Combined calcium balance and radioactive calcium turnover studies have been performed in a series of normal and paralyzed adults. The purpose of this investigation was to evaluate the kinetic factors responsible for disuse osteoporosis. Patients with acutely developing disuse osteoporosis were found to have bone formation rates from normal to twice normal and bone resorption rates from two to three times normal. The increased bone resorption rates more than accounted for the negative calcium balances of these subjects. Patients with chronic, stable (but severe) disuse osteoporosis were found to be in calcium equilibrium, with bone formation and resorption rates either normal or slightly low. These observations indicate clearly that the absence of mechanical stresses did not, of itself, reduce bone forming activity, and that a primary increase in bone resorption was responsible for the development of disuse osteoporosis. In vivo uptake measurements of Sr85 in one subject confirmed the kinetic observations, to the effect that a more severely paralyzed extremity took up more isotope than did its less severely involved mate. Treatment of five of the paralyzed subjects with anabolic steroids produced the expected improvement in calcium balance, but kinetic analysis indicated that in the acute group the effect was entirely anticatabolic: i.e., there was no increase in bone forming activity, but a considerable decrease in bone resorption. Measurement of gastrointestinal calcium absorption in all subjects studied revealed gross depression of absorption efficiency in the acute stage of osteoporosis. This change, together with elevations in both serum calcium and serum phosphorus, are interpreted as indications of suppression of endogenous parathyroid function. As such, this evidence precludes any possible role of parathyroid hormone in the genesis of disuse osteoporosis.
All Science Journal Classification (ASJC) codes