Abstract

Recent studies have identified a mildly elevated circulating homocysteine level as a new and potentially modifiable risk factor for osteoporotic fractures. However, these studies do not establish a causal relationship between increased serum homocysteine and fractures. In the present paper the current data on the effect of lowering homocysteine levels on fracture incidence is discussed. Furthermore, an overview is given of the different cellular and molecular mechanisms that can link high homocysteine concentrations and/or associated B vitamins with bone metabolism.

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