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Acne is a common skin disorder affecting both genders and all ethnic groups. In fact, the condition affects at least 80% of adolescents and young adults to some degree. Research also shows that a large number of women over 25 have acne, and the prevalence of acne remains constant until approximately 44, at which time there is a decrease in its incidence.1 It is important to understand the epidemiology and causes of acne and oily skin to truly appreciate the science and benefit behind today’s acne treatment products.
Acne can substantially impact a client’s quality of life. Clients with moderate or severe acne generally have higher levels of behavioral and emotional difficulties than those with clearer skin. The most prominent psychological impact acne has on clients is lower self-confidence, embarrassment, and reduced self-esteem and self-image. The psychosocial impact of this skin condition should never be underestimated.
Acne is a self-limiting disease that involves the hair follicle (pilosebaceous) unit. A pilosebaceous unit is comprised of a follicle or pore and an oil gland (sebaceous gland). Characteristic skin lesions are created by pathology in the pilosebaceous unit and include blackheads (comedones), red papules, pustules, red nodules and cysts.
The cause of acne is multifactorial. The female and male hormones that impact the pilosebaceous gland are in higher concentrations after puberty. Stress can also influence hormone levels, related in part to increased adrenal gland secretion, causing and aggravating acne. Altered keratinization and abnormal skin cell growth in the pore create a dead skin cell/protein/lipid complex that plugs the pilosebaceous gland (microcomedone). Abnormal sebum production and swollen sebaceous glands are present in acne-prone individuals. Also, the composition of free fatty acids secreted by acne-prone individuals differs from those in acne-free individuals. Abnormal bacterial colonization in the pilosebaceous unit occurs in acne-prone individuals. Lastly, an exaggerated immune and inflammatory response to microcomedones, sebum and follicular bacteria produce papules, pustules, nodules and cysts in acne-prone individuals.
The initial lesion in acne caused by a combination of etiologies is the comedone. A comedone starts in the upper portion of the pilosebaceous gland as an expanding mass of cellular debris, keratin protein and lipid material. Bacteria (Proprionebacterium acnes) populate the blocked pilosebaceous gland. Bacteria produce an inflammatory response by the chemical breakdown of lipids within the plugged pilosebaceous unit. This starts the development of small, red papules. As they grow in size, the follicle wall thins, and the follicle itself stretches and swells. Comedones become inflamed when the follicle wall is ruptured, which releases small amounts of cellular and lipid material into the dermis—papules and pustules. Release of all the bacteria, cellular and lipid material in a single comedone produces a full inflammatory response—nodules and cysts. (Editor’s note: To learn more about the physiology of the skin as it relates to acne, check out Skin Inc. Video Education at learn.SkinInc.com.)