Uterine receptivity: alterations associated with benign gynecological disease

Abstract

The role of the endometrium is to establish and maintain pregnancy. Endometrial receptivity is established during the mid-secretory phase, between cycle day (CD) 20 to 24, or 6 to 10 days after ovulation. In some cases of infertility or recurrent pregnancy loss, implantation failure is due to a lack of expression of specific critical participating proteins such as cell adhesion molecules. Numerous cell adhesion molecules (including integrins, selectins, and cadherins) are expressed by the endometrium and appear to be necessary for the successful interaction of the embryo with the endometrium. One of the best-characterized cell adhesion molecules are the integrins. Integrins are transmembrane glycoproteins that belong to a large family comprising alpha and beta subunits, and are present on virtually all cells in the body. Women with various benign gynecologic disorders, including endometriosis, polycystic ovarian syndrome, hydrosalpinges, and luteal phase defect, appear to exhibit decreased uterine receptivity and abnormal expression of endometrial biomarkers. This review addresses proposed mechanisms of implantation and endocrine and paracrine signals responsible for the establishment of endometrial receptivity as well has the possible mechanisms of dysfunction in certain types of infertility in women with benign gynecologic disease.