Dandruff and Seborrheic Dermatitis

W. Steven Pray, PhD, RPh, Professor of Nonprescription Products and Devices, School of Pharmacy, Southwestern Oklahoma State University, Weatherford, OK

US Pharmacist. 2001;26(4) 

In This Article

Etiology

Abnormal Cell Turnover

Epidermis is composed of five distinct layers. The innermost layer, next to the dermis, is known as the stratum germinativum. Epidermal cells formed here gradually begin to migrate upwards to the next layers, eventually reaching the uppermost layer, the stratum corneum. By this time, they have lost their nuclei and gained keratin, a tough substance. This process ensures that outer skin can withstand the various minor environmental assaults to which it is exposed. In other words, we are encased in a layer of dead, keratinized cells that act to protect the living tissues beneath them. The time frame required for stratum germinativum cells to lose their nuclei and become optimally keratinized is 25-30 days. For the most part, normal cell shedding is not noticed, and causes no symptoms. Proponents of the cell turnover etiology of dandruff and seborrheic dermatitis assert that, for some patients, cell turnover is accelerated. In dandruff, cell turnover is commonly 13-15 days. Seborrheic dermatitis may result from a cell turnover of only 9-10 days. The FDA OTC Review panel, in a 1982 report on dandruff and seborrheic dermatitis, stated, "The cause of dandruff has not been clearly defined, but it is known to involve an increase in the rate of epidermal turnover. This rapid transit of cells to the surface does not allow for complete keratinization of new cells."[1] The FDA mentioned this etiology again in its consumer publication in 1994, although it also briefly explored the theory of an invasive fungus.[2]

Fungal Etiology

A great deal of research on dandruff and seborrheic dermatitis has centered on the possible causative role of fungi. In 1873, a researcher affected with seborrheic dermatitis of the beard isolated an organism that was also noticed in 1874 by a researcher named Malassez. The fungus carried the name of the latter investigator for decades, being known as Malassezia furfur.[3,4] While many other names have been used for this organism, current practice is to call it by a name it was given in 1913, Pityrosporum ovale. This lipophilic yeast is known to be a normal inhabitant of human skin (follicles).

Although the fungal etiology was once widely believed, it fell into disrepute for two reasons. One is that there were no antifungals powerful enough to eradicate the condition. Another is that corticosteroid therapy seemed to produce benefit, leading to the conclusion that cell hyperproliferation might be the root cause.

At the time of the 1982 FDA OTC Review Panel Report, the view provided by the experts was: "Proponents of this [fungal] theory support the use of antimicrobials in controlling dandruff, but the Panel has concluded that there is not a definite correlation between the presence of P. ovale and the development of dandruff."[1]

In 1984, however, a researcher reviewed the literature, coming to the conclusion that P. ovale fulfilled all of Koch's postulates for dandruff and seborrheic dermatitis.[5] Coupled with the efficacy of ketoconazole in those conditions, medical opinion has slowly begun to swing back toward the fungal etiology.

Current treatments for dandruff and seborrheic dermatitis may in fact be effective through dual antifungal approaches, if in fact the cell turnover theory has any validity.

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