Are cardiovascular disease and osteoporosis directly linked?
For years, osteoporosis and cardiovascular disease were thought to be two independent consequences of aging; however, mounting evidence supports an association between these diseases. Recently, a widespread class of cholesterol-lowering drugs known as statins have demonstrated (in rodents and cell cultures) the ability to induce bone formation. This finding is significant since current therapies are limited to the prevention or slowing down of bone loss rather than (enhancing/improving) bone formation. In humans, the ability of statins to generate new bone has not been consistent; however, several investigations have demonstrated a dramatic decrease in fracture risk. Although it has been proposed that statins induce new bone via increased bone morphogenetic protein-2, other conditions affected by statins such as dyslipidaemia, vascular calcification, endothelial dysfunction and impaired nitric oxide expression, may also contribute to the cardiovascular and bone health paradigm. Furthermore, the role of physical activity and its influence on cardiovascular and bone health, especially in postmenopausal women, may contribute to the discrepancy of findings in human data. In summary, it remains to be determined if statins contribute to bone health via improvements in vascular health or by pleiotropic properties unique to their pharmacology. This review provides information on our current understanding of the bone and cardiovascular association, as well as on novel areas of research to further our current understanding of these conditions.
Whitney
Crystal
C
Healthy Heart Program, St Paul's Hospital, Vancouver, British Columbia V6T 1Z3, Canada.
Warburton
Darren E R
DE
Frohlich
Jiri
J
Chan
Sammy Y
SY
McKay
Heather
H
Khan
Karim
K
D000818:Animals; D001161:Arteriosclerosis / Q000378:metabolism / Q000503:physiopathology; D001842:Bone and Bones / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology; D015444:Exercise / Q000502:physiology; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology; D050356:Lipid Metabolism; D008055:Lipids / Q000097:blood; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism; D010024:Osteoporosis / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology*
D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008055:Lipids; D009569:Nitric Oxide