It is well known that the glucocorticoid suppresses the osteoblast and the calcitonin suppresses the osteoclast. If the calcitonin prevents the osteoporosis with increased Tc-99m MDP uptake in the long-term use of glucocorticoid, then the calcitonin has some activating effect on the bone formation. The immobilization operation was done on the left hind-leg of 16 male Sprague-Dawley rats weighing about 300 g each. For 12 weeks after operation,8 rats were injected 0.5 mg/kg dexamethasone, and the other 8 rats were injected 0.5 mg/kg dexamethasone and $1;ar{u}/kg$ eel calcitonin. The bone mineral content was measured by the single photon absorptiometry and the Tc-99m MDP uptake was used as an index of the osteoblastic activity. 1) The Tc-99m MDP uptakes in the dexamethasone treated group were lower than those in the dexamethasone and calcitonin treated group, and there was no significant difference in Tc-99m MDP uptakes between the immobilized and normal femurs. 2) The bone mineral contents in the dexamethasone treated group were significantly lower than in the dexamethasone and calcitonin treated group, and the immobilized femurs had tower BMC than normal femurs. 3) The slope of regression between the BMC and Tc-99m MDP uptake was stiff in the dexamethasone treated group, and flat in the dexamethasone and calcitonin group, which shows discrepancy between the bone resorption and formation resulting prevention of net bone loss in the dexamethasone and calcitonin treated group. In conclusion, the calcitonin has some effect on the bone formation, and further studies with urinary hydroxyproline and cyclic AMP are expected.