Increasing numbers of cross-sectional studies on general populations and chronic kidney disease (CKD) or end-stage renal disease (ESRD) patients have reported relationships between cardiovascular calcifications and bone disorders, including osteoporosis, osteopenia and high or low bone activity. The mechanisms underlying this bone-cardiovascular axis and biological links between bone and arterial abnormalities are suggestive of bone-vascular cross-talk. The nature of these links is not well understood and could result from: 1) common factors acting on bone remodeling and arterial calcification; 2) compromised bone blood supply responsible for arteriosclerosis of bone vessels and reduced perfusion; and/or 3) direct action of bone cells (osteoblasts/osteocytes) on vascular biology and structure. Inflammation and accumulation of reactive oxygen species are the principal common pathways linking bone and arterial pathologies.