The underexplored crosstalk between hemostasis and bone metabolism: from mechanisms to clinical implications

Abstract

Hemostasis and bone metabolism, traditionally considered as distinct physiological systems, are now recognized to share a complex and bidirectional interplay. Emerging evidence reveals that several components of the hemostatic cascade-including coagulation factors and platelets-may modulate bone cell function and remodeling. Conversely, key regulators of bone and mineral metabolism, such as calcium, vitamin D, and parathyroid hormone, exert significant effects on vascular and hemostatic pathways. This interplay is especially relevant in aging populations, where the incidence of thrombotic disorders and skeletal fragility increases, and the 2 conditions often coexist, with long-term use of anticoagulants or osteoporosis therapies potentially affecting both systems. In this narrative review, we synthesize current insights into the molecular and cellular mechanisms involved in the hemostasis-bone interaction. We also discuss how disorders of mineral metabolism influence coagulation and, conversely, how hemostatic conditions may affect skeletal health. Moreover, we examine how pharmacologic agents-such as anticoagulants and osteoporosis therapies-may impact the hemostasis-bone axis. While most available evidence is preclinical or observational, emerging data point to potential clinical implications that warrant further investigation. A deeper understanding of this interplay could support more effective therapeutic strategies and improve risk assessment in patients with concurrent coagulation and skeletal disorders.

Keywords: anticoagulants; bone remodeling; coagulation; osteoporosis; vitamin K.