Glucocorticoid inhibits bone regeneration after osteonecrosis of the femoral head in aged female rats.

Idiopathic osteonecrosis of the femoral head (ION) is a painful disease of the hip, the pathogenic mechanism of which is still unclear. The most common extraneous factor is steroid treatment. Steroids have inhibiting effects on bone formation and resorption. When bone regenerative treatments are indicated for ION patients who are exposed to steroids, we cannot ignore the effects of corticosteroid itself on bone healing. The aim of this study was to investigate the effects of glucocorticoid on bone regeneration after osteonecrosis of the femoral head in a rat model. Osteonecrosis was induced surgically on the left femoral heads of aged female rats (about 6 months old) on day 0. Methylprednisolone sodium succinate (MPSS) or normal saline was administrated at a dose of 100 mg/kg/day from day 7 to 11. Femoral heads were analyzed histologically. There were no pathological findings in the right femoral heads of the MPSS-treated and saline-treated rats, as control for the contralateral injury. The newly formed bone volume and the osteoclast number were significantly smaller in the MPSS-treated group. The normal bone marrow was regenerated in the saline-treated group, whereas most of the bone marrow space still contained fibroblast-like spindle-shaped cells in the MPSS-treated group on day 42. Alkaline phosphatase-positive cells were only seen in the areas around the regenerated bone marrow cavities. Thus, MPSS inhibits bone formation by suppressing osteoblast proliferation and resorption by suppressing the recruitment of osteoclast precursors. These findings may be useful when designing treatments for ION patients exposed to steroids.