State Key Laboratory of Oral Disease, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Department of Oral Implantology, Shanghai Ninth Peoples' Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, National Clinical Research Center for Oral Diseases, Shanghai Key Laboratory of Stomatology & Shanghai Research Institute of Stomatology, Shanghai, China.
J Histotechnol. 2023 Sep;46(3):139-150. doi: 10.1080/01478885.2023.2188705. Epub 2023 May 15.
Diabetes and periodontitis are prevalent diseases that considerably impact global economy and diabetes is a major risk factor of periodontitis. Mitochondrial dynamic alterations are involved in many diseases including diabetes and this study aims to evaluate their relevance with diabetes aggravated periodontitis. Sixty mice are randomly divided into 4 groups: control, periodontitis, diabetes and diabetic periodontitis. Periodontitis severity is evaluated by alveolar bone loss, inflammation and oxidative stress status. Mitochondrial structural and functional defects are evaluated by the mitochondrial fission/fusion events, mitochondrial reactive oxygen species (ROS) accumulation, complex activities and adenosine triphosphate (ATP) production. Advanced glycation end product (AGE) and are closely related to periodontitis occurrence and development. Human gingival fibroblast cells (HGF-1) are used to investigate the AGE role and lipopolysaccharide (LPS) from (P-LPS) in aggravating diabetic periodontitis by mitochondrial dynamic and function alterations. In vivo, diabetic mice with periodontitis show severe bone loss, increased inflammation and oxidative stress accumulation. Among mice with periodontitis, diabetic mice show worse mitochondrial dynamic perturbations than lean mice, along with fusion protein levels inducing more mitochondrial fission in gingival tissue. In vitro, AGEs and P-LPS co-treatment causes severe.
糖尿病和牙周炎是常见疾病，对全球经济有重大影响，而糖尿病是牙周炎的主要危险因素。线粒体动力学改变与包括糖尿病在内的许多疾病有关，本研究旨在评估其与糖尿病加重牙周炎的相关性。60 只小鼠随机分为 4 组：对照组、牙周炎组、糖尿病组和糖尿病牙周炎组。通过牙槽骨丧失、炎症和氧化应激状态来评估牙周炎的严重程度。通过线粒体分裂/融合事件、线粒体活性氧（ROS）积累、复合物活性和三磷酸腺苷（ATP）产生来评估线粒体结构和功能缺陷。晚期糖基化终产物（AGE）与牙周炎的发生和发展密切相关。人牙龈成纤维细胞（HGF-1）用于研究 AGE 的作用以及脂多糖（LPS）从（P-LPS）通过线粒体动力学和功能改变加重糖尿病牙周炎。在体内，患有牙周炎的糖尿病小鼠表现出严重的骨质流失、炎症增加和氧化应激积累。在患有牙周炎的小鼠中，糖尿病小鼠的线粒体动力学紊乱比瘦小鼠更严重，牙龈组织中融合蛋白水平诱导更多的线粒体裂变。在体外，AGEs 和 P-LPS 共同处理会导致严重的。
