Academic journal article International Journal of Child Health and Human Development

Acne

Academic journal article International Journal of Child Health and Human Development

Acne

Article excerpt

Introduction

Acne vulgaris is a chronic, multifactorial, inflammatory disorder of the sebaceous glands as well as ducts and the hair follicles with a strong genetic predisposition (1-5). It is found in areas of increased sebaceous density, i.e, the face, chest, upper arms, and back. Though acne can be seen at any age, it typically begins at puberty and its onset as well as severity is influenced by genetic factors as well as the host immune response to inflammation.

Epidemiology

Acne can be found in all ages of childhood (neonatal, infantile, childhood) and adulthood (6-8). Acne vulgaris is found in as many as 40% in those between 8 and 10 years of age, 90% of mid-adolescent males (i.e., ages 13 to 17) and 80% of similar aged females; severe acne is noted in 10% of adolescents and young adults. Severe acne may occur in young adults even if they only had mild acne as adolescents. Concern with acne accounts for 14% of visits to primary care clinicians and 27% of visits to dermatologists. Table 1 provides a classification of acne and its many variants. The direct cost of acne management is over $2.2 billion per year in the United States (9). Acne rosacea is reviewed in the next section (10).

Pathogenesis

The pathogenesis of acne vulgaris involves three main components: sebum, keratin plug, and the microbial skin flora (11). Sebum is made by the sebaceous glands and is composed of approximately two thirds triglycerides and one-third wax esters along with steroid esters and squalene. The protein secreted by keratinocytes is called keratin while sebum is secreted into hair follicles through the sebaceous duct. Sebum production is influenced in adolescence by the adrenal and gonadal androgens. Acne is an inflammatory condition and starts with follicular keratinocytes becoming so sticky that a keratin plug forms which then occludes the follicle with trapping of sebum. Trapped sebum leads to perifollicular inflammatory and secondary impaction. Seborrhea may be mild to severe and is not specifically linked to acne vulgaris.

Local bacteria contribute to the acne process and this flora includes Propionibacterium acnes (formerly known as Corynebacterium acnes) that has been implicated in acne pathogenesis since 1896. This bacterium is an anaerobic Gram-positive diphtheroid that increases during adolescence and colonizes at pilosebaceous follicles. This important microbe converts triglycerides to free fatty acids and produces mediators as well as chemotactic factors that leads to the inflammatory nature of acne (vide infra). Other flora implicated in acne include coagulase-negative Staphylococcus epidermidis and the yeast Pityrosporum oval.

An important etiologic component in adolescent acne development is the increasing level of plasma testosterone in which testosterone is converted in the skin to dihydrotestosterone by 5-α-reductase. This conversion leads to direct stimulation of sebaceous gland enlargement via a cyclic cAMP (adenosine monophosphate) mechanism. Estrogen can inhibit gland stimulation and acne exacerbations in females may occur during periods of reduced estrogen stimulation, such as before menstruation. Youth can have normal hormonal levels but still have severe acne, partially due to increased free testosterone levels and DHEAS along with lowered levels of SHBG (sex hormone-binding globulin).

Acne vulgaris typically initiates with the development of microcomedones, the primary, noninflammed acne lesions which are due to occluded hair follicles. The microcomedone is due to excessive sebum from desquamated epithelial cells in the follicular wall, as noted above; microcomedones become overt comedones. Closed comedones are called whiteheads while open comedones or blackheads have pigmented epithelial cells and are due to retained melanin. The open or closed comedo obstructs the follicle duct and sebum outflow leading to follicle distention and potential rupture.

Inflammatory pathogenesis

Ongoing distention results in local tissue injury that is worsened by conversion of sebum triglycerides to irritant free fatty acids. …

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