Abstract
The ability of bone to resist fracture depends on the intrinsic properties of the materials that comprise the bone matrix mineralization, the amount of bone (i.e. mass), and the spatial distribution of the bone mass (i.e. microarchitecture). Antiresorptive agents may prevent the decay of cancellous bone and cortical thinning, with no improvement of bone microstructure, leading to a partial correction of the principal bone quality defect in osteoporosis, the disruption of trabecular microarchitecture. Anabolic agents promote bone formation at both trabecular and endocortical surfaces, resulting in an increase of cancellous bone volume and cortical thickness. The improvement of cortical bone strength may be limited by an increase in cortical porosity. strontium ranelate improves trabecular network and cortical thickness that will contribute to anti-fracture efficacy at both vertebral and non-vertebral sites. The results of clinical and experimental studies are consistent with the mode of action of strontium involving dissociation between bone formation and resorption leading to a stimulation both trabecular and cortical bone formation without increasing cortical porosity.
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