Reconstruction of irregular oral-maxillofacial bone defects with an inflammatory microenvironment remains a challenge, as chronic local inflammation can largely impair bone healing. Here, we used magnesium silicate nanospheres (MSNs) to load microRNA-146a-5p (miR-146a) to fabricate a nanobiomaterial, MSN+miR-146a, which showed synergistic promoting effects on the osteogenic differentiation of human dental pulp stem cells (hDPSCs). In addition, miR-146a exhibited an anti-inflammatory effect on mouse bone marrow-derived macrophages (BMMs) under lipopolysaccharide (LPS) stimulation by inhibiting the NF-κB pathway via targeting tumor necrosis factor receptor-associated factor 6 (TRAF6), and MSNs could simultaneously promote M2 polarization of BMMs. MiR-146a was also found to inhibit osteoclast formation. Finally, the dual osteogenic-promoting and immunoregulatory effects of MSN+miR-146a were further validated in a stimulated infected mouse mandibular bone defect model via delivery by a photocuring hydrogel. Collectively, the MSN+miR-146a complex revealed good potential in treating inflammatory irregular oral-maxillofacial bone defects.

具有炎症微环境的不规则口腔颌面部骨缺损的重建仍然是一个挑战，因为慢性局部炎症会在很大程度上损害骨愈合。在这里，我们使用硅酸镁纳米球（MSNs）负载microRNA-146a-5p（miR-146a）来制造纳米生物材料MSN+miR-146a，该材料对人牙髓干细胞（hDPSCs）的成骨分化表现出协同促进作用）。此外，miR-146a通过靶向肿瘤坏死因子受体相关因子6（TRAF6）抑制NF-κB通路，对脂多糖（LPS）刺激下的小鼠骨髓源性巨噬细胞（BMM）表现出抗炎作用， MSNs 可以同时促进 BMMs 的 M2 极化。MiR-146a 还被发现可以抑制破骨细胞的形成。最后，通过光固化水凝胶递送，在受刺激的感染小鼠下颌骨缺损模型中进一步验证了 MSN+miR-146a 的成骨促进和免疫调节双重作用。总的来说，MSN+miR-146a 复合物在治疗炎症性不规则口腔颌面部骨缺损方面显示出良好的潜力。