Acne biology information
 
ACNE BIOLOGY

Acne, the most common of all skin disorders and the bane of almost every adolescent face, is caused due to various biological factors mostly related to the function of the sebaceous glands.

Acne develops from the combination and intertwining of several complex biological processes. Evidence suggests the involvement of sebaceous hyperplasia or excessive sebum production by the sebaceous glands, follicular hyperkeratinization, colonization of the hair follicle by Propiobacterium acnes, as well as immune reactions and discharge of chemical inflammatory mediators into the skin.

Relation of acne to sebaceous glands

The sebaceous glands are situated in the hair follicles and the epidermis and found all over, especially in the area of the face and scalp, but not on the palms or soles of the feet. Sebaceous glands are a holocrine secreting tissue and its most important function is the secretion of sebum, the excess of which manifests as the development of acne. Sebum is a lipid rich fluid which is released onto the surface of the skin when mature sebocytes in the sebaceous glands rupture. The sebum is made up of cholesterol, fatty acids, fatty alcohols, glycerides, wax esters and sterol esters.

Increase in sebum secretion reaches its peak on the fist week after birth in infants. After this the sebum secretion subsides and only rises again at around 9 years of age and continues to reach another paek at about 17 years of age. This is the reason behind infant acne and adolescent acne respectively. Acne in childhood develops into severe acne in adolescence.

The sebaceous gland functions associated with acne are proinflammatory lipids, locally produced cytokines, periglandular peptides, neuropeptides, and substance P, which is release at the endings of nerves in the sebaceous glands.

The function of androgens in acne development

Androgens bring about the differentiation in sebaceous glands. The sebaceous glands are vital areas where active androgens are formed. The role of androgens in the pathogenesis of acne has been proven both clinically and through experimental evidence. 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 as well.

Hormones and acne

Hormones are thought to have a tremendous impact on the development of acne. They also act on the hyperkeratinization of hair follicles, which also helps lead to acne. Growth hormones that are secreted in the pituitary glands may also be involved in the manifestation of acne. So acne mostly occurs in the adolescent years when there is high secretion of the growth hormone and the serum levels of the somatomedians or growth factors are highest and the excess of which leads to seborrhea and acne. Estrogen, glucorticoids and prolactin in women influence sebaceous gland function and therefore have effect on the development of acne.

Neuropeptides and acne

Corticotrophin releasing hormone from the nerves of the skin and sebocytes are produced and discharged when the cutaneous nervous system senses stress and damage of skin and deals with the cell damaging signals in this manner. The nerves near the sebaceous glands of acne sufferers release this neuropeptide substance.

Acne as a primary inflammatory disease

It is now accepted that acne vulgaris is an inflammatory disease, which occurs as an immune reaction to the P. acnes bacteria. Follicular hyperkeratinisation leads to a change of the hair follicle make up with consecutive proliferation of bacteria, chiefly Propionibacterium acnes, in the hair follicle. This leads to further increased production of the pro-inflammatory cytokines and tumour necrosis factor [alpha] by T cells and keratinocytes, which gives rise to yet more proliferation of bacteria. In response, follicular keratinocytes produce hypergranulosis similar to the impermeable skin outer layer, resulting in the formation of microcomedones. These microcomedones are more simply described as small lumps of dead skin and oils mixed together – the seeds for the subsequent plugging of the hair follicles and the development of acne. Further inflammatory responses lead to the development of increasing degrees of severity in inflammatory forms of acne.
Sebaceous lipids responsible for acne formation

Sebaceous lipids secreted by the sebaceous glands are also responsible for the development of acne. The lipid mixture is made up of squalene and wax esters, triglycerides and cholesterol. The sebaceous lipids are functional in three dimensional skin surface lipid organization and also synthesize free fatty acids on the skin surface. The stimulation of sebaceous glands by androgens during puberty leads to a rise in lipid synthesis and the formation of acne. These lipids have pro-inflammatory properties, which lead to acne development. The lipids are also food for the bacteria and so the increase in lipids present also promotes the proliferation of P. acnes.

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.