The connections between vascular calcification and bone health

Abstract

Vascular calcification, bone loss and increased fracture risk are age-associated disorders. Several epidemiological studies have suggested a relationship between vascular calcification, impaired bone metabolism and increased mortality. So far, this relationship had been underestimated as osteoporosis and vascular calcification have been considered nonmodifiable disorders of aging. Recent data suggest that this association is not simply an artefact of age, stressing that the coincidence of vascular calcification with low bone activity and osteoporosis could be biologically linked. During the development of vascular calcification, the transition of vascular smooth muscle cells towards an osteoblast-like phenotype promotes the release of the vesicular structures, and mineralization within these structures is promoted by several players, including those related to mineral metabolism, like phosphorus, calcium or PTH, which influence either the supersaturation within the structure or the expression of osteogenic factors. However, an intriguing question is whether the presence of vascular calcification impacts bone metabolism, thus demonstrating true cross-talk between these tissues. Evidence is now emerging, suggesting that some inhibitors of the Wnt pathway, such as secreted frizzled proteins 2 and 4 and DKK-1, may play a role linking vascular calcification and bone loss. An additional important question to answer, from the patient’s perspective, is whether or not progression of vascular calcification can be prevented or restricted and whether altering this progression we can efficiently impact patients’ outcomes. Several evidences suggest the control of the CKD-MBD components, particularly serum phosphorus are the main targets to maintain normal bone turnover and protect against vascular calcification.