The prevention of fractures induced by inflammatory bone disease remains a clinical challenge. This is because of a lack of bone formation to fill in the bone defects, which are believed to be due in part to persistent inflammation caused by the imbalance of M1 over M2 macrophages. In this study, gold nanoparticles (AuNPs) were synthesized to shift the balance of macrophages at the site of bone damage to improve osteanagenesis in a mouse model of LPS-induced inflammatory bone erosion. Specifically, the AuNPs treatment improved bone structure and increased bone mineral density (BMD) by ~14% compared with model group. Macrophages recruited by LPS treatment were reduced by ~11% after AuNPs injection. Compared to LPS treatment only, the percentage of M2 macrophages increased threefold by AuNPs, while the proportion of M1 macrophages decreased by 59%. This promoted the regeneration of bone matrix proteins in the bone defect site, which finally leads to increased bone mass and improved bone structure in model mice. These data suggest that AuNPs could be a novel candidate therapeutic for inflammatory bone disease rather than a drug carrier.

预防由炎症性骨病引起的骨折仍然是一个临床挑战。这是因为缺乏骨形成来填补骨缺损，这被认为部分是由于 M1 相对于 M2 巨噬细胞失衡引起的持续性炎症。在这项研究中，合成金纳米粒子 (AuNPs) 以改变骨损伤部位巨噬细胞的平衡，以改善 LPS 诱导的炎症性骨侵蚀小鼠模型中的骨生成。具体而言，与模型组相比，AuNPs 治疗改善了骨骼结构，并使骨矿物质密度 (BMD) 增加了约 14%。在注射 AuNPs 后，LPS 处理募集的巨噬细胞减少了约 11%。与仅 LPS 处理相比，AuNPs 使 M2 巨噬细胞的百分比增加了三倍，而 M1 巨噬细胞的比例减少了 59%。这促进了骨缺损部位骨基质蛋白的再生，最终导致模型小鼠的骨量增加和骨结构改善。这些数据表明，AuNPs 可能是炎症性骨病的新型候选治疗剂，而不是药物载体。