Journal of Prevention and Treatment for Stomatological Diseases ›› 2019, Vol. 27 ›› Issue (11): 739-744.DOI: 10.12016/j.issn.2096-1456.2019.11.010

• Review Articles • Previous Articles     Next Articles

Research progress of periodontitis and periodontal dysbiosis

GUO Xinwei,ZHAO Hongyan(),YANG Yaoyao,QIAN Xin,LING Xiaoxu,ZHANG Zhimin()   

  1. Department of Endodontics, Hospital of Stomatology, Jilin University, Changchun 130021, China
  • Received:2018-07-04 Revised:2019-09-14 Online:2019-11-20 Published:2019-12-03
  • Contact: Hongyan ZHAO,Zhimin ZHANG

牙周炎菌群失调研究进展

郭馨蔚,赵洪岩(),杨瑶瑶,钱鑫,凌晓旭,张志民()   

  1. 吉林大学口腔医院牙体牙髓科,吉林 长春(130021)
  • 通讯作者: 赵洪岩,张志民
  • 作者简介:郭馨蔚,在读硕士研究生,住院医师,Email:1255088144@qq.com
  • 基金资助:
    吉林省自然科学基金项目(20160101003JC)

Abstract:

In recent years, the etiology of periodontitis has tended to be based on the theory of flora imbalance. That is, periodontitis is not caused by specific bacteria but by the breakdown of the oral flora balance, which leads to an immune imbalance. Imbalanced bacterial flora cooperate with each other to produce virulent factors that destroy organism tissues and induce immune cells to produce abnormal levels of cytokines, causing greater damage. This article reviews the initiation of a flora imbalance, the interaction between bacteria, the immune damage of the host and the prevention and treatment of the flora imbalance. The literature review shows that peroxidase released by inflammatory reactions, host immune responses to pathogenic microorganisms and some systemic factors, such as diabetes, can trigger flora imbalance. As a result, ion transport, substance synthesis and metabolism of bacteria change; virulence factors increase; and the oral flora balance is disrupted. Red complex bacteria enter gingival epithelial cells, produce adhesin, and selectively inhibit the expression of specific chemokines, which is beneficial for other pathogenic bacteria to enter gingival epithelial cells. Toxicity factors increase throughout the body, directly destroying body tissues and inducing innate and adaptive immune responses, thus causing related immune damage. The dysbacteriosis model of periodontitis provides a new idea for the prevention and treatment of periodontitis, such as using biological factors, bacteriophages, probiotics and other methods to reduce the number of periodontal pathogens to restore the steady state of periodontal flora.

Key words: periodontitis, dysbiosis, bacterial interaction, gingival epithelial cells, immune response, periodontitis flora imbalance model, phagotherapy

摘要:

牙周炎的病因学说近年来趋向于菌群失调学说,即牙周炎不是由于某种特定细菌作用而成,而是由于口腔菌群平衡被打破,进而引起免疫失调。失衡的菌群间相互协同,产生毒力因子破坏机体组织,诱导免疫细胞产生异常增多的细胞因子,造成更大的损害。本文就菌群失调的启动、细菌间的相互作用、宿主的免疫损伤及菌群失调的防治进行综述。文献复习结果显示,机体由于炎症反应释放的过氧化物酶、宿主对病原微生物的免疫应答及一些系统性因素如糖尿病等可启动菌群失调,继而细菌的离子转运、物质合成代谢等功能会发生改变,毒力因子增强,口腔菌群平衡被打破。红色复合体细菌首先进入牙龈上皮细胞,产生黏附素,并选择性抑制特定趋化因子的表达,利于其他致病菌进入牙龈上皮细胞,整体毒力因子产生增多,直接破坏机体组织,并诱发机体固有免疫和适应性免疫反应,产生相关的免疫损伤。牙周炎菌群失调模型为牙周炎的防治提供了新思路,如采用生物因子、噬菌体、益生菌等方法降低牙周致病菌的数量,使牙周菌群恢复稳态。

关键词: 牙周炎, 菌群失调, 细菌间相互作用, 牙龈上皮细胞, 免疫应答, 牙周炎菌群失调模型, 噬菌体疗法

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