Vascular calcification is an active,cell-regulated process,characterized by the deposition of hydroxyapatite crystal in vascular wall,resulted from high-calcium/phosphate-environment,up-regulation of mineralization inducers and down-regulation of mineralization inhibitor in local or systemic sites.In this process,the protective system against vascular mineralization is exhausted,and mesenchyma,such as vascular smooth muscle cells(VSMC),lose the intrinsic phenotypes,but gain the osteogenic phenotypes.Consequently,mineralized cells release some lipid vesicles,which have two forms at least in vascular wall,such as matrix vesicle and apoptosis body.Lipid vesicles provide appropriate nucleating micro-environments for vascular calcification,and vascular elastin provides the bracket structure for hydroxyapatite deposition.So,under the condition that the balance between calcium deposition(mediated by osteoblast-like cells)and calcium absorption(mediated by osteoclast-like cells)is disrupted,ectopic calcification of vascular intima,media or aortic valve may be developed.Intervention on the mechanisms and risk factors of vascular calcification may bring some beneficial effects on the reverse and regression of vascular calcification.In particular,up-regulation on the number and activity of osteoclasts or osteoclast-like cells in calcification lesion may be a more efficient therapeutic strategy.However,it will be a difficult problem in future how to coordinate the relation between normotopic bone formation and ectopic calcification absorption because of calcification paradox in bone-vascular axis.