慢性牙周炎的氧化应激

Parveen Dahiya, Reet Kamal, R. Gupta, A. Puri
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引用次数: 4

摘要

文献表明,牙周病的主要病原是一种多微生物复合物,主要是龈下生物膜内的革兰氏阴性厌氧或兼性细菌。这些细菌触发细胞因子的释放,导致多形核细胞(pmn)的数量和活性升高。作为细菌抗原刺激的结果,PMNs通过呼吸爆发产生活性氧(ROS)超氧化物,作为宿主对感染反应的一部分。人体确实含有一系列抗氧化防御机制,可以在有害活性氧形成时立即清除它们,并防止它们的有害影响。这篇综述主要集中在活性氧和抗氧化防御系统在牙周炎病理生物学中的作用,以期确定未来宿主调节疗法的特定治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Oxidative stress in chronic periodontitis
It is well documented that the primary etiological agent of periodontal disease is a polymicrobial complex, predominantly gram-negative anaerobic or facultative bacteria within the subgingival biofilm. These bacteria trigger the release of numbers of cytokines, leading to elevated numbers and activity of polymorphonucleocytes (PMNs). As a result of stimulation by bacterial antigens, PMNs produce the reactive oxygen species (ROS) superoxide via the respiratory burst as part of the host response to infection. The human body does contain an array of antioxidant defence mechanisms to remove harmful ROS as soon as they are formed and to prevent their deleterious effects. This review focuses predominantly on the role of ROS and antioxidant defence systems in the pathobiology of periodontitis, with a view to identify specific therapeutic targets for future host-modulating therapies.
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