According to the different studies carried out so far, there appear to be several mechanisms by which endometriosis causes female sterility:
- Decreased ovarian reserve implants, cysts, or endometriomas that affect the ovaries reduce the quantity and quality of a woman’s eggs. Healthy tissue from the ovary is gradually being lost and it is being replaced by this endometriotic tissue, so the formation of the follicles that contain the ovules (folliculogenesis) is altered.
- Reduced tubal patency Adhesions may appear that decrease the permeability of the tubes. In most cases, patency is adequate but the functionality of the tubes is poor. This prevents or hinders the sperm from reaching the egg and the proper transport of the embryo to the uterine cavity.
- Decreased ability of the tubes to collect the egg the increased volume of the peritoneal fluid and the presence of inhibitors of oocyte capture in this flow prevent the interaction between the ovum and the fimbriae of the fallopian tube, which is why it may not reach the tube after ovulation.
- Impaired immune system peritoneal macrophages can phagocytose sperm that travel up the female reproductive tract. Likewise, inflammatory molecules are produced that can affect female fertility in different ways and anti-sperm antibodies can appear.
- Embryo implantation problems the inflammatory environment that is generated can be toxic to the embryo. On the other hand, these patients may have low endometrial receptivity, since different molecules necessary for implantation are affected, especially the integrins that the endometrium must express.
- Increased oxidative stress and changes in the hormonal environment They can affect both ovarian production and the receptivity of the endometrium or the interaction of the ovum and the sperm, among others.
Problems derived from endometriosis and affecting fertility may also appear, such as alterations in carbohydrate metabolism, ranging from insulin sensitivity with low glucose levels to insulin resistance.