According to the various studies conducted so far, there appear to be several mechanisms by which endometriosis causes female infertility:
- Decrease in ovarian reserve
- implants, cysts or endometriomas that affect the ovaries reduce the quantity and quality of the woman's eggs. Healthy ovarian tissue is gradually lost and replaced by this endometriotic tissue, so that the formation of follicles containing the eggs (folliculogenesis) is altered.
- Reduction of tubal patency
- Adhesions may develop, decreasing tubal patency. In most cases, patency is adequate but tubal function is poor. This prevents or hinders the sperm from reaching the egg and the correct transport of the embryo to the uterine cavity.
- Decreased ability of the fallopian tubes to pick up the egg
- Increased peritoneal fluid volume and the presence of oocyte capture inhibitors in the peritoneal fluid prevent interaction between the egg and the fallopian tube fimbriae, so that the egg may not reach the tube after ovulation.
- Immune system impairment
- Peritoneal macrophages may phagocytose sperm ascending the female reproductive tract. In addition, inflammatory molecules are produced which may affect female fertility in different ways and anti-sperm antibodies may appear.
- Embryo implantation problems
- the inflammatory environment generated may be toxic to the embryo. On the other hand, these patients may present low endometrial receptivity, as different molecules necessary for implantation are affected, especially the integrins that must be expressed by the endometrium.
- Increased oxidative stress and changes in the hormonal environment
- can affect both ovarian production and endometrial receptivity or the interaction of the egg and sperm, among others.
Endometriosis can also cause problems that affect fertility, such as alterations in carbohydrate metabolism, ranging from insulin sensitivity with low glucose levels to insulin resistance.
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