sebum production in the neonate may manifest as cradle cap. Once maternal hormone control subsides, sebum production does not begin again until puberty, at which time sex hormone control affects sebum production. As sebum production increases, Malassezia proliferates in response to new food sources. Proliferation of Malassezia increases lipid metabolism, which causes scalp itching and flaking.

Microbial Metabolism

Malassezia species are lipid-dependent microorganisms that adapt to the narrow niche provided by sebum-rich skin. Malassezia globosa and a second species M. restricta predominate on dandruff scalp. Malassezia globosa likely initiates dandruff formation due to its high lipase activity.

Malassezia restricta and M. globosa require lipids. Due to its inability to metabolize its own lipids, Malassezia species rely on the lipids present in sebum. Sebum is degraded to free fatty acids from triglycerides and saturated fatty acids are consumed . Unsaturated fatty acids are left behind: penetration of unsaturated fatty acids results in inflammation, irritation and scalp flaking.

There remains a lack of correlation between the number of Malassezia cells and the development and severity of dandruff and other forms of dermatitis. However, there may be a correlation between specific Malassezia metabolites and severity of infection, specifically irritating free fatty acid metabolites (e.g. oleic acid).

Procter & Gamble Genome Exploration

In its quest to understand the role of Malassezia and other microorganisms in the development and treatment of dandruff, seborrhea, eczema and other types of dermatitis, Procter & Gamble sequenced the Malassezia genome. Procter & Gamble hoped to understand the structure and function of the yeast-like fungus in order to later manipulate it. M. globosa was found to have very few repeated elements in its genome making it one of the most efficient organisms identified.

M. globosa lacks the ability to synthesize fatty acids: it is highly adaptive but niche dependent and is commonly found on the scalp, back, face and chest where the highest levels of sebum are produced. M. globosa excretes more than 50 different enzymes to help metabolize hair and scalp.

M. globosa is capable of mating. Although its mating ability may seem irrelevant at first glance, it may affect the ability of M. globosa to change and adapt in response to its environment and future needs.

Susceptibility of Individual

Malassezia metabolism results in increased oleic acid levels that lead to the symptoms of dandruff and other forms of dermatitis in some individuals.

Treatment of Malassezia

Pyrithione zinc is highly effect against Malassezia species found on scalp. Reduction in the number of fungi reduces free fatty acid metbolism, in turn reducing scalp flaking and itch.

Interesting Facts:

Ten liters of fungus is equal to the amount on the heads of the entire population of London (approximately 10,000,000 people).

Sources:

Dawson TL Jr. Malassezia globosa and restricta: Breakthrough Understanding of the Etiology and Treatment of Dandruff and Seborrheic Dermatitis through Whole-Genome Analysis. J Investig Dermatol Symp Proc. 2007 Dec;12(2):15-19.

Ro BI, TL Jr. Dawson. The role of sebaceous gland activity and scalp microfloral metabolism in the etiology of seborrheic dermatitis and dandruff. J Investig Dermatol Symp Proc. 2005 Dec;10(3):194-7

DeAngelis YM, CW Saunders, KR Johnstone et al. Isolation and expression of a Malassezia globosa lipase gene, LIP1 (PDF). J Invest Dermatol. 2007 Sep;127(9):2138-46.