What is acne

Acne lesions develop from the sebaceous glands associated with hair follicles—on the face, external auditory meatus, back, chest, and anogenital area. (Sebaceous glands are also found on the eyelids and mucosa, prepuce and cervix, where they are not associated with hair follicles.) The sebaceous gland contains holocrine cells that secrete triglycerides, fatty acids, wax esters, and sterols as "sebum". The main changes in acne are:

an increase in sebum secretion;

thickening of the keratin lining of the sebaceous duct, to produce blackheads or comedones—the colour of blackheads is due to melanin, not dirt; an increase in Propionibacterium acnes bacteria in the duct;

an increase in free fatty acids;

inflammation around the sebaceous gland, probably as a result of the release of bacterial enzymes.

Underlying causes

There are various underlying causes of these changes. Hormones

Androgenic hormones increase the size of sebaceous glands and the amount of sebum in both male and female adolescents. Oestrogens have the opposite effect in prepubertal boys and eunuchs. In some women with acne there is lowering of the concentration of sex hormone binding globulin and a consequent increase in free testosterone concentrations. There is probably also a variable increase in androgen sensitivity. Oral contraceptives containing more than 50 micrograms ethinyloestradiol can make acne worse and the combined type may lower sex hormone binding globulin concentrations, leading to increased free testosterone. Infantile acne occurs in the first few months of life and may last some years. Apart from rare causes, such as adrenal hyperplasia or virilising tumours, transplacental stimulation of the adrenal gland is thought to result in the release of adrenal androgens—but this does not explain why the lesions persist. It is more common in boys.

Fluid retention

The premenstrual exacerbation of acne is thought to be due to fluid retention leading to increased hydration of and swelling of the duct. Sweating also makes acne worse, possibly by the same mechanism.


In some patients acne is made worse by chocolate, nuts, and coffee or fizzy drinks.

Acne cysts and scars

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Sebaceous gland— histology of acne

Sebaceous gland— histology of acne

Blocked pore

Blocked pore

Excess grease from enlarged sebaceous gland | V

Sebaceous gland— pathology in acne

Hormones—the cause of all the trouble

- increase the size of sebaceous glands

- increase sebum secretion

• Androgenic adrenocorticosteroids—have the same effect

• Oestrogens—have the opposite effect


Acne often improves with natural sunlight and is worse in winter. The effect of artificial ultraviolet light is unpredictable.

External factors

Oils, whether vegetable oils in the case of cooks in hot kitchens or mineral oils in engineering, can cause "oil folliculitis", leading to acne-like lesions. Other acnegenic substances include coal tar, dicophane (DDT), cutting oils, and halogenated hydrocarbons (polychlorinated biphenols and related chemicals). Cosmetic acne is seen in adult women who have used cosmetics containing comedogenic oils over many years.

Iatrogenic factors

Corticosteroids, both topical and systemic, can cause increased keratinisation of the pilosebaceous duct. Androgens, gonadotrophins, and corticotrophin can induce acne in adolescence. Oral contraceptives of the combined type can induce acne, and antiepileptic drugs are reputed to cause acne.

Types of acne Acne vulgaris

• Affects comedogenic areas

• Occurs mainly in puberty, in boys more than girls

• Familial tendency Infantile acne

• Clears spontaneously Severe acne

• Acne conglobata

Pyoderma faciale

• Gram negative folliculitis Occupational acne

• Chlorinated phenols

• DDT and weedkillers Steroids

• Systemic or topical Hormones

• Combined type of oral contraceptives and androgenic hormones

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