Is a change in bone mineral density a sensitive and specific surrogate of anti-fracture efficacy?

Abstract

Anti-resorptive agents perturb steady state remodeling; they suppress, but do not abolish, the birth rate of new basic multicellular units (BMUs). In doing so, remodeling goes to completion with bone formation in the many BMUs created before treatment but now with fewer resorption cavities appearing concurrently. As a result, cortical porosity and trabecular stress concentrators decrease reducing bone fragility. From this improved bone strength, steady state is re-established at a slower remodeling rate that again produces bone fragility but more slowly as fewer new BMUs, each with a less negative BMU balance, produce cortical thinning and porosity, trabecular thinning and loss of connectivi..