Parathyroid hormone (PTH) is well known to increase bone mass in several osteoporosis animals due to its effects of increasing bone formatidn. We examined the effect of recombinant human PTH(I84) on mass and strength of bone in a steroidtreated-rat model of reduced bone formation. SD male rats received 30 mg/kg of prednisolone (PRD) twice a week and concomitant daily injections of PTH(I-84) for 12 weeks at doses of 12.5, 50 and 200 ~g/kg; all by the subcutaneous route. After sacrificing the animals, spinal and femoral bone mineral density (BMD) were measured by a dual X-ray absorptiometer, and compressive strength of the L5 spine was also assessed. Body weights and femoral lengths were significantly reduced in all PRD-treated groups at the end of the experiment; PTH(I-84) did not ameliorate these effects. Although BMD was not significantly altered in spine and femur from PRDtreated controls, PTH(I-84) in comparative experiments caused dose-dependent increases; significant effects occurred at more than 50 ~g/kg for spine and more than 12.5 ~g/kg for femur. Furthermore, compressive strength, as assessed by a maximum load and structural stiffness of the L5 spine, markedly and dose-dependently increased fin PTH(l-84)-treated groups. These findings indicate that PTH(I-84) increases both mass and strengthof bone in steroid-induced osteopenia, even when bore formation is inhibited. This may result from an induction of bone formation in the animals. In conclusion, PTH(I-84) is a therapeutic agent for secondary osteoporosis as well as for postmenopausal and senile osteoporosis.