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.
This study examined the correlations between isokinetic muscle strength of knee and elbow flexors and extensors with vertebral and femoral bone mineral density in a population of 106 women between the ages of 44 and 87 years. The absolute value of muscle strength correlated significantly with bone mineral density; muscle strength of the upper limb appeared to be more closely correlated with bone mass, while muscle strength in the lower limb was more specific for femoral mineral bone density. The most important finding that these results demonstrated was a concomitant decline in muscle strength of the upper limb and bone mineral density between the 5th and 6th decades. In contrast, they also showed a decline in muscle strength of the lower limbs after the 6th decade, occurring before the decline in bone mineral density observed between the 7th and 8th decades. From these results it would appear that other studies are required to examine the relationship between the essentially hormonal role in postmenopausal decline in muscle strength and the decline in physical activity during the senile period. These elements are important because they must be taken into account in physical exercise programmes designed to prevent osteoporosis.
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