Genetic Polymorphisms and Molecular Pathogenesis of Endometriosis

The most widely accepted theory to explain endometriosis is that viable endometrial cells reach the peritoneal cavity through retrograde menstruation along the fallopian tubes. Some of the cells then adhere to the peritoneal surface and proliferate in response to the ovarian hormones. However, it is well established that menstrual debris is present in the peritoneal cavity of 90% of menstruating women, suggesting that endometrial cells from only ‘some women’ are capable of establishing ectopic endometrial implants. Why does this happen in only ‘some (10-15%) women’? There are several possible explanations for disease susceptibility, including differences in genetic predisposition (Bischoff FZ et al, 2000), increased exposure to menstrual debris, abnormal eutopic endometrium, altered peritoneal environment, reduced immune-surveillance (Sinaii N et al, 2002), and increased angiogenic capacity (Absenger Y et al, 2004).