**Abstract**

Polycystic ovary syndrome (PCOS) is a frequent disorder affecting women of reproductive age characterized by infertility. Affected endometrial receptivity seems to contribute to decreased fertility of these patients as suggested by several studies. Understanding the mechanism behind this reduced endometrial receptivity could contribute to discovery of new therapeutic targets for infertility of PCOS. The aim of the paper is to review the current data regarding endometrial receptivity in PCOS patients, the potential mechanisms involved with particular focus on recent findings as the impact of gut microbiota on endometrium, the relationship between vitamin D and endometrial receptivity and the different impact of letrozole and clomiphene citrate on endometrial receptivity in infertile PCOS women.

**Keywords:** polycystic ovary syndrome, endometrial receptivity, endometrium, implantation, pregnancy

### **1. Introduction**

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of reproductive age, having a prevalence of 8 to 13% and of 21% in high-risk groups [1]. Moreover, it is a leading cause of female infertility [2, 3] and the most common cause of anovulatory infertility [4]. A systematic review from 2020 [5] found that there is significant variation in prevalence probably according to ethnic background and design of the published studies, but also to diagnosis criteria used to identify the disease. Thus, they found that the reported prevalence of PCOS vary between 2,2% and 15–20%, with the studies using the Rotterdam criteria reporting the highest prevalence [5].

PCOS has significant consequences on the women health, being associated with infertility, menstrual irregularities, metabolic abnormalities, cardiovascular risk and psychological disturbances [6] and, therefore, impairing the quality of life. The latest guidelines [7] recommend the use of Rotterdam Consensus criteria for PCOS diagnosis, which assumes that two out of the following three features are present: oligo- or anovulation, hyperandrogenism (clinical or biochemical) and polycystic ovaries [8]. The use of these criteria generates several clinical phenotypes with variate impact on reproductive potential and metabolic profile, with some of them diagnosed with difficulty due to a scarce clinical picture. Therefore, PCOS can be a challenging disorder in the reproductive medicine practice.

Hyperandrogenism is a key feature of PCOS, being the result of increased production of both ovarian and adrenal androgens. Ovarian over-secretion of androgens is the consequence of LH stimulation and also the action of high insulin levels on insulin receptors from the ovarian theca cells. Moreover, bioavailability of androgens is increased due to insulin effect to reduce the hepatic production of sex-hormone binding globulin.
