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Acne Biology

Acne, though not deadly, still requires treatment. Acne is a common skin disorder and an annoying problem for both teenagers and adults, caused by biological factors affecting the functions of the sebaceous glands.

Acne is the result of the interrelationship of many various biological processes. It seems that sebaceous hyperplasia (excessive sebum production by the sebaceous glands), follicular hyperkeratinization, colonization of the hair follicle by Propiobacterium Acnes, immune reactions, and discharge of chemical inflammatory mediators into the skin are involved with the skin disorder.

Acne and the sebaceous glands

Sebaceous glands are glands responsible for releasing sebum, the oily substance excreted from the chest, face, neck and back areas. Sebaceous glands are attached to hair follicles in the epidermis and are a holocrine secreting tissue. Sebaceous glands excrete sebocytes, which when mature forms sebum. Excess sebum is the main cause of acne, and is made up of cholesterol, glycerides, fatty acids and alcohols, sterol esters, and wax esters.

Sebum secretion has three noted peaks in a person’s lifetime: (1) during the first week after birth; (2) at around nine years of age; and (3) at 17 years of age. This is why acne seems to attack more frequently and aggressively on infants and adolescents. It has also been found that a child suffering from acne develops more severe attacks in adolescence.

Sebaceous gland functions associated with acne include locally produced cytokines, periglandular peptides, neuropeptides, proinflammatory lipids, and substance P, which is released at sebaceous gland nerve endings.

Androgens in acne development

Androgens have been proven clinically and through experimental evidence to play an important role in the pathogenesis of acne. Androgens bring about the differentiation in sebaceous glands, and are produced therein as well. The adrenal precursor hormone – primarily dehydroepiandrosterone sulfate (DHEAS) – produce androgens in the sebaceous glands. Heightened levels of serum DHEAS, which incidentally is also a precursor for testosterone, is a cause of acne during pre-puberty, and is associated with the increase of sebum production and development of comedonal and severe inflammatory acne.

Androgen is found in the vital areas of a sebaceous gland. It serves as the pathogenesis of acne. The adrenal precursor hormone is the one responsible of the production of androgen in the sebaceous gland. Dehydroepiandrosterone sulfate (DHEAS) is related to the serum which is said to be a precursor for the testosterone. In other words if the serum increases the surely the DHEAS will also increase. When both of the serum and the DHEAS rise then we will be facing a severe case of inflammatory acne and of the comedonal acne. This is where the acne problem would be called an inflammatory disease.

Hormones and acne

Aside from sebaceous glands, hormones are also a factor in acne formation by acting on the hyperkeratinization of hair follicles. Acne occurs mostly during the adolescent stage due to the high secretion of growth hormones during this stage, and the serum levels of the somatomedians (growth factors) once again reach its peak. Women also have a tendency to suffer more acne problems than men due to estrogen, glucorticoids and prolactin.

Neuropeptides and acne

When the cutaneous nervous system senses stress and skin damage, the nerves near the sebaceous glands of acne sufferers release a neuropeptide substance to deal with the skin damaging signals. This substance is composed of a corticotrophin-releasing hormone from the nerves of the skin, and sebocytes.

Acne as a primary inflammatory disease

Acne vulgaris is today accepted as an inflammatory disease occurring as an immune reaction to the P. acne bacteria. When bacteria proliferates in the hair follicle, follicular hyperkeratinisation results and leads to the formation of Propionibacterium acnes. In this event, the production of pro-inflammatory cytokines and tumor necrosis factor [alpha] by the T cells and keratinocytes increases. It leads to an even greater increase of bacteria and creates small lumps (microcomedones) on the skin composed of dead skin cells and oil. Microcomedones worsen and aggravate inflammation, leading to severe acne formation.

Sebaceous lipids responsible for acne formation

The sebaceous glands also secrete sebaceous lipids that facilitate acne development. These lipids are composed of squalene and wax esters, triglycerides, and cholesterol. These sebaceous lipids are functional in three-dimensional skin surface lipid organization, and synthesize free fatty acids on the skin surface as well. During puberty, the stimulation of sebaceous glands causes a rise in lipid synthesis and, consequently, acne development. Bacteria also feed on these lipids, promoting their growth and propagation.

These biological factors should be taken into account when considering acne treatment. As well as reducing sebum production and Propionibacterium acnes, pro-inflammatory lipids in sebum should be controlled to hinder the accumulation of inflammatory cells around the hair follicles.