Beh？et's disease is a multisystem inflammatory disorder characterized by recurrent oral aphthous ulcers, genital ulcers, uveitis, and skin lesions. The cause of Beh？et's disease remains unknown, but epidemiologic findings suggest that an autoimmune process is triggered by an environmental agent in a genetically predisposed individual. An infectious agent could operate through molecular mimicry, and subsequently the disease could be perpetuated by an abnormal immune response to an autoantigen in the absence of ongoing infection. Potentia bacterial are Saccharomyces cerevisiae, mycobacteria, Borrelia burgdorferi, Helicobacter pylori, Escherichia coli, Staphylococcus aureus, and Mycoplasma fermentans, but the most commonly investigated microorganism is Streptococcus sanguinis. The relationship between streptococcal infections and Beh？et's disease is suggested by clinical observations that an unhygienic oral condition is frequently noted in the oral cavity of Beh？et's disease patients. Several viral agents, including herpes simplex virus-1, hepatitis C virus, parvovirus B19, cytomegalovirus, Epstein-Barr virus and varicella zoster virus, may also have some role. 1. Introduction Beh？et’s disease is a multisystem inflammatory disorder characterized by recurrent oral aphthous ulcers, genital ulcers, uveitis, and skin lesions and generally presents with remissions and exacerbations. It can frequently involve the joints, gastrointestinal tract, and central nervous system [1, 2]. 2. Epidemiology Beh？et’s disease is most prevalent along the “Silk Road,” an ancient trading route between the Mediterranean and East Asia, where it is a major cause of morbidity. In Turkey, the country with the highest incidence of the disease, the prevalence is estimated to be between 110 and 420 per 100.000, whereas that in Japan is 13–20 per 100.000, and the prevalence in the UK and USA is estimated at 1-2 per 100.000. The typical age of onset is in the third or fourth decade of life and the male-to-female ratio varies with ethnic origin [1, 3, 4]. The study of migrant populations led to interesting epidemiological findings. Individuals from endemic areas who have immigrated to areas with low prevalence of the disease have an intermediate risk for developing the disease, which points that environment has some role in Beh？et’s disease. Turkish individuals who have emigrated to Germany have a significantly lower risk of disease than individuals of Turkish origin living in Turkey, although their risk remains higher than that of the native German population. Similarly, the disease is
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