The effects of endometrial polyps, leiomyomas, adenomyosis, and endometriosis on endometrial receptivity: phenotype, molecular pathways, and clinical implications

Purpose of review: This review synthesizes current evidence on how endometrial polyps, leiomyomas, adenomyosis, and endometriosis influence endometrial receptivity, emphasizing phenotype-specific effects, molecular mechanisms, and implications for embryo transfer outcomes. Recent findings: Impaired endometrial receptivity, when present, is mediated by a limited set of convergent pathways, including Homeobox gene ( HOX ) A10/HOXA11 suppression, inflammatory cytokine dysregulation, and progesterone resistance. Leiomyomas and adenomyosis alter decidualization through paracrine signaling, including TGF-β–mediated pathways. Adenomyosis is consistently associated with defective decidualization and altered estrogen–progesterone signaling. Endometriosis alone appears to have limited direct effects on receptivity, and many studies are confounded by unrecognized coexisting adenomyosis. Clinical benefit from polypectomy and myomectomy is phenotype-dependent, with the strongest support for submucous fibroids and selected polyps. Commercial receptivity assays (e.g. BCL6 -based testing) remain insufficiently validated to guide clinical decision-making. Summary: These pathologies do not uniformly impair endometrial receptivity. When impairment occurs, it is phenotype-specific and mediated through shared molecular pathways. Current evidence supports targeted surgical intervention in selected phenotypes, but at present, there are no available tests, such as those assessing relevant endometrial expressions, to guide more specific case selection. Future work should link phenotype-specific treatment to restoration of validated molecular markers and live birth outcomes.