This review evaluates the mechanistic basis of cannabinoid efficacy in endometriosis-associated pain, integrating preclinical (in vitro and animal model) and human epidemiological evidence on the endocannabinoid system (ECS) as a therapeutic target.
Cannabinoids act on three main pain mechanisms in endometriosis: (1) suppressing nociceptive signaling via cannabinoid and non-cannabinoid receptors in lesions, (2) attenuating inflammation by inhibiting proinflammatory cytokines and reducing mast cell/peritoneal macrophage mediator release, and (3) exerting antiproliferative effects on endometriotic lesions in preclinical models.
No clinical trial data are available; evidence is largely from in vitro studies and animal models, limiting direct translation to humans. The mechanisms underlying self-reported cannabis use in women with endometriosis remain poorly characterized.
The ECS represents a biologically plausible and multi-mechanistic target for endometriosis pain, but no clinical trials have yet established safety or efficacy of cannabinoid therapies in this population. Clinicians should note patient-driven cannabis use is already prevalent while awaiting rigorous trial data.
Explore related topics
