Endometriosis-related peritoneal adhesion formation: molecular mechanisms and clinical significance

Becky Macpherson, Joel Zindel, Michael D. Mueller, Erin Greaves
Human Reproduction Update · 2026 · doi:10.1093/humupd/dmag021 · PMID:42600047 · W7203496921
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This narrative review examines how endometriosis-specific factors like chronic inflammation and iron exposure lower the threshold for peritoneal adhesion formation, highlighting the need for targeted pharmacological therapies to prevent these adhesions.

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Abstract

BACKGROUND: Peritoneal adhesions are a major and often under-recognized cause of morbidity following abdominopelvic inflammation and surgery, contributing to chronic pelvic pain, infertility, bowel obstruction, and surgical complications. Endometriosis, affecting 10-11% of reproductive-age women, is strongly associated with adhesions; however, whether adhesion formation in endometriosis reflects general peritoneal injury or disease-specific mechanisms remains unclear. OBJECTIVE AND RATIONALE: This narrative review examines (i) physiological peritoneal healing and mechanisms of adhesion formation, (ii) how the altered peritoneal microenvironment in endometriosis may modify adhesiogenesis, and (iii) current and theoretical therapeutic and preventative strategies for adhesions in endometriosis. This will improve current understanding of adhesiogenesis and the implications of adhesions in women with endometriosis, and will identify areas for future research to reduce morbidity in this patient population. SEARCH METHODS: Literature searches were performed in PubMed, Embase and Cochrane Library using combinations of the terms 'endometriosis', 'adhesions', 'pelvic', 'abdominal', 'peritoneal' between January 2000 and February 2026. Randomized-controlled trials, observational studies, systematic reviews, and relevant experimental studies were included. Case reports and non-English publications were excluded. A total of 124 studies were included in this literature review. OUTCOMES: Adhesion formation results from dysregulated peritoneal repair involving inflammation, coagulation-fibrinolysis imbalance, and fibroproliferative remodelling. Evidence suggests that endometriosis creates a peritoneal environment characterized by chronic inflammation, altered immune responses, repeated tissue injury, and exposure to menstrual debris and iron, which may promote adhesiogenesis. However, much mechanistic understanding is derived from experimental models, and direct evidence from patients remains limited. Prevention of adhesiogenesis in endometriosis currently focuses on intra-operative interventions to limit adhesion development following endometriosis-related surgery, rather than preventing disease-related adhesiogenesis in the absence of surgery. We discuss potential pharmacotherapies, including hormonal treatments, identified by experimental studies, which may perturb endometriosis-related adhesiogenesis. WIDER IMPLICATIONS: Current data support a model in which adhesion biology in endometriosis largely reflects conserved wound-healing pathways but develop within a chronically altered peritoneal microenvironment that lowers the threshold for adhesiogenesis and promotes persistence and recurrence. Clarifying endometriosis-specific drivers and generating robust human data are essential to develop targeted adhesion-prevention strategies and improve long-term outcomes for affected patients. Notably, there are currently no effective pharmacological therapies to prevent or treat adhesions, representing a major unmet clinical need in endometriosis care. REGISTRATION NUMBER: N/A.

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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. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (100)

SciLite annotations

organisms 2
noordeloos 2009062 human
chemicals 1
iron

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