Department of Prosthodontics, School and Hospital of Stomatology, Tianjin Medical University, Tianjin, 300070, China; Department of Genetics, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.
Department of Genetics, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.
Biochem Biophys Res Commun. 2022 Jul 23;614:22-28. doi: 10.1016/j.bbrc.2022.04.039. Epub 2022 May 5.
Periodontitis, one of the most common oral complications of diabetes mellitus (DM), causes a reduction in alveolar bone height and loss of alveolar bone mass. It has been shown that DM aggravates the progression of periodontitis, but the mechanism remains inconclusive. The hyperglycemic environment of DM has been proven to generate reactive oxygen species (ROS). Since telomeres, guanine-rich repeats, are highly susceptible to oxidative attack, we speculate that the excessive accumulation of ROS in DM could induce telomere damage resulting in dysfunction of periodontal ligament cells, especially periodontal ligament stem cells (PDLSCs), which reduces the ability of tissue repair and reconstruction in diabetic periodontitis. In this study, our current data revealed that oxidative telomere damage occurred in the periodontal ligaments of diabetic mice. And Micro-CT scans showed reduced alveolar bone height and impaired alveolar bone mass in a diabetic periodontitis model. Next, cultured mouse PDLSCs (mPDLSCs) were treated with the oxidant tert-butyl hydroperoxide (t-BHP) in vitro, as we expected telomere damage was observed and resulted in cellular senescence and dysfunction. Taken together, oxidative stress in DM causes telomere dysfunction and PDLSCs senescence, which influences periodontal bone tissue regeneration and reconstruction and ultimately exacerbates bone loss in periodontitis.
牙周炎是糖尿病（DM）最常见的口腔并发症之一，会导致牙槽骨高度降低和牙槽骨量丧失。研究表明，DM 会加重牙周炎的进展，但具体机制尚不清楚。DM 的高血糖环境已被证明会产生活性氧（ROS）。由于富含鸟嘌呤的端粒对氧化攻击非常敏感，我们推测 DM 中过多的 ROS 积累可能会导致端粒损伤，从而导致牙周韧带细胞（尤其是牙周韧带干细胞 [PDLSCs]）功能障碍，这会降低糖尿病性牙周炎组织修复和重建的能力。在这项研究中，我们目前的数据显示，糖尿病小鼠的牙周韧带中存在氧化端粒损伤。Micro-CT 扫描显示，糖尿病牙周炎模型中的牙槽骨高度降低，牙槽骨量受损。接下来，我们在体外用氧化剂叔丁基过氧化物（t-BHP）处理培养的小鼠牙周韧带干细胞（mPDLSCs），正如我们所预期的那样，观察到端粒损伤导致细胞衰老和功能障碍。综上所述，DM 中的氧化应激导致端粒功能障碍和 PDLSCs 衰老，从而影响牙周骨组织的再生和重建，最终导致牙周炎中的骨丢失加剧。
