Centre for Oral Immunobiology & Regenerative Medicine, Institute of Dentistry, Bart's & The London School of Dentistry & Medicine, Queen Mary University of London, London, UK.
Centre for Oral Clinical Research, Institute of Dentistry, Bart's & The London School of Dentistry & Medicine, Queen Mary University of London, London, UK.
J Periodontal Res. 2021 Apr;56(2):330-338. doi: 10.1111/jre.12825. Epub 2020 Dec 26.
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.
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).
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.
SR may promote bone formation in calvarial defects in healthy and osteoporotic rats, albeit in a moderate extent.
背景/目的：SR 是一种专为治疗骨质疏松症而开发的化学制剂。在体外，SR 可促进成骨细胞前体细胞的复制和骨形成。在去卵巢大鼠中，SR 可防止骨生物力学恶化，而非去卵巢大鼠中，SR 可增强骨结构并增加小梁和皮质骨量。本研究旨在评估 SR 对去卵巢和未去卵巢大鼠颅骨临界尺寸缺损用脱蛋白牛骨矿物质（DBBM）和胶原屏障（CM）治疗后骨愈合的影响。
使用 64 只 4 月龄的 Wistar 雌性大鼠。一半大鼠通过卵巢切除术和缺钙饮食诱导骨质疏松症。16 只去卵巢（OSR）和 16 只健康（HSR）大鼠接受 SR 治疗，而其余 16 只健康（H）和 16 只去卵巢（O）大鼠未接受任何药物治疗。在卵巢切除后 6 周，每只动物的每块顶骨上均形成 5mm 大小的缺损。一个缺损用 DBBM 和 CM 处理，而对侧不处理。在 30 和 60 天愈合时进行定性和定量组织学分析。使用广义估计方程检验评估 SR 和骨质疏松症对新骨形成（NB）的影响。
在 30 天愈合时，未处理缺损中的 NB 分别为 O、OSR、H 和 HSR 组的 3.4%±1.7%、4.3%±6.2%、3.2±4.5%、15.9±23.5%；60 天时，NB 分别为 4.7%±4.3%、11.3%±7%、7.1%±13.2%、12.1%±13.5%。在 GBR 处理的缺损中，在 30 天时，NB 分别为 O、OSR、H 和 HSR 组的 2.6%±1.4%、2.4%±1.6%、4.5%±4.1%、10.3%±14.4%；在 60 天时，NB 分别为 2.2%±1.6%、4.3%±4.2%、7%±5.1%、10.8%±17.4%。骨质疏松症（p=0.008）和缺乏雷奈酸锶治疗（p=0.01）对 NB 有负面影响。
SR 可能促进健康和骨质疏松症大鼠颅骨缺损中的骨形成，尽管程度适中。
