Despite the high frequency of endometriosis and the significant consequences for the patients and for the health systems also, the exact pathogenesis of the disease has not yet been deciphered. Many theories have been described to explain the presence of ectopic endometrial tissue, some of which are contradictory to each other. Today retrograde menstruation is a widely accepted mechanism for the presence of ectopic endometrial tissue but it does not explain the fact that retrograted cells do not survive, attach and multiply in all women. More specifically, retrograde menstruation occurs in more than 90% of women, but only 15-20% of women suffer from endometriosis. The causative factor for endometriosis remains a mystery but there are indications that immunological - inflammatory factors participate in its pathogenesis. It is well established that in women with endometriosis peritoneal fluid (PF) is modestly increased and is abandoned from phagocytic macrophages-monocytes, natural killer (NK) cells, cytotoxic T lymphocytes, B cells and inflammatory mediators—complement and cytokines. Whether inflammation is the cause rather than the result of endometriosis, has not been clarified yet and can not be studied in women since it is unethical. However, studies in baboon and mice indicate that inflammation is the result rather than the cause of endometriosis. More specifically in baboon menstruation, has been associated with increased PF volume, reach in white blood cells and inflammatory cytokines, which seem to be even more elevated in baboon with spontaneous endometriosis. Furthermore the percentage of CD4+ and IL2R+ cells has been correlated to the stage of endometriosis. However induction of endometriosis in an inflammatory peritoneal cavity of thioglycolate medium-treated mice, negatively affected the development of endometriosis.