The last decades have seen increased scientific interest in the extra skeletal effects of the vitamin D system, including its role in muscular function. The hypothesis that this seco-steroid was involved in muscle activity derives from the observation that vitamin D-deficient children affected by rickets experience serious muscular impairment, defined as “myopathia rachitica”. In the first half of the last century, to better understand the pathophysiological mechanisms of such muscular damage, a theory was formulated based on the key role of alterations of phosphoric ester concentrations in muscle tissue. This theory, however, did not take into account the effects on skeletal muscle of secondary hyperparathyroidism due to hypovitaminosis D. In fact, it is known that the hyperparathyroidism leads to significant muscular damage characterized by muscle atrophy due to the loss of mainly type II fibers. This damage is different from pathognomonic alterations of primary myopathy, in which there is degeneration or even necrosis of muscle fibers, together with a proliferation of the endomysial connective tissue.
