Y Fujita1, T Konoo, K Maki. 1. Division of Developmental Stomatognathic Function Science, Department of Growth and Development of Functions, Kyushu Dental College, Kitakyushu, Japan.
Abstract
OBJECTIVES: To analyse the effects of short-term treatment with etidronate on the glucocorticoid-induced retardation of bone growth and deterioration of bone structure in the prepubertal rat mandible. MATERIALS AND METHODS: Fifty 5-week-old male rats were divided into five groups. Etidronate or vehicle treatment (5 mg/kg/day, daily, subcutaneous injection) was initiated after glucocorticoid administration (30 mg/kg/day, on alternate days, orally) for 6 weeks and was continued for 3 weeks. Then, bone growth was measured using lateral cephalometric analysis. Peripheral quantitative computed tomography was used to determine bone density, bone cross-sectional area and bone strength. RESULTS: Glucocorticoid-treated rats had significantly lower body weight, mandibular length, cortical bone density, bone strength and cross-sectional area in trabecular and cortical bone, but had significantly higher trabecular bone density than untreated rats. No significant difference in mandibular height was observed between the glucocorticoid-treated group and the untreated control group. Etidronate treatment improved the glucocorticoid-induced decrease in bone strength and increased density in trabecular and cortical bone above the untreated control level, but had no significant effects on the reduction in mandibular length. CONCLUSION: These findings suggest that etidronate can potentially reverse the glucocorticoid-induced deterioration of internal bone structure, but has no beneficial effects on the glucocorticoid-induced retardation of bone growth in the growing rat mandible.
OBJECTIVES: To analyse the effects of short-term treatment with etidronate on the glucocorticoid-induced retardation of bone growth and deterioration of bone structure in the prepubertal rat mandible. MATERIALS AND METHODS: Fifty 5-week-old male rats were divided into five groups. Etidronate or vehicle treatment (5 mg/kg/day, daily, subcutaneous injection) was initiated after glucocorticoid administration (30 mg/kg/day, on alternate days, orally) for 6 weeks and was continued for 3 weeks. Then, bone growth was measured using lateral cephalometric analysis. Peripheral quantitative computed tomography was used to determine bone density, bone cross-sectional area and bone strength. RESULTS: Glucocorticoid-treated rats had significantly lower body weight, mandibular length, cortical bone density, bone strength and cross-sectional area in trabecular and cortical bone, but had significantly higher trabecular bone density than untreated rats. No significant difference in mandibular height was observed between the glucocorticoid-treated group and the untreated control group. Etidronate treatment improved the glucocorticoid-induced decrease in bone strength and increased density in trabecular and cortical bone above the untreated control level, but had no significant effects on the reduction in mandibular length. CONCLUSION: These findings suggest that etidronate can potentially reverse the glucocorticoid-induced deterioration of internal bone structure, but has no beneficial effects on the glucocorticoid-induced retardation of bone growth in the growing rat mandible.