In recent years, the association between osteoporosis and atherosclerotic disease has been described, regardless of patients’ age, and highlighted epidemiologic and pathophysiologic similarities between arterial wall calcification and osteogenesis.^, Cross-sectional, prospective studies have pointed out significant negative association between cardiovascular mortality and low bone mass, osteoporotic fractures, vascular calcification, extension of coronary artery disease and abdominal aortic injury.^– Concomitant occurrence of both diseases seems to result from common pathophysiologic and molecular mechanisms between these conditions. However, it is still controversial whether a low bone mass is caused by arterial calcification or vice-versa, or whether these conditions only have the same pathophysiological mechanism.

Risk factors for osteoporosis and atherosclerotic disease include estrogen, parathyroid hormone, homocysteine and vitamin K deficiency, lipid oxidation products, inflammatory process, vitamin D excess, molecular pathways involved in both bone and vascular mineralization, and similar mechanisms of calcification involving vascular and bone structures. Arterial calcification is found in more than 90% of atherosclerotic lesions. The process starts with formation of vesicles in the endothelial matrix, followed by proliferation and mineralization of the arterial intima-media wall, similarly to the bone tissue. Many bone remodeling regulators have been described in calcified atherosclerotic lesions, including osteocalcin, hydroxyapatite crystals, osteopontin, bone morphogenetic protein 2 osteoprotegerin, sclerostin, dickkopf factor (DKK), leptin, oxidized lipids and calcium sensor-related factor.

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