Hidradenitis suppurativa (HS) starts with a defect in hair follicles, not with an infection or poor hygiene. The follicles become blocked, rupture beneath the skin, and trigger a powerful inflammatory response that leads to painful lumps, abscesses, and tunneling wounds in areas like the armpits, groin, and under the breasts. No single factor causes HS on its own. It results from a combination of genetics, immune dysfunction, hormones, and environmental triggers that together create a cycle of chronic inflammation.
How the Disease Starts in Hair Follicles
The process begins when a hair follicle becomes clogged. Skin cells lining the follicle multiply abnormally and create a plug, similar to what happens with a blocked pore. But unlike ordinary acne, the blockage in HS goes deeper. The plugged follicle eventually ruptures below the surface, spilling its contents (proteins like keratin and any bacteria present) into the surrounding tissue. The body treats this like an invasion, flooding the area with immune cells.
That immune response creates abscesses and destroys the original follicle, but it doesn’t stop there. The inflammation spreads to nearby tissue, and the skin forms tunnels (sometimes called sinus tracts) that connect lesions beneath the surface. Oil-producing glands in the affected skin also become less functional over time. This is why HS tends to worsen progressively rather than simply flaring and resolving like a regular skin infection.
Genetics and Family History
HS runs in families. Researchers have identified mutations in a group of genes that code for a protein complex called gamma-secretase, specifically in genes known as NCSTN, PSENEN, and PSEN1. Gamma-secretase plays a role in how skin cells develop and communicate, particularly in the lining of hair follicles. When it doesn’t work properly, follicles are more prone to the abnormal cell buildup that triggers the disease.
These specific mutations account for rare, often severe familial forms of HS. Many people with HS don’t carry these exact mutations, which suggests other genetic variations also contribute. Having a first-degree relative with HS significantly raises your risk, though the condition can also appear without any known family history.
An Overactive Immune Response
HS is fundamentally a disease of inflammation, not infection. The immune system in people with HS overreacts to the ruptured follicle and then fails to shut that response down. Research measuring inflammatory signaling molecules in HS skin lesions has found striking numbers: one study showed a 149-fold increase in IL-17A (a key inflammation driver) in affected skin compared to healthy skin, along with a 115-fold increase in IL-1β, another potent inflammatory signal.
These molecules belong to a network that normally helps fight off bacteria and fungi. In HS, they’re produced in massive excess. IL-17 ramps up the production of antimicrobial compounds and chemical signals that recruit even more immune cells to the area, creating a self-reinforcing loop. IL-1β drives the activity of specialized immune cells called Th17 cells, which in turn produce more IL-17. This feedback cycle is a major reason HS lesions persist and recur rather than healing cleanly. It also explains why treatments targeting these specific pathways (similar to therapies used for psoriasis and inflammatory bowel disease) can help control the condition.
The Role of Hormones
Hormones, particularly androgens like testosterone, clearly influence HS. The disease typically first appears around puberty and follows hormonal patterns throughout life. Between 43% and 77% of female patients report their symptoms worsen in the days before menstruation, when hormone levels shift. Flares also commonly worsen after pregnancy.
Studies have found that HS patients tend to have higher testosterone levels and a higher free androgen index (the ratio of testosterone to a protein that binds it) compared to people without the condition. HS lesions themselves show increased androgen receptor activity, meaning the affected skin is more responsive to these hormones. In transgender men receiving testosterone therapy, HS has been reported to worsen or appear for the first time, further supporting the hormonal link.
The hormonal picture is not identical for everyone. The connection to androgens appears strongest in female patients, while the role of hormones in male HS is less clear. This may partly explain why gender distribution varies across populations. In Western countries and Latin America, HS is diagnosed more often in women (roughly 65% to 74% of cases in Latin American studies, with one Argentinian study finding a 2.15:1 female-to-male ratio). In several Asian countries, the pattern reverses, with men making up 62% to 84% of HS patients in studies from South Korea and Japan.
Smoking and Nicotine
Smoking is one of the strongest modifiable risk factors for HS. Nicotine directly affects the structures involved in the disease. It stimulates secretion from sweat glands in the skin folds where HS occurs, contributing to follicular blockage. It also causes the outer layer of skin and hair follicles to thicken abnormally, which is the same kind of overgrowth that plugs follicles in the first place.
Nicotine receptors are heavily expressed in the skin around and within hair follicles, making follicular tissue particularly sensitive to tobacco exposure. Beyond these local effects, smoking raises levels of inflammatory molecules in the blood. HS patients who smoke have been found to have elevated levels of IL-36 (a family of inflammatory signals), which feeds into the same inflammatory pathways already overactive in the disease. Nicotine also promotes the growth of Staphylococcus aureus, a bacterium that can colonize HS lesions and worsen symptoms.
Obesity and Mechanical Friction
Higher body weight is strongly associated with HS severity, and the relationship works through two separate mechanisms. The first is purely mechanical: excess weight increases skin-on-skin contact in the folds where HS develops. That friction irritates hair follicles and creates a warm, moist environment that favors blockage and bacterial growth.
The second mechanism is metabolic. Fat tissue is not passive storage. It releases inflammatory signals and attracts immune cells called macrophages, which promote a state of low-grade, body-wide inflammation. For someone already predisposed to HS, this additional inflammatory load can push the immune system further toward the overactive state that drives the disease. Weight loss doesn’t cure HS, but many patients experience fewer and less severe flares when they reduce friction in affected areas and lower their overall inflammatory burden.
Bacteria Are Not the Root Cause
Because HS lesions can produce pus and have an unpleasant odor, many people assume the disease is a skin infection. It is not. HS is not contagious, and it is not caused by poor hygiene. The bacterial involvement in HS is secondary: bacteria colonize lesions after they form, but they do not initiate the disease process. Research on the skin microbiome in HS has found that bacterial communities shift as the disease progresses, though whether those changes contribute to worsening or are simply a consequence of the altered skin environment remains unclear.
This distinction matters because it affects treatment. Antibiotics can help manage secondary bacterial overgrowth and reduce some inflammation, but they don’t address the underlying follicular and immune dysfunction. HS is frequently misdiagnosed as boils, folliculitis, or even a sexually transmitted infection, which delays appropriate treatment by an average of several years. Understanding that the root cause is internal, not external, is the first step toward effective management.