Abstract

Statins inhibit HMG-CoA reductase and reduce the intracellular formation of mevalonate. They are chemical compounds able to reduce total cholesterol by 15-40% and LDL cholesterol by 20-60%, and to increase HDL cholesterol by 5-15%. They also reduce triglycerides by 10- 30%. Statins, blocking the mevalonate pathway, inhibit the prenylation of proteins, which is essential to perform their biological function. A great deal of research has documented the positive effect of statins on bone formation and the importance of bone morphogenetic protein-2 (BMP-2) in mediating this effect. Statins are also able to decrease osteoblast apoptosis. The positive effect of statins on bone formation is accompanied by an inhibition of osteoclast activity, which gives statins the ability to uncouple the bone remodeling processes. Patients taking statins have a higher femoral bone density than those who do not. The lipophilic statins seem to be more effective than the hydrophilic statins in protecting bone. In several clinical trials, but not in all, the use of statins had been associated with a reduction in the fracture risk. In conclusion, statins have a positive effect on bone in vitro, but such an efficacy in humans has yet to be clearly demonstrated. Randomized, controlled trials are needed to provide a satisfactory answer on this issue.