There are many theories exist as to the development of endometriosis, the most generally accepted one is that it may be initiated by retrograde menstrual flux through the Fallopian tubes. Epithelial progenitor cells derived from the shedding of endometrial tissue can implant on the peritoneum, ovaries, or in the rectovaginal pouch. Once established, these hormone-responsive and cyclically active endometriotic lesions drive acute then chronic inflammatory reactions, and lead to pelvic adhesions, pain, and infertility. Individual susceptibility to endometriosis, however, is influenced by genetic, anatomical, endocrine, and environmental factors.
Among women with minimal/mild endometriosis, approximately 50% will be able to conceive without treatment, whereas in women with moderate disease, only 25% will conceive spontaneously, and few spontaneous conceptions occur in the case of severe disease.
Possible causes for reduced fertility in women with endometriosis
- Adhesions
- Chronic intraperitoneal inflammation
- Disturbed folliculogenesis
- Luteinized unruptured follicle
- Luteal phase defects
- Progesterone resistance
- Detrimental effects on spermatozoa
- Anti-endometrial antibodies
- Reduced endometrial receptivity
- Dysfunctional uterotubal motility
- Reduced ovarian response secondary to chronic inflammation
- Disturbed hypothalamic -pituitary ovarian axis