Endometrial Hemostasis in Normal Menstruation and Heavy Menstrual Bleeding

Heavy menstrual bleeding (HMB) affects up to one-third of reproductive-age women and remains a major cause of gynecologic consultations and impaired quality of life. While some cases are attributable to structural uterine abnormalities, many occur without identifiable pathology, and the mechanisms regulating menstrual blood loss remain incompletely understood. Emerging evidence suggests that menstrual hemostasis depends on coordinated local vascular and hemostatic processes within the endometrium, including spiral artery remodeling, vasoconstriction, transient hemostatic plug formation, and tightly regulated coagulation and fibrinolysis. Disruption of these mechanisms, through abnormal vessel remodeling, impaired thrombus formation, or excessive fibrinolytic activity, may contribute to excessive bleeding. In this review, we synthesize current evidence on endometrial vascular biology and hemostatic regulation during menstruation and propose a hypothetical, multiphase biomechanical framework, yet to be validated, in which permissive fibrinolysis, nonocclusive coagulation clots, vasoconstriction, and occlusive shear-induced platelet aggregation successively dominate menstrual hemostasis. Within this framework, unexplained HMB is hypothesized to arise when impaired spiral artery vasoconstriction prevents local wall shear from reaching the range that supports mechanically robust, platelet-rich occlusion. Although this proposed framework is intended as a testable hypothesis, it generates specific, falsifiable predictions and identifies measurements needed to evaluate it. By highlighting key knowledge gaps in the control of menstrual hemostasis, this work aims to guide future research toward mechanism-based, fertility-preserving therapies for women with HMB.