ABSTRACT
There is now a consensus that osteoporosis should be defined as a disease of decreased bone strength rather than a disease of decreased bone mass, and that all efficacious drugs should demonstrate increases in bone strength as evidenced by a decrease in fracture incidence. Bone strength primarily reflects the integration of bone density and bone quality1. From a skeletal metabolism standpoint, osteoporosis may be defined as a consequence of the imbalance of the physiological process of bone turnover (or coupling), i.e. a lack of equilibrium between the activity of osteoblasts (bone-forming cells) and osteoclasts (bone-resorbing cells), with a relative increase in the activity of the latter2.
