Endometriosis reshapes peritoneal healing and raises the odds of adhesions
Peritoneal adhesions remain one of the most consequential but underappreciated complications in abdominopelvic disease. In endometriosis, they are tied to chronic pelvic pain, infertility, bowel obstruction, and technically difficult surgery, yet the biology behind their formation is still incompletely defined. The review by Macpherson, Zindel, Mueller, and Greaves places adhesion formation inside the broader framework of impaired peritoneal repair, where inflammation, coagulation, fibrinolysis, and fibroproliferative remodeling intersect. Endometriosis does not appear to create an entirely separate adhesion pathway; rather, it seems to load the same wound-healing machinery with a persistently abnormal inflammatory burden.
The review searched PubMed, Embase, and the Cochrane Library for studies published between January 2000 and February 2026 and included randomized trials, observational studies, systematic reviews, and experimental work. In all, 124 studies informed the synthesis. The breadth of the literature is useful, but it also reveals how much of the field still depends on animal and laboratory models rather than direct human evidence. The resulting picture is biologically coherent and clinically troubling: the peritoneum in endometriosis appears primed to scar, adhere, and remain stuck in a cycle of recurrent injury.
A chronically inflamed peritoneum is primed for scar formation
Normal peritoneal repair depends on a tightly coordinated sequence of hemostasis, fibrin deposition, fibrinolysis, and mesothelial regeneration. When that process stalls, fibrin persists, fibroblasts migrate, collagen accumulates, and adhesions mature. Endometriosis complicates each of those steps. Repeated bleeding, inflammatory signaling, and exposure to menstrual debris create a microenvironment that can delay clearance of fibrin and encourage fibrotic remodeling. Iron from hemorrhagic material may further intensify oxidative stress, adding another layer of tissue injury.
A single sentence captures the clinical consequence: the pelvis becomes a site where healing and scarring compete, and scarring often wins.
This matters because adhesion biology is not simply a passive consequence of surgery. The review supports a model in which endometriosis-related peritoneal disease lowers the threshold for adhesiogenesis even when the initiating injury is modest. Chronic immune activation, altered macrophage behavior, and repeated tissue disruption may help explain why adhesions are so common in this population and why they may recur after surgical treatment. The biologic logic is straightforward: if the surrounding tissue is already inflamed and repair pathways are dysregulated, then any additional injury is more likely to resolve with fibrosis rather than restoration of normal anatomy.
Surgical injury remains the main target for prevention
Current prevention strategies are still centered on the operating room. In women undergoing endometriosis-related surgery, efforts focus on limiting tissue trauma, reducing desiccation and ischemia, and using intra-operative measures intended to reduce adhesion development. Those measures address the point at which the peritoneum is most vulnerable, when fresh injury meets an inflammatory milieu already shaped by disease.
What remains conspicuously absent is a proven drug that can reliably prevent adhesions or reverse them once established. The review is direct on this point: no effective pharmacological therapy exists for adhesion prevention or treatment. Experimental work has suggested that hormonal therapies might influence adhesiogenesis, presumably by modifying inflammation and the hormonal responsiveness of ectopic and eutopic endometrial tissue. Still, these signals remain preclinical or indirect, and they have not yet translated into a treatment that changes everyday care.
The absence of a drug-based solution leaves surgeons and patients in a difficult position. Surgery may relieve pain, excise lesions, or restore anatomy, yet it can also create the very tissue injury that seeds future adhesions. In endometriosis, this paradox is especially sharp because the disease itself already appears to distort the peritoneal healing response.
Human data lag behind the biology
The strongest mechanistic arguments in this field come from experimental studies. Human evidence is thinner, and that gap shapes how confidently the field can move from association to intervention. The review makes clear that direct patient data are limited, even though the clinical burden is obvious. Adhesions contribute to pain, infertility, bowel symptoms, and surgical complications, but the exact proportion of that burden attributable to disease-specific mechanisms rather than generalized peritoneal injury remains unsettled.
This uncertainty should not be mistaken for irrelevance. It points to a more precise research agenda. Endometriosis-associated adhesions may not be fundamentally distinct from other postoperative adhesions at the level of core wound-healing pathways, but they likely arise in a peritoneal environment that is already primed for persistence and recurrence. Identifying which components of the inflammatory and fibrotic response are truly disease-specific would allow future studies to separate broad surgical prevention from targeted therapy.
Why the unanswered biology matters at the bedside
For clinicians, adhesions in endometriosis are not an abstract histologic finding. They influence operative difficulty, increase the chance of unintended organ injury, and may help explain why symptoms persist after apparently successful treatment. They also complicate fertility care, where distorted pelvic anatomy can interfere with oocyte pickup, tubal function, or the mobility of pelvic structures. When adhesions recur, the consequences are cumulative.
The review argues for a more refined view of adhesiogenesis in endometriosis: conserved wound-healing pathways operating within a disease-altered peritoneal microenvironment. That framework is clinically useful because it explains why broad anti-inflammatory or anti-fibrotic concepts have appealed to investigators, while also explaining why translation has been slow. A therapy that succeeds in a laboratory model may still fail in patients if it does not address the complexity of chronic pelvic inflammation, repeated microtrauma, and the interaction between endometrial debris and host repair systems.
A sharper human evidence base is still missing.
Future progress will depend on studies that link molecular findings to operative findings, symptoms, fertility outcomes, and recurrence after surgery. The field now needs robust patient-centered data on which women are most likely to develop adhesions, which molecular pathways are most active in human peritoneal tissue, and whether hormonal or other pharmacologic strategies can meaningfully alter that course. Until then, the review supports a cautious but important conclusion: endometriosis appears to amplify adhesion risk by distorting normal peritoneal repair, yet the absence of validated pharmacologic prevention leaves a major therapeutic gap in routine care.