[Osteoporosis and cardiovascular disease--two sides of the same coin?].
BACKGROUND
Osteoporosis and cardiovascular disease have numerous epidemiologic changes, health economic consequences, and molecular mechanisms in common, which are highlighted in this short review.
The incidence of osteoporosis and cardiovascular disease is increasing in western societies, and genetic background, nutrition and psychologic factors play important roles in the pathogenesis of both diseases. The presence of a decreased bone mass or osteoporotic vertebral fractures are associated with an increased cardiovascular mortality. Calcaneal bone loss of 1 SD (standard deviation) as measured by osteodensitometry is associated with a 1.31 times increased risk for the occurrence of stroke.
The observed increase in interleukin-6 and tumor necrosis factor serum concentrations during the menopause contributes to osteoporotic bone loss and is associated with arteriosclerosis. Furthermore, the presence of hydroxyapatite in arteriosclerotic plaques supports the notion of common pathogenetic mechanisms for both, osteoporosis and arteriosclerosis. Osteopontin, bone GLA protein and bone morphogenetic protein-2, which have first been isolated from the organic bone matrix, are also present in arteriosclerotic plaques. 1,25-dihydroxycholecalciferol potently stimulates bone matrix mineralization and is also a negative regulator of the renin-angiotensin system; therefore vitamin D(3) deficiency in addition to bone metabolism also affects blood pressure. Osteoporosis and arteriosclerosis develop in mice lacking the osteoprotegerin gene and also in klotho gene knockout mice.


CONCLUSIONS
Diagnosis of osteopenia, osteoporosis and osteoporotic vertebral or hip fractures indicates the presence of an increased cardiovascular risk which needs to be addressed by the physician who cares for patients with osteoporosis. The experimental finding of an osteoanabolic effect of statins supports the possibility of common pathogenetic disturbances which may be responsible for the simultaneous and frequent manifestation of osteoporosis and arteriosclerosis in elderly patients.
Nawroth
Peter
P
Abteilung Innere Medizin I und Sektion Osteologie, Universität Heidelberg.
Pirzer
Rainer
R
Fohr
Berthold
B
Schilling
Tobias
T
Ziegler
Reinhard
R
Bierhaus
Angelika
A
Kasperk
Christian
C
D000818:Animals; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000235:genetics / Q000401:mortality; D015984:Causality; D002762:Cholecalciferol / Q000172:deficiency; D015897:Comorbidity; D005598:Fractures, Spontaneous / Q000209:etiology / Q000235:genetics / Q000401:mortality; D005966:Glucuronidase; D006023:Glycoproteins / Q000235:genetics; D006801:Humans; D000090265:Klotho Proteins; D008565:Membrane Proteins / Q000235:genetics; D051379:Mice; D018345:Mice, Knockout; D010024:Osteoporosis / Q000209:etiology* / Q000235:genetics / Q000401:mortality; D053244:Osteoprotegerin; D018160:Receptors, Cytoplasmic and Nuclear / Q000235:genetics; D018124:Receptors, Tumor Necrosis Factor; D012306:Risk; D016103:Spinal Fractures / Q000209:etiology / Q000235:genetics / Q000401:mortality
D006023:Glycoproteins; D008565:Membrane Proteins; D053244:Osteoprotegerin; D018160:Receptors, Cytoplasmic and Nuclear; D018124:Receptors, Tumor Necrosis Factor; C506030:TNFRSF11B protein, human; C506031:Tnfrsf11b protein, mouse; D002762:Cholecalciferol; D005966:Glucuronidase; D000090265:Klotho Proteins