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糖尿病与牙周炎的主要交汇点为细胞内紊乱。

Diabetes Mellitus and Periodontitis Share Intracellular Disorders as the Main Meeting Point.

机构信息

Department of Periodontology, Dental School, University of Seville, C/Avicena, s/n, 41009 Seville, Spain.

Biomedical Research Center (CIBM), Department of Physiology, University Campus of Cartuja, Institute of Nutrition and Food Technology "José Mataix Verdú", University of Granada, 18071 Granada, Spain.

出版信息

Cells. 2021 Sep 13;10(9):2411. doi: 10.3390/cells10092411.

DOI:10.3390/cells10092411
PMID:34572060
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8467361/
Abstract

Diabetes and periodontitis are two of the most prevalent diseases worldwide that negatively impact the quality of life of the individual suffering from them. They are part of the chronic inflammatory disease group or, as recently mentioned, non-communicable diseases, with inflammation being the meeting point among them. Inflammation hitherto includes vascular and tissue changes, but new technologies provide data at the intracellular level that could explain how the cells respond to the aggression more clearly. This review aims to emphasize the molecular pathophysiological mechanisms in patients with type 2 diabetes mellitus and periodontitis, which are marked by different impaired central regulators including mitochondrial dysfunction, impaired immune system and autophagy pathways, oxidative stress, and the crosstalk between adenosine monophosphate-activated protein kinase (AMPK) and the renin-angiotensin system (RAS). All of them are the shared background behind both diseases that could explain its relationship. These should be taken in consideration if we would like to improve the treatment outcomes. Currently, the main treatment strategies in diabetes try to reduce glycemia index as the most important aspect, and in periodontitis try to reduce the presence of oral bacteria. We propose to add to the therapeutic guidelines the handling of all the intracellular disorders to try to obtain better treatment success.

摘要

糖尿病和牙周炎是全球最常见的两种疾病,它们会降低患者的生活质量。它们属于慢性炎症性疾病群,或者如最近所提到的,非传染性疾病,炎症是它们的共同特征。炎症包括血管和组织的变化,但新技术提供了细胞内水平的数据,可以更清楚地解释细胞如何对攻击做出反应。本综述旨在强调 2 型糖尿病和牙周炎患者的分子病理生理学机制,其特点是不同的中央调节受损,包括线粒体功能障碍、免疫系统和自噬途径受损、氧化应激以及单磷酸腺苷激活蛋白激酶 (AMPK) 和肾素-血管紧张素系统 (RAS) 之间的串扰。所有这些都是这两种疾病背后的共同背景,可以解释它们之间的关系。如果我们想要改善治疗效果,就应该考虑到这些因素。目前,糖尿病的主要治疗策略是降低血糖指数,作为最重要的方面,而在牙周炎中,则试图减少口腔细菌的存在。我们建议在治疗指南中增加处理所有细胞内紊乱的内容,以尝试获得更好的治疗效果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d3b/8467361/c263e63631a0/cells-10-02411-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d3b/8467361/776a8c8669bf/cells-10-02411-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d3b/8467361/f83eb2f1435b/cells-10-02411-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d3b/8467361/f3f1b8a3e05c/cells-10-02411-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d3b/8467361/c263e63631a0/cells-10-02411-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d3b/8467361/776a8c8669bf/cells-10-02411-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d3b/8467361/f83eb2f1435b/cells-10-02411-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d3b/8467361/f3f1b8a3e05c/cells-10-02411-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d3b/8467361/c263e63631a0/cells-10-02411-g004.jpg

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Diabetes fuels periodontal lesions via GLUT1-driven macrophage inflammaging.糖尿病通过 GLUT1 驱动的巨噬细胞衰老引发牙周病损。
Int J Oral Sci. 2021 Mar 24;13(1):11. doi: 10.1038/s41368-021-00116-6.
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Association of mitochondrial DNA copy number with metabolic syndrome and type 2 diabetes in 14 176 individuals.
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J Inflamm Res. 2025 Jul 2;18:8689-8704. doi: 10.2147/JIR.S521430. eCollection 2025.
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Antioxidants (Basel). 2025 Jun 13;14(6):725. doi: 10.3390/antiox14060725.
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