BACKGROUND/ OBJECTIVES: SR is a chemical agent developed for the treatment of osteoporosis. In vitro, SR enhanced replication of osteoprogenitor cells and bone formation. In vivo, in ovariectomized rats SR prevented the biomechanical deterioration of bone while in non-ovariectomized rats, enhanced bone architecture and increased trabecular and cortical bone mass. The aim of this study was to evaluate the effect of SR on bone healing of calvarial critical size defects treated with a deproteinized bovine bone mineral (DBBM) and a collagen barrier (CM), in healthy and osteoporotic rats.

MATERIAL AND METHODS: Sixty-four, 4-month-old Wistar female rats were used. Osteoporosis was induced by ovariectomy and calcium-deficient diet in half of them. Sixteen ovariectomized (OSR) and 16 healthy (HSR) rats were treated with SR while no medication was administered in the remaining 16 healthy (H) and 16 ovariectomized (O) rats. At 6 weeks after ovariectomy, a 5mm defect was created in each parietal bone of every animal. One defect was treated with DBBM and CM, while the contralateral was left untreated. Qualitative and quantitative histological analysis was performed at 30 and 60 days of healing. A generalized estimating equations test was performed to evaluate the effect of SR and osteoporosis, on new bone formation (NB).

RESULTS: After 30 days of healing, NB in the untreated defects was 3.4%±1.7%, 4.3%±6.2%, 3.2±4.5%, 15.9±23.5% in O, OSR, H and HSR groups, respectively; after 60 days, NB was 4.7%±4.3%, 11.3%±7%, 7.1%±13.2, 12.1%±13.5%, respectively. In the GBR-treated defects, after 30 days, NB was 2.6%±1.4%, 2.4%±1.6%, 4.5%±4.1%, 10.3%±14.4% in O, OSR, H and HSR groups, respectively; after 60 days, NB was 2.2%±1.6%, 4.3%±4.2%, 7%±5.1%, 10.8%±17.4%, respectively. Osteoporosis (p=0.008) and the absence of strontium ranelate treatment (p=0.01) had a negative impact on NB.

CONCLUSION: SR may promote bone formation in calvarial defects in healthy and osteoporotic rats, albeit in a moderate extent.