Hadidi Lina, Ge Susan, Comeau-Gauthier Marianne, Ramirez-Garcia Luna Jose, Harvey Edward J, Merle Geraldine
McGill University Division of Orthopedic Surgery, Montreal General Hospital, Montreal, QC, Canada.
Department of Experimental Surgery, Faculty of Medicine, McGill University, Montreal, QC, Canada ; and.
J Orthop Trauma. 2021 May 1;35(5):e165-e170. doi: 10.1097/BOT.0000000000001974.
To evaluate if local delivery of boron can accelerate bone healing and examine if the bioactive salt impacts the osteogenic response of bone-derived osteoclasts and osteoblasts by the regulation of the Wnt/β-catenin pathway.
Bilateral femoral cortical defects were created in 32 skeletally mature C57 mice. On the experimental side, boric acid (8 mg/kg concentration) was injected locally, whereas on the control side, saline was used. Mice were euthanized at 7, 14, and 28 days. MicroCT was used to quantify bone regeneration at the defect. Histological staining for alkaline phosphatase and tartrate-resistant acid phosphatase was used to quantify osteoblast and osteoclast activity, respectively. Immunohistochemical antibodies, β-catenin, and CD34 were used to quantify active β-catenin levels and angiogenesis, respectively.
The boron group exhibited higher bone volume and trabecular thickness at 28 days on microCT. Both alkaline phosphatase activity and β-catenin activity was significantly higher in the boron group at 7 days. In addition, CD34 staining revealed increased angiogenesis at 14 days in boron-treated groups. We found boron to have no association with osteoclast activity.
This study shows that local delivery of boron is associated with an increase in osteoblast activity at early phases of healing. The corresponding increase in β-catenin likely supports that boron increases osteoblast activity by the Wnt/β-catenin pathway. Increased angiogenesis at 14 days could be a separate mechanism of increasing bone formation that is independent of Wnt/β-catenin activation.
评估硼的局部递送是否能加速骨愈合，并研究这种生物活性盐是否通过调控Wnt/β-连环蛋白信号通路影响骨源性破骨细胞和成骨细胞的成骨反应。
在32只骨骼成熟的C57小鼠上制造双侧股骨皮质缺损。在实验侧局部注射硼酸（浓度为8mg/kg），而在对照侧注射生理盐水。分别在第7、14和28天对小鼠实施安乐死。使用微型计算机断层扫描（MicroCT）对缺损处的骨再生进行定量分析。采用碱性磷酸酶和抗酒石酸酸性磷酸酶的组织学染色分别对成骨细胞和破骨细胞活性进行定量分析。分别使用免疫组化抗体β-连环蛋白和CD34对活性β-连环蛋白水平和血管生成进行定量分析。
在第28天的MicroCT检查中，硼组的骨体积和小梁厚度更高。硼组在第7天时碱性磷酸酶活性和β-连环蛋白活性均显著更高。此外，CD34染色显示硼处理组在第14天时血管生成增加。我们发现硼与破骨细胞活性无关。
本研究表明，硼的局部递送与愈合早期成骨细胞活性增加有关。β-连环蛋白相应增加可能支持硼通过Wnt/β-连环蛋白信号通路增加成骨细胞活性。第14天时血管生成增加可能是增加骨形成的另一种机制且独立于Wnt/β-连环蛋白激活。
