The role of sebaceous gland activity and scalp microfloral metabolism in the etiology of seborrheic dermatitis and dandruff.

Most common scalp flaking disorders show a strong correlation with sebaceous gland (SG) activity. Early SG activity in the neonate results in microfloral colonization and cradle cap. After maternal hormonal control subsides, there is little SG activity until puberty, when the SG turns on under sex hormone control. When the SG activity increases, the present but low Malassezia population has a new food source and proliferates, resulting in the scalp itching and flaking common to greater than 50% of adults. Dry scalp flaking, dandruff, and seborrheic dermatitis are chronic scalp manifestations of similar etiology differing only in severity. The common etiology is a convergence of three factors: (1) SG secretions, (2) microfloral metabolism, and (3) individual susceptibility. Dandruff and seborrheic dermatitis (D/SD) are more than superficial stratum corneum disorders, including alteration of the epidermis with hyperproliferation, excess lipids, interdigitation of the corneal envelope, and parakeratosis. The pathogenic role of Malassezia in D/SD has recently been elucidated, and is focused on their lipid metabolism. Malassezia restricta and M. globosa require lipids. They degrade sebum, free fatty acids from triglycerides, consume specific saturated fatty acids, and leave behind the unsaturates. Penetration of the modified sebaceous secretions results in inflammation, irritation, and scalp flaking.