Glucocorticoid-Induced Osteoporosis in Growing Mice Is Not Prevented by Simultaneous Intermittent PTH Treatment

Glucocorticoids (GCs) are widely used in medicine for treatment of chronic diseases. Especially in children, prolonged treatment causes growth retardation and early onset of osteoporosis. Human parathyroid hormone (PTH) has an anabolic effect on bone when administrated intermittently. The aim of the present study was to examine whether a combined therapy of dexamethasone (DEX) and PTH could prevent the detrimental effects of GC on cortical and trabecular bone in the femur and vertebrae of growing mice. Three-week-old female FVB mice were treated with control, DEX, PTH, or a combination of DEX and PTH by daily subcutaneous injections. After 4 weeks, animals were killed and the femur and L5 vertebra were isolated. Cortical and trabecular bone parameters and relative calcium density were measured by high-resolution X-ray micro-computed tomography (micro-CT). In the femur, PTH can reverse the effects of DEX on bone volume to control. However, it cannot reverse the undermineralization, which most likely is a strong contributor to bone fragility. In the vertebra, PTH improves bone volume to some extent but does not restore the values to normal. It augments the negative effect of DEX on mineralization. We conclude that the detrimental effects of DEX in the growing skeleton cannot be prevented by simultaneous PTH treatment.