There is no certainty about the cause of this disorder, but the bacterial species Staphylococcus aureus has a central role and can be detected in the lesions of most patients. It is unclear if another primarily sterile process with secondary colonization by Staphylococcus aureus is present, or if Staphylococcus aureus starts the process by causing a strong immune reaction. Another possibility is that Staphylococcus aureus produces toxins that act as superantigens which directly activate the T-cells over the variable domain of T-cell receptors. Nonetheless Staphylococcus aureus can by found in almost all patients affected by this disorder, while it is detected in only 20–30% of non-affected people. As Staphylococcus aureus is not always found in people that suffer from<unk> , other factors must be present. Through examinations in families it was found that there is a family connection to the occurrences, which leads to the conclusion that there is a genetic predisposition for it; for example, patients with<unk>  could have a hereditary different opening of the hair follicle that could facilitate the lodging of the bacteria. Immunologically, another possibility is that especially strong intercellular fixation protein ICAM-1 contributes to inflammation with its strong effect of attracting white blood cells such as granulocytes and lymphocytes.
Folliculitis decalvans
Streptococcal intertrigo
Hidradenitis suppurativa
Lichen myxedematosus
Keratosis follicularis spinulosa decalvans
Granuloma faciale
Tinea capitis
Acroangiodermatitis