Periodontitis is an inflammatory disease caused by bacteria. The prolonged and repeated occurrence of this disease results from immune system disorders and leads to the destruction of surrounding tissues. Research on new antibacterial materials that can regulate autoimmunity and promote repair can effectively treat periodontal inflammation. Hence, metal–phenolic networks (MPNs) were loaded onto the surface of branched AuAg nanoparticles (NPs), denoted as AuAg@PC-Fe. The procyanidin (PC)-Fe network not only enhanced the photothermal properties of AuAg NPs to achieve effective photothermal antibacterial activity against periodontal pathogens but also alleviated oxidative stress and excessive inflammation. The mechanism of action is as follows: AuAg@PC-Fe promotes the polarisation of alternatively activated macrophages by activating the phosphoinositide 3-kinase/protein kinase B signaling pathway and upregulates nuclear factor erythroid 2-related factor 2, scavenging reactive oxygen species and subsequently inhibiting the nuclear factor kappa-B signaling pathway to regulate immunity. The ability of periodontal inflammatory tissue to repair was improved in vivo. This design provides new ideas for applying MPNs to photothermal therapy and immunotherapy. It presents a new therapeutic platform for treating periodontitis and other infectious diseases.

牙周炎是由细菌引起的炎症性疾病。这种疾病的长期和反复发生是由免疫系统紊乱引起的，并导致周围组织的破坏。研究调节自身免疫、促进修复的新型抗菌材料，可有效治疗牙周炎症。因此，金属-酚网络 (MPNs) 被加载到支链 AuAg 纳米粒子 (NPs) 的表面，表示为 AuAg@PC-Fe。原花青素 (PC)-Fe 网络不仅增强了 AuAg NPs 的光热性能，以实现对牙周病原体的有效光热抗菌活性，而且还减轻了氧化应激和过度炎症。作用机制如下：AuAg@PC-Fe 通过激活磷酸肌醇 3-激酶/蛋白激酶 B 信号通路促进交替激活的巨噬细胞的极化，并上调核因子红细胞 2 相关因子 2，清除活性氧并随后抑制核因子 kappa-B 信号调节免疫力的途径。体内牙周炎症组织修复能力得到提高。该设计为将 MPNs 应用于光热疗法和免疫疗法提供了新的思路。它为治疗牙周炎和其他感染性疾病提供了一个新的治疗平台。体内牙周炎症组织修复能力得到提高。该设计为将 MPNs 应用于光热疗法和免疫疗法提供了新的思路。它为治疗牙周炎和其他感染性疾病提供了一个新的治疗平台。体内牙周炎症组织修复能力得到提高。该设计为将 MPNs 应用于光热疗法和免疫疗法提供了新的思路。它为治疗牙周炎和其他感染性疾病提供了一个新的治疗平台。