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Many people mistakenly believe dandruff is caused by dry scalp, frequent shampooing or poor hygiene. These popular misconceptions can lead to ineffective, and sometimes inappropriate, treatments, and make it even harder on those who have dandruff - half of adults with dandruff are more self-conscious about their appearance.

Researchers now believe dandruff is a medical condition caused by an overabundance of an organism that normally exists on everyone's scalp - even people who don't have the condition. This is important information for the millions of Americans who feel self-conscious and embarrassed about their appearance due to dandruff.   

Dandruff typically begins to appear in puberty, and the incidence is highest at age 40. Because people with dandruff often do not seek medical attention, no one knows exactly how widespread the problem is, but an estimated 63 million Americans - or one in three adults - have experienced dandruff symptoms. 

Additionally, 12.4 million people suffer from seborrheic dermatitis, a more severe form of dandruff that affects scalp and skin. In fact, more people in the U.S. have dandruff problems than arthritis (40 million) and smoking addiction (48 million).

Unfortunately, these millions needlessly suffer the flaking, itchiness, redness and scalp inflammation caused by dandruff. Most people do not realize that these symptoms, which range from slight to severe discomfort, can be successfully treated. 

What causes dandruff?

Dandruff is a minor infection of the scalp caused by an overabundance of a micro-organism called Pityrosporum ovale (P. ovale), a yeast-like fungus that is part of the normal skin flora.

The notion that P. ovale might contribute to dandruff was first proposed more than 100 years ago, but only in the past 20 years has research been able to substantiate this theory. Understanding that dandruff is a medical condition is essential in selecting a treatment that will return the scalp to its natural balance.

Dandruff is a medical - not cosmetic - condition
In the past, dandruff and seborrheic dermatitis were seen as two different conditions. Seborrheic dermatitis was treated with corticosteroids and dandruff was viewed as more of a cosmetic concern, and treated with shampoos and potions supplied by the cosmetics industry.

Around the 1960s and '70s, dermatologists began to use a number of new techniques to study skin structure and functions, including the growth of epidermal cells, which showed that epidermal cell turnover (the production and shedding of the uppermost layer of the skin) was increased in patients with dandruff. At that time, dermatologists assumed that it was the increased epidermal cell turnover, or "hyperproliferation," that was causing dandruff, and that P. ovale colonization was secondary.

It is now evident that the opposite is true: P. ovale overgrowth occurs first, and increased epidermal cell turnover is secondary. Hyperproliferation occurs because the skin is growing and flaking more rapidly as a result of the yeast presence.

How does P. ovale cause dandruff?
The research supporting the idea that P. ovale is a primary culprit emerged during the 1980s, and is based on the findings that:
  • P. ovale is present in both patients with seborrheic dermatitis and dandruff, as well as normal subjects who have neither;
  • reinfection with P. ovale causes the recurrence of dandruff problems; and
  • if the condition is treated with drugs whose common mechanism or mode of action is antipityrosporal, it improves.

The rapid growth of P. ovale often is triggered by an imbalance in environmental factors such as climate, heredity, diet, hormones and stress. As the body's natural defenses fight the excessive growth of this organism, the results are the symptoms of dandruff - flaking, scaling and itching.

Under normal conditions, P. ovale yeasts can live on the skin without causing any problems. For example, one study found that yeast-like organisms made up 46 percent of scalp flora in people without dandruff problems; 74 percent in those who had dandruff, and 82 percent in those who were diagnosed with seborrheic dermatitis.

Other causes of dandruff
However, the presence of P. ovale is not the sole factor contributing to dandruff problems. When, for whatever reason, the body's balance is disturbed, one of several immune responses often are produced in dandruff patients.
  • One is the production of antibodies, which are immunoglobulin molecules that react with a specific antigen (a substance capable of inducing a specific immune response and reacting with the products of that response). 

    Certain studies show the highest titers of antibodies to P. ovale are found in patients with the highest amounts of dandruff.

  • Hypersensitivity, or an overreaction of the immune system to an antigen, also probably contributes to dandruff. Hypersensitivity reactions have the same mechanisms as those of protective immunity, except that while the latter protects against disease, hypersensitivity leads to tissue damage and disease. 

    The environmental factors linked to dandruff may contribute to hypersensitivity reactions in dandruff patients.

  • Additionally, there is substantial evidence that P. ovale feed off the lipids and proteins present in the skin and then secrete lipase or other enzymes. 

    The increased P. ovale found in dandruff patients may facilitate lipase activity, during which the organisms digest skin lipids and turn them into irritant fatty acids, causing skin inflammation and tissue damage. This may lead to the skin reaction associated with dandruff. 

    This lipase activity indicates that in addition to hypersensitivity, the P. ovale release toxic substances or chemicals that may contribute to the development of a fungal infection.
For a long time, effective therapy for dandruff and seborrheic dermatitis has been seen with compounds whose only common link was antipityrosporal activity. But proof of this relationship was lacking until the introduction of antifungal drugs - in particular, ketoconazole.

The role of ketoconazole in dandruff therapy The mechanism of action of ketoconazole has been extensively studied. Studies with various fungal species have shown that ketoconazole acts primarily by damaging the fungal cell wall, leading to its death.

While many of antifungal drugs have produced a good inhibitory effect on P. ovale, studies have shown that ketoconazole was the most powerful.


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