The pathogenesis of acne

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Acne vulgaris, the bane of almost every adolescent face is caused due to the dysfunction of the sebaceous glands located in the skin, secondary to multiple biological factors. Excessive sebum production by the sebaceous glands, increased production of epithelial cells by the ducts of the gland, bacteria such as Propiobacterium acnes, as well as immune reactions and chemical inflammatory mediators have all been implicated in the pathogenesis ofr acne.

A) Sebaceous glands and acne:

Sebaceous glands are glands located at the root of hair follicles and are found all over the body, most predominantly in the face and scalp. They produce sebum that is made up of cholesterol, fatty acids, fatty alcohols, glycerides, wax esters and sterol esters and functions to keep skin and hair smooth and soft. The sebaceous lipids help to synthesize free fatty acids on the skin surface and helps in lipid organization that in turn help to keep the skin and hair oily and smooth.

Sebum secretion reaches its peak on the fist week after birth in infants. After it subsides and only rises again at around 9 years of age. It peaks again at the age of 17 years. This is the reason behind infant acne and adolescent acne respectively. Acne in childhood can develop into severe acne in adolescence.

Acne formation results from the excess of sebum, which leads to blockage of the ducts forming comedones. Sebum also contains proinflammatory lipids that can lead to increased inflammatory reaction around the gland if produced in excess.

B) Hormones and acne:

Androgens are sex-hormones that peak during adolescence and young adulthood. The role of androgens in the pathogenesis of acne has been proven both clinically and through experimental evidence. They bring about the differentiation in sebaceous glands and stimulate the production of sebum. Androgens are produced in the sebaceous glands from the adrenal precursor hormone - primarily dehydroepiandrosterone sulfate (DHEAS). The occurrence of acne during pre puberty is related to the heightened levels of serum DHEAS, which is also a precursor for testosterone. The rise in DHEAS is associated with an increase in sebum production and development of comedonal acne and severe inflammatory acne.

Other hormones:
Besides androgens, other hormones also are thought to have a tremendous impact on the development of acne. Growth hormones that are secreted in the pituitary glands can cause hyperkeratinization of the sebaceous glands, i.e. increase the epithelial cell production in the ducts and inner lining of the gland and lead to acne. Again, growth hormones reach their peak during adolescence which increases the propensity of this age group to have acne. Estrogen, glucorticoids and prolactin in women also influence sebaceous gland function and in turn have an effect on the development of acne.

Certain proteins are released by nerve ending near sebaceous glands, called neuropeptides that are released in response to stress or skin damage in surrounding skin. These also effect sebaceous gland secretion and function and can lead to acne.

C) Inflammation and acne:

It is now accepted that acne vulgaris is an inflammatory disease, which occurs as an immune reaction to the Propiobacterium acnes bacteria. The bacteria stimulate the over production of epithelial cells in the hair follicle and sebaceous glands also known as follicular hyperkeratinisation. They also increase the production of chemical signals such as pro-inflammatory cytokines and tumour necrosis factor alpha, which potentiates the proliferation of bacteria. In response to this, follicular cells (known as keratinocytes or epithelial cells) proliferate and produce small clumps of dead skin and oils that are called microcomedones. These microcomedones are the seeds for the subsequent plugging of the hair follicles and sebaceous glands and the development of acne. Greater the inflammatory response of the skin to the Propiobacterium, the greater is the severity of the acne and scar formation.

Sebaceous lipids responsible for acne formation
Sebaceous lipids secreted by the sebaceous glands are also responsible for the development of acne. The stimulation of sebaceous glands by androgens during puberty leads to a rise in lipid synthesis which has pro-inflammatory properties that can lead to acne development. The lipids are also food for the bacteria and so any increase in lipids also promotes the proliferation of Propiobacterium acnes bacteria.

Treatments aimed at controlling acne should therefore take into consideration all these biological factors so as not only to reduce sebum production and Propionibacterium acnes, but also try and control pro-inflammatory lipids in sebum and inhibit accumulation of inflammatory cells around the hair follicles.

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