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Acne


 
Introduction Back to Top
What should I know about Acne?

Acne vulgaris is the most common skin disease, affecting 80% of the population between the ages of 12 and 25.(1) It usually has a limited life span of its own; however, some cases may persist for years and the more severe cases may potentially lead to scarring and disfigurement. The lesions of acne are generally classified as inflammatory or noninflammatory, and occur most frequently on the face, neck, chest, and back.

The causes of acne are very complex and involve many different systems and chemicals within the body. Hormones, enzymes, and the immune system all interact together resulting in different reactions in each individual. Understanding this complex system has kept dermatologists busy for decades.

One of the factors responsible in the development of acne is called sebum, which is produced by the sebaceous glands. Sebaceous glands are located throughout the body except for the palms of the hands, soles of the feet, and the lower lip. Each person has approximately 5,000 sebaceous follicles. These glands are the largest and most numerous on the face, back, chest, and upper outer arms. Sebaceous glands are large at birth, and then reduce in size until adolescence. They once again enlarge during pre-puberty with changes in hormone levels influencing sebaceous gland secretion. This increase in production of sebum is the reason that acne is so prevalent in adolescents and teenagers.

When there is excess sebum, bumps called comedones, appear because there is a blockage of follicles by this excess sebum. Inside these comedomes, there are bacteria and yeast that work on the sebum causing it to release free fatty acids. When this happens, there is inflammation and sometimes a rupture of the bump or comedome. Sebum levels are increased when testosterone is converted into dihydrotestosterone in the skin. When this happens the dihydrotestosterone acts directly on the sebaceous gland to increase its size and metabolic rate. Estrogens, on the other hand, work differently and actually decrease sebaceous gland secretion. Early acne lesions result from blockage of the follicle canals. These canals become blocked when sebum mixes with keratin, which is also affected by hormonal changes. This new mixture increases the number of cornified cells that stick to the walls of the canal and a plug is formed just above the opening of the sebaceous gland duct. All of this change that occurs within the follicle is important, but not fully understood. It is not known whether this activity is a cause of or a result of irritation and other factors.(2)

The earliest lesions that are most often seen in adolescence are mildly inflamed or non-inflamed comedones on the forehead. Comedones may be open (blackhead), or closed (whitehead). The contents of closed comedones are usually not easily expressed, and are often the first sign of the inflammatory lesions of acne vulgaris. It is unsure where open comedones get their black color. It is not from accumulation of dirt, and may not even be the accumulation of melanin, which was the source most recently thought to be the cause. Open comedones generally do not result in inflammatory acne lesions, are easily expressible, and contain oxidized, darkened, oily debris.

The severest forms of acne are most frequently seen in males, but acne is generally more persistent in females. Also, females tend to have flare-ups prior to menstrual periods. This may continue until menopause. Low grade, persistent acne is often found in professional women. One author thinks that chronic stress leads to enhanced secretion of adrenal androgens, resulting in the production of comedones.(3)

Acne is considered an inherited disease, although it is impossible to know which members of a family may suffer from the disease, and which members will not. Acne is not caused by greasy foods, and is not caused by dirt. Avoiding all g

Additional Links Back to Top
Footnotes Back to Top
1 Leyden JJ. Therapy for acne vulgaris. N Engl J Med. 1997;336:1156-1162.
2 Han NH, et al. Acne and Psorasis. In: DiPiro JT, et al, eds. Pharmacotherapy, A Pathophysiologic Approach, 4th ed. Stamford CT: Appleton & Lange; 1999:1490-1496.
3 Kligman AM. Postadolescent acne in women. Cutis. 1991;48:75-77.
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This information is educational in context and is not to be used to diagnose, treat or cure any disease. Please consult your licensed health care practitioner before using this or any medical information.