month in normal couples to 2%-5% per month in women with endometriosis (8, 9). This review will focus on mechanisms of infertility and strategies for preserving and optimizing fertility in endometriosis patients. Mechanisms of infertility There are multiple proposed mechanisms of infertility associated with endometriosis. First, anatomic distortion due to pelvic adhesions may prevent ovum capture and fertilization. Second, inflammatory cytokines, prostaglandins, and metalloproteinases may alter ovarian, tubal and endometrial function, resulting in abnormal folliculogenesis or failure of fertilization or implantation. Additionally, peritoneal fluid high in cytokines, inflammatory mediators, and macrophages may be toxic to sperm and reduce embryo survival (2, 10-13). Furthermore, abnormalities of the eutopic endometrium, including progesterone resistance, may result in implantation failure. Studies detailing the gene expression profiles of the endometrium in women with and without endometriosis show that several genes influenced by progesterone are dysregulated during implantation, when levels of progesterone in the endometrium are highest (1, 14). Although it is well established that advanced endometriosis decreases fertility due to distorted pelvic anatomy, it remains controversial whether women with early-stage endometriosis have impaired fertility. Studies of women with endometriosis who have undergone in vitro fertilization (IVF) provide mixed data. A 2002 meta-analysis of women undergoing IVF reported pregnancy rates among women with endometriosis that were half those of women with tubal factor infertility. Additionally, women with endometriosis showed a decreased response to gonadotropin stimulation, as well as lower fertilization and implantation rates compared to