What Is Acne

Acne is a hormonally driven condition which affects the pilosebaceous gland. Sebaceous glands are found on most parts of the human body except for the palms of the hands and the soles and dorsum of the feet. They are found predominantly on the face and scalp, but also exist in relatively large numbers on the chest and back. This explains the tendency for acne to appear in these areas. There is considerable variability in the size of the glands both between individuals and on different anatomical sites on any single individual.

The sebaceous glands respond to circulating androgens by producing sebum. In acne, sebum production is increased either because the sebaceous gland becomes overly sensitive to circulating androgens or because the levels of circulating androgens are particularly high. Testosterone is the primary androgen associated with acne. It is produced in the adrenal glands, the ovaries in women and testes in men. Whilst generally thought of as a male hormone, testosterone is present in both males and females and becomes an important factor at puberty when the reproductive organs become active.

There are four key processes which occur to produce acne lesions:

1. Increased production of sebum;
2. Hyperkeratinisation within the hair follicle leading to follicular plugging;
3. Increased bacterial activity within the follicle as there is enhanced colonisation with Propionibacterium acnes;
4. Release of inflammatory mediators (e.g. cytokines, tumour necrosis factor) into the follicle and surrounding dermis causing increased inflammation as shown in figure below.

Each of these four processes will now be considered in turn.

Increased sebum production

The response of the body to increased circulating androgens (which generally begins to occur at 7–8 years of age) is twofold. Firstly, the androgens drive changes in both sebocytes and follicular keratinocytes which lead to microcomedone formation. Microcomedones are non-inflammatory lesions which are considered the first lesions of acne, i.e. both inflammatory and non-inflammatory acne lesions are preceded by a microcomedone. Secondly, the androgens lead to an increase in sebum production.

Sebum is made up of lipids (triglycerides, waxes, free fatty acids and squalene) and the debris of dead fat-producing cells. As a substance in itself, it is odour free; however, bacterial activity
on the sebum does produce a distinctive odour known as body odour. Its purpose is to waterproof the skin and protect it from becoming dry and brittle. Sebum has the unique ability to support the growth of the bacteria P. acnes and as such acne cannot occur without the presence of sebum. If the amount of sebum produced can be reduced, there is a consequent decrease in P. acnes.

Follicular plugging

In a normal follicle, the keratinocytes are shed as single cells into the follicular channel and then excreted. It is not fully understood what stimulates the hyperkeratinisation in which the dead keratinocytes remain adherent in the follicular channel leading to blockage, which can be either partial or complete. However, initially these blockages lead to small virtually invisible changes which are the microcomedones. They may take up to 2–3 years before they proceed into more significant acne lesions. As the microcomedone gets bigger and the swelling increases behind the blockage, comedones develop. These are always the precursor lesions to acne.

Comedones can either be open or closed. Open comedones (otherwise known as blackheads) are where the blockage of the follicle is high up and contents of the follicle are pushed through the follicle opening, thus being exposed to the air. The black colour of blackheads is not caused by dirt, although there appears to be disagreement about its origins. Texts vary, with some saying it is due to the presence of melanin, others to the way that light is reflected of the tightly compacted horny cells and yet others stating it is caused by the oxidising effect of the air on the contents of the comedone.

Closed comedones (otherwise known as whiteheads) do not have their contents exposed to the air as the blockage is further down the hair follicle. Blackheads and whiteheads are the non-inflammatory stage of acne as shown in figure on the left. Acne can resolve spontaneously at this stage never progressing to the inflammatory form of the disease. The blockage within the follicle allows for a build up of sebum which becomes the ideal environment for P. acnes to proliferate.

Increased bacterial activity and resulting inflammation

Even where there is no evidence of active acne, P. acnes exists on the skin surface; indeed, there does not seem to be any correlation between the levels of P. acnes on the skin surface and severity of acne. However, some aspect of the hair follicle itself and the microenvironment found there causes P. acnes to proliferate and colonise the hair follicle leading to inflammation. The intensity of the inflammation varies depending on the individual which may, in part, be due to the individual’s sensitivity to the inflammatory mediators associated with P. acnes. Although the mechanisms are not fully understood, it is thought that the action of the proliferating bacteria causes release of inflammatory cytokines, primarily CD4+ T-lymphocytes. Initially, papules and pustules are seen. Pustules form the typical yellow spot of acne. Because of the inflammatory response, lots of white blood cells are attracted to the area where there are increased levels of bacteria. Pus is formed largely from the dead white blood cells.

As these inflammatory mediators move out into the surrounding dermis, the lesions are more likely to be nodular and/or cystic and there is an increased likelihood of permanent scarring. Nodules are solid and larger than pustules extending deeper into the layers of skin. They are caused when large comedones rupture releasing their inflammatory contents into the surrounding skin. Because they extend deeper into the skin affecting the dermis as well as epidermis, they do lead to scarring. Cysts occur less frequently than nodules but when they do they are even more destructive, leading to greater levels of scarring. They are not as solid as a nodule and will often occur where there are two or three nodules close together as shown in figure on the left.

Acne conglobata and acne fulminans

Acne conglobata describes a situation where there is severe nodular acne causing deep abscesses, sinuses in the skin and skin breakdown leading to ulceration. There are also usually large numbers of blackheads affecting the face, neck, upper arms and trunk. Acne fulminans is a severe form of acne conglobata where the patient becomes systemically unwell. Patients will present with nodular cystic acne plus a number of other symptoms including malaise, fever, joint pain and/or swelling. It nearly always affects males and is characterised by an abrupt onset along with the above symptoms and a raised white blood cell count. It may be precipitated by the illegal use of testosterone to boost muscle growth; however, it can just occur spontaneously (New Zealand Dermatological Society Incorporated, 2009). It is considered a dermatological emergency and a patient presenting with acne fulminans must be referred urgently to see a dermatologist. Acne conglobata and fulminans can present as part of a syndrome known as SAPHO. This syndrome must include any combination of the following:

• Synovitis (inflamed joints)
• Acne (conglobata or fulminans)
• Pustulosis (thick blister containing yellow pus)
• Hyperostosis (increase in bone substance)
• Osteitis (inflammation of the bones)

Treatment will be multifactorial involving care from dermatologists and rheumatologists in order to treat all of the symptoms.