Many women with endometriosis fail to ovulate, although no one knows if this is a direct result of the disease or if it is coincidental. One thought is that if an ovarian follicle that has been stimulated by luteinizing hormone fails to rupture and expel the ovum, the ovum cannot be fertilized.
This is called luteinized unruptured follicle syndrome. Even if the ovum is fertilized, problems can occur. You can also check out online sources to get detailed information about how endometriosis and fertility are related.
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For instance, when the smooth muscle of the uterus and fallopian tubes becomes irritated, the contractile waves diminish, thus making it difficult for the ovum, fertilized or not, to move along its path to the uterus.
Other barriers to fertility in endometriosis include:
Irritation and inflammation produced by retrograde menstruation, or by the endometrioma themselves, can cause an immune reaction and formation of an excessive number of macrophages (scavenger cells), which destroy foreign invaders such as sperm.
Various autoimmune responses (a condition in which one is "allergic" to oneself) arise as a result of misplaced endometrium. Autoantibodies prevent implantation or cause the uterus to reject the zygote (fertilized ovum). Endometriosis is now beginning to be regarded as an autoimmune disease, like lupus erythematosus or rheumatoid arthritis.
Increased or overactive prostaglandins can decrease sperm motility. Moreover, ectopic (misplaced) endometrium secretes prostaglandins that affect a number of reproductive mechanisms. Anatomic distortions and obstructions of the fallopian tubes, as well as anovulation, luteal phase defects, and hormonal abnormalities can inhibit fertility.