Endometriosis is a complex trait with significant environmental and genetic influences that are likely to affect its phenotype. Natural history of the disease varies from one individual to another. The gold standard of surgical diagnosis is limited in accuracy by visibility and recognition of lesions by the attending surgeon. Several lines of evidence suggest that pelvic endometriosis results from the reflux of viable endometrial tissue through the fallopian tubes. Endometriosis is an inflammatory disease that nuclear factor kappa B pathway may play an important role in its pathogenesis. Endometriotic lesions demonstrate increased aromatase expression in association with increased cyclo-oxygenase-2 expression, especially in red lesions which represent earlier stages of inflammation. Estrogen and progesterone receptor expressions vary according to the morphology and the inflammatory status of the endometriotic lesions. Normal endometrial tissue fragments can adhere and implant to peritoneum. Aromatase expression, a possible intrinsic survival factor for endometrial tissue, is inducible in human endometrial fragments by androstenedione at physiological concentrations found in peritoneal fluid. Inflammatory response to ectopic endometrial tissue, which may vary in each individual seems to be important in disease progression. Current therapies for endometriosis include surgical and medical approaches aimed at cytoreduction or hormonal suppression. However, the disease have tendency to recur in many symptomatic women. Although new management approaches are emerging, properly designed clinical trials are desperately needed in treatment of pain and subfertility associated with endometriosis. Future studies should also focus on identifying risk population to develop preventive strategies, since the treatment of endometriosis is costly and challenging.