Immobilization and Post-traumatic Osteopenia

Over 300 years ago Galileo and Vesalius suspected skeletal architecture might depend on mechanical usage [1] and more than 100 years ago Julius Wolff stated the relationship between bone function and its architecture [2]. Therefore, the effects of reduced mechanical usage on bone have been known for a long time. In 1924, J.W. Dowden wrote: “the musculature of a limb is reflected in the bones, so that it is easy to distinguish the long bone of a strong man, by its solidity and powerful ridges for muscular attachment, from the bone of a disuse limb, by the lightness and smoothness of the latter. The results of disuse are rapidly seen, even in the X-ray photographs” [3], In 1941, Albright and colleagues reported the case of a young boy who developed hypercalcemia as a consequence of the immobilization for a fracture. During the 1940s and 1950s, alterations in calcium and phosphorus metabolism were described by Whendon and colleagues in poliomyelitic patients and immobilized volunteers and an elevated rate of bone turnover after fracture was described by Bauer [4] and confirmed by others [5,6].