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线粒体功能障碍与糖尿病加重牙周炎有关。

Mitochondrial dysfunction is involved in the aggravation of periodontitis by diabetes.

机构信息

Department of Periodontology, School and Hospital of Stomatology, Wenzhou Medical University, Wenzhou, China.

Institute of Stomatology, School and Hospital of Stomatology, Wenzhou Medical University, Wenzhou, China.

出版信息

J Clin Periodontol. 2017 May;44(5):463-471. doi: 10.1111/jcpe.12711. Epub 2017 Apr 12.

DOI:10.1111/jcpe.12711
PMID:28207937
Abstract

AIM

To elucidate whether mitochondrial dysfunction contributes to aggravated periodontitis in diabetes.

MATERIALS AND METHODS

Sixty-four wistar rats were randomly assigned into four groups: control, periodontitis, diabetes, and diabetic periodontitis. Two weeks after induction of diabetes, periodontitis was induced by silk ligation for 2 weeks and thereafter evaluated by assessing alveolar bone loss and apoptosis of periodontium cells. Mitochondrial oxidative stress was detected by MitoSOX staining. Mitochondrial function was determined by measuring ATP production, and by assessing mitochondrial DNA copy number, activities of electron transport chain complexes, and biogenesis with real-time PCR.

RESULTS

Significantly severer bone loss, enhanced periodontium cell apoptosis, and mitochondrial oxidative stress were found in the rats with diabetic periodontitis than the others. Furthermore, diabetic rats with periodontitis presented severer mitochondrial dysfunction than lean rats with periodontitis, as reflected by compromised ATP production, decreased mitochondrial DNA copy number, reduced gene expression of electron transport chain complex I subunits, and impaired mitochondrial biogenesis (p < 0.05). Multiple regression analysis further indicated a close correlation between these mitochondrial events and bone loss in diabetic periodontitis.

CONCLUSIONS

Mitochondrial dysfunction was positive correlated to aggravated periodontitis in diabetes and might represent a therapeutic target for diabetic periodontitis.

摘要

目的

阐明线粒体功能障碍是否导致糖尿病加重牙周炎。

材料和方法

64 只 wistar 大鼠随机分为四组:对照组、牙周炎组、糖尿病组和糖尿病牙周炎组。糖尿病诱导 2 周后,通过丝线结扎诱导牙周炎 2 周,并通过评估牙槽骨丧失和牙周细胞凋亡来评估。通过 MitoSOX 染色检测线粒体氧化应激。通过测量 ATP 产生、评估线粒体 DNA 拷贝数、电子传递链复合物的活性和实时 PCR 评估线粒体生物发生来确定线粒体功能。

结果

糖尿病牙周炎大鼠的骨丢失明显加重,牙周细胞凋亡增加,线粒体氧化应激增强。此外,与单纯牙周炎的瘦大鼠相比,患有糖尿病和牙周炎的大鼠的线粒体功能障碍更为严重,表现为 ATP 产生减少、线粒体 DNA 拷贝数降低、电子传递链复合物 I 亚基的基因表达减少以及线粒体生物发生受损(p<0.05)。多元回归分析进一步表明,这些线粒体事件与糖尿病牙周炎的骨丢失密切相关。

结论

线粒体功能障碍与糖尿病加重的牙周炎呈正相关,可能成为糖尿病牙周炎的治疗靶点。

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