Immobilization osteoporosis: a review

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Abstract
Bone mass is not only subject to systemic hormonal homeostatic mechanisms, but also to local mechanical influences. The importance of the mechanical balance of bone has been more recently stressed by the research on the effect of weightlessness on bone, and by the introduction of the concept of “mechanostat” in the pathogenesis of osteoporotic conditions. Immobilization osteoporosis has clinical (fractures, sometimes hypercalcemia, urinary lithiasis) and radiological features. Immobilization has an effect on bone modeling and remodeling, through an increased activation of remodeling loci, and a decrease of the osteoblastic stimulus. This leads directly to a local reduction in bone mass, the increased activation multiplying the effect of the deficit in bone formation. The prevention is based on exercise if the load is applied intermittently for a daily period. It seems also that muscle weight is an important determinant of bone mass. There is a potential for recovery during the active early phase of immobilization osteoporosis that may disappear in the subsequent late (about six months) inactive phase. Permanent losses could be prevented by appropriate measures, pharmacology or exercises, applied during the first months of immobilization. No recovery has been demonstrated after the inactive phase has been reached, whatever the treatment. The cumulative effect of repeated periods of immobilization remains hypothetical.