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

Michelle N Han, Han MN, Michelle Han, Goldrath KE, Kathryn E Goldrath, Kathryn Goldrath, Munro MG, Malcolm G Munro
Current opinion in obstetrics & gynecology · 2026 · vol. 38(4) , pp. 261–269 · doi:10.1097/gco.0000000000001115 · PMID:42145181 · W7161604041
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This review examines how endometrial polyps, leiomyomas, adenomyosis, and endometriosis affect endometrial receptivity through shared molecular pathways, with phenotype-specific clinical implications for surgical interventions.

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⚙ AI-generated deep summary by claude@2026-07, 2026-07-17 · read from full text ⓘ

This review synthesizes evidence on how endometrial polyps, leiomyomas, adenomyosis, and endometriosis affect endometrial receptivity, integrating phenotype differences, proposed molecular pathways, and implications for embryo transfer outcomes. It reports that when receptivity is impaired, the mechanism involves a limited set of convergent pathways such as HOXA10/HOXA11 suppression, inflammatory cytokine dysregulation, and progesterone resistance, while leiomyomas and adenomyosis can disrupt decidualization via paracrine signaling including TGF-β–mediated pathways; adenomyosis is described as consistently linked to defective decidualization and altered estrogen–progesterone signaling. A key caveat emphasized is that endometriosis studies may be confounded by unrecognized coexisting adenomyosis, and receptivity assays like BCL6-based testing are noted as insufficiently validated to guide decisions. This paper is centrally about endometriosis and adenomyosis — it reviews how adenomyosis (and also endometriosis) influences endometrial receptivity through phenotype-specific molecular pathways.

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Abstract

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.
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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.

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Condition tags

endometriosisadenomyosis

MeSH descriptors

Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (76)

SciLite annotations

chemicals 3
progesterone estrogen progesterone

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last seen: 2026-07-26T06:08:39.051465+00:00
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