There are several events involved in the triggering and progression of HS. It is thought that people who get HS are susceptible to it because of their genes (see ‘Is it hereditary?’). Blockage of hair follicles is believed to be the event that triggers the disease. Bacterial infection and hormones also play a part in the progression of the disease.

Blockage of hair follicles
Just under the skin are tiny structures called pilosebaceous-apocrine units. These consists of:

• an apocrine gland
• a sebaceous gland
• a hair follicle

Skin surface

It is thought that HS is triggered when the hair follicle in a pilosebaceous-apocrine unit gets blocked and inflammed.

To understand how they get blocked, take a look at these two pictures below. Picture 1 shows how a pilosebaceous-apocrine unit works normally. Picture 2 shows what happens when the hair follicle gets blocked.

Picture 1.
Picture 1 shows that fluid from glands go into the hair follicle and escape out of the neck of the hair follicle.

Picture 2.
Picture 2 shows what happens in HS. A build up of skin cells block the neck of the hair follicle.4 This means the fluid have no way of escaping from the hair follicle. This causes the fluid to build up in the hair follicle. The hair follicle then becomes swollen and inflamed and bursts.

When the hair follicle bursts the fluid is released into the fat around it or onto the skin surface. This causes a lot of inflammation (hence the pain and redness).

The inflammation can produce tunnels under the skin. Skin cells can grow in these tunnels forming a lining inside them. This allows pus to be persistently released from these tunnels. These skin-lined tunnels are known as sinus tracts or sinuses.

Bacteria play a role in the progression of the disease after the HS has already been triggered by blockage and inflammation of the pilosebaceous-apocrine units.
The bacteria that are thought to be involved are:

• staphylococci
• anaerobic streptococci
• Streptococcus milleri
• Other less common bacteria including the Bacteroides species.

Many other bacteria are present but most of these are not thought to play any active part in the disease. It is thought that their presence is due to the fact that bacteria thrive on the areas of skin that have been damaged by chronic HS.

Hormones affect the process of HS. The evidence for this comes from the following observations:

• HS does not develop until puberty, when increased levels of sex hormones begin to circulate in the blood.
• Some women find that they have premenstrual and menstrual flares.
• The combined oestrogen/progestogen oral contraceptive pill has been associated with several cases of HS, particularly those pills with a low oestrogen/progestogen ratio.
• Most women find that their HS improves during pregnancy.
• Many women find that their HS improves after the menopause.
• The disease is much more common amongst women

These observations suggest that when the oestrogen level is very low (such as before puberty and after menopause) HS is less likely to occur. When the levels have risen after puberty but are still relatively low such as pre-menstrually or when a woman is on the oral contraceptive pill, HS is most likely to occur. During periods of very high oestrogen such as pregnancy HS may improve. Figure 1 shows the variation in oestrogen levels at different times.

Figure 1

Some studies have shown higher levels of testosterone in women with HS than unaffected women but most affected women will have testosterone levels within the normal range.

In rare cases, HS is associated with an underlying hormone disorder such as an imbalance of the sex hormones (increased testosterone in women) or acromegaly (excessive secretion of growth hormone).

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