Diabetes-associated periodontitis (DP) aggravates diabetic complications and increases mortality from diabetes. DP is caused by diabetes-enhanced host immune-inflammatory responses to bacterial insult. In this study, we found that persistently elevated CCL2 levels in combination with proinflammatory monocyte infiltration of periodontal tissues were closely related to DP. Moreover, inhibition of CCL2 by oral administration of bindarit reduced alveolar bone loss and increased periodontal epithelial thickness by suppressing periodontal inflammation. Furthermore, bindarit suppressed the infiltration of proinflammatory monocytes and altered the inflammatory properties of macrophages in the diabetic periodontium. This finding provides a basis for the development of an effective therapeutic approach for treating DP.

糖尿病相关牙周炎 (DP) 会加重糖尿病并发症并增加糖尿病死亡率。DP 是由糖尿病增强的宿主对细菌损伤的免疫炎症反应引起的。在这项研究中，我们发现持续升高的 CCL2 水平与牙周组织的促炎性单核细胞浸润与 DP 密切相关。此外，通过口服 bindarit 抑制 CCL2 可减少牙槽骨丢失并通过抑制牙周炎症增加牙周上皮厚度。此外，bindarit 抑制促炎性单核细胞的浸润并改变糖尿病牙周组织中巨噬细胞的炎症特性。这一发现为开发治疗 DP 的有效治疗方法提供了基础。