Oil secretions are controlled by hormones and become more active during puberty because of the increase in androgens, particularly testosterone, though hormonal changes can continue into adult life with many varying causes. This increase of sebum production will eventually outweigh the secretion capacity, which leads to a blockage of sebum in the hair follicle resulting in inflammation.

Treatments that inhibit sebaceous gland activity such as oral or topical retinoids, anti-androgens and estrogens are an integral part of managing acne. With this in mind it is essential to understand that skin dryness actually exacerbates the pathogenic cycle of acne, so it is important not to use cleansers/agents that will strip the skin of all its oils causing more irritation and compromising the skins barrier function.

Studies have shown that washing the skin with a non-comedogenic agent in an emollient cleanser actually accelerates the pace of acne resolution.

The follicle is like an indentation of the skin, so just as the skins cells progress from the basal layer to the surface and eventually slough off (a process called keratinisation) this will also happen in the follicle.

In acne patients these skin cells (keratinocytes) tend to stick together which then block the pore/follicle creating a comedone. This becomes a great nutritional source for bacteria for which they become naturally attracted.

Once the immune system recognises the presence of bacteria it will launch an immune response resulting in redness, pus and inflammation creating a ‘pimple’. It is likely that most of the inflammation occurs via mediators that are released when bacteria digest sebum.

The exact role of bacteria is unclear as Propionibacterium acnes (P. acnes) is found in both teenagers with acne but not without and adults both with or without acne. It is thought that the bacteria is unlikely to be a direct cause of acne breakouts but is the main culprit of inflammation as discussed in ‘Changes in follicular keratinization‘.