Embryo implantation and endometriosis

Is it the embryos or endometrium claimed guilty for implantation failure in women with endometriosis

Key Points

Highlights:

• The literature is controversial for targeting the defective side of implantation failure in endometriosis.
• The inflammation seems to affect both oocyte quality and endometrial receptivity.

Importance:

• The review aims to find a target for infertility of patients with endometriosis searching for oocyte alterations, hormonal imbalance, endometrial receptivity, and progesterone resistance.
• Inflammation seems a feasible reason for failure, however, future studies are still required.

What's done here:

• The PubMed database has been searched for the words “endometriosis” and “embryo implantation”, including studies published up to April 2022 and only written in English.
• 21 articles have met the criteria.

Key Results:

• Most of the studies concluded that poor oocyte and embryo quality endorses lower pregnancy rates, more than the endometrium itself in women with endometriosis.
• But results are NOT reliable in comparing different types, stages, and operative histories of included patients.
• Robust evidence supports that endometrium is defective but future research is needed to explain how endometriotic lesions affect decidualization. Until then freeze all strategy seems feasible.
• The hormonal imbalance observed in the endometrium of endometriotic patients, including high estrogen dominance, stimulates lesion growth, diminishes steroidogenesis, causes changes in secretory phase stabilization, and impairs embryo implantation.
• Progesterone resistance causes impaired antagonism to estrogen, inappropriate stromal differentiation, increased inflammation, and decreased endometrial receptivity. But the genes that might cause those are still not well-defined.
• In women with adenomyosis, impaired peristalsis increased ROS production with inflammation, and altered endometrial receptors might also affect implantation.

Limitations:

• The review summarized the literature about endometriosis and impaired implantation rates but as the studies are heterogeneous the mechanisms are not clear and the argument continues.

Lay Summary

Infertility is one of the main symptoms of endometriosis. And unfortunately, monthly fecundity rates decrease from 15% to 2-10% for women with endometriosis. The reason for these decreases is controversial and still not known whether it is because of impaired oocyte quality or endometrial receptivity.

In the review conducted by Astrid Boucher et al, the main reasons are underlined. The PubMed database has been searched for the words “endometriosis” and “embryo implantation”, including studies published up to April 2022 and only written in English, published in the Journal of Clinical Medicine.

Twenty-one articles have met the criteria. Most of the studies concluded that poor oocyte and embryo quality endorses lower pregnancy rates, more than the endometrium itself in women with endometriosis. However, results are not reliable in comparing different types, stages, and operative histories of included patients.

Robust evidence supports that endometrium is defective but future research is needed to explain how endometriotic lesions affect decidualization. Until then freeze all strategy seems feasible.

The hormonal imbalance observed in the endometrium of endometriotic patients, including high estrogen dominance, stimulates lesion growth, diminishes steroidogenesis, causes changes in secretory phase stabilization, and impairs embryo implantation.

Progesterone resistance causes impaired antagonism to estrogen, inappropriate stromal differentiation, increased inflammation, and decreased endometrial receptivity. But the genes that might cause those are still not well-defined.  

In women with adenomyosis, impaired peristalsis increased ROS production besides inflammation and altered endometrial receptors might also affect implantation.

Even the review summarized the literature about endometriosis and impaired implantation rates, as the studies are heterogeneous the mechanisms are not clear and the argument continues.

Research Source: https://pubmed.ncbi.nlm.nih.gov/36143011/