Although it is not clear what causes LS, several theories have been postulated. Lichen Sclerosus is not contagious; it cannot be caught from another person. Several risk factors have been proposed, including autoimmune diseases, infections and genetic predisposition. There is evidence that LS can be associated with thyroid disease. Genetic Lichen sclerosus may have a genetic component. Higher rates of lichen sclerosus have been reported among twins and among family members. Autoimmunity Autoimmunity is a process in which the body fails to recognize itself and therefore attacks its own cells and tissue. Specific antibodies have been found in LS. Furthermore, there seems to be a higher prevalence of other autoimmune diseases such as diabetes mellitus type 1, vitiligo, alopecia areata, and thyroid disease. Infection Both bacterial as well as viral pathogens have been implicated in the etiology of LS. A disease that is similar to LS, acrodermatitis chronica atrophicans is caused by the spirochete Borrelia burgdorferi. Viral involvement of HPV and hepatitis C are also suspected. A link with Lyme disease is shown by the presence of Borrelia burgdorferi in LSA biopsy tissue. Hormones Since LS in females is primarily found in women with a low estrogen state (prepubertal and postmenopausal women), hormonal influences were postulated. To date though, very little evidence has been found to support this theory. Local skin changes Some findings suggest that LS can be initiated through scarring or radiation, although these findings were sporadic and very uncommon.
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