Glucocorticoids induce bone loss by increasing bone resorption and decreasing bone formation. In this study we have investigated the potential of salmon calcitonin to attenuate glucocorticoid-induced bone loss in a dog model. Male beagles were divided into three groups: 1) untreated controls, 2) prednisone-treated dogs (1 mg.kg-1.day-1 orally), and 3) prednisone-calcitonin-treated dogs (1.5 U.kg-1.day-1 calcitonin subcutaneously and 1 mg.kg-1.day-1 prednisone orally). Assessment of bone mass by dual energy X-ray absorptiometry demonstrated that bone density remained stable in controls throughout 48 wk. Prednisone-treated dogs lost 13.2% of their initial bone mass by 48 wk. Concomitant calcitonin treatment attenuated prednisone-induced bone loss to only 3.2% at 48 wk. Bone histomorphometry of the spine showed reduced trabecular bone volume in prednisone-treated dogs, whereas control and prednisone-calcitonin-treated animals maintained normal trabecular bone volume. Both prednisone- and prednisone-calcitonin-treated dogs acquired a defect in osteoblastic function as evidenced by a reduction in mean wall thickness and trabecular thickness. Thus calcitonin attenuates the early bone loss induced by glucocorticoids. However, calcitonin failed to prevent glucocorticoid-induced osteoblast dysfunction.