The statins may act on bone by the inhibition of bone resorption and the stimulation of bone formation. There is some clinical evidence to support these actions. There appears to be a reduction in the risk of fractures in patients taking statins, based on observational studies. There appears to be a small improvement in bone mineral density and a small increase in bone formation markers in patients taking statins. However, in the randomised controlled trials, there appears to be no effect of statins on fracture risk; since hyperlipidaemia is associate with obesity and this, in turn, is associated with a decreased risk of vertebral and hip fracture, then the association reported in observational studies could be an artefact. Statins increase BMP-2 production by osteoblasts, an important anabolic agent. This effect appears to be mediated by nitric oxide. Further, statins act on the mevalonate pathway and have effects on intermediary compound such as farnesyl pyrophosphate that mimics the nitrogen-containing bisphosphonates. Thus, there are plausible mechanisms through which statins could exert their effects on bone cells. However, the statins may not achieve sufficiently high doses in bone in order to exert these effects. We need to conduct randomised controlled trials in patients with osteoporosis to evaluate the effect of statins on bone fully.
03 - 05 Nov 2003
Society for Endocrinology