Abstract
In rabbits, cortisone administration induces osteoporosis, a low or unbalanced Ca/P diet accelerating this change so that in young rabbits spontaneous fractures occurred within 12 days. This rapid rarefaction of bone was mainly due to an increased rate of resorption associated with large numbers of osteoclasts at trabecular margins. Microradiograms of the skull showed that this change initially took place around vascular channels, which rapidly widened to form large spaces within the bone itself. Old rabbits responded in the same way, although the bone changes occurred more slowly and fractures were not observed. The anti-anabolic hypothesis of the development of osteoporosis is thus not applicable to cortisone-induced rarefaction of bone in the rabbit.