Role of reactive oxygen species and antioxidants in periodontal disease

Q3 Biochemistry, Genetics and Molecular Biology
H. Saluja, Shivani Sachdeva, Amit Mani
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引用次数: 1

Abstract

Recent epidemiological studies reveal that more than two-third of the world’s population suffers from one of the chronic forms of periodontal disease. The primary etiological agent of this inflammatory disease is a polymicrobial complex, predominantly Gram negative anaerobic or facultative bacteria within the sub-gingival biofilm. These bacterial species initiate the production of various cytokines such as interleukin-8 and TNF-α, further causing an increase in number and activity of polymorphonucleocytes (PMN) along with these cytokines, PMNs also produce reactive oxygen species (ROS) superoxide via the respiratory burst mechanism as the part of the defence response to infection. ROS just like the interleukins have deleterious effects on tissue cells when produced in excess. To counter the harmful effects of ROS, human body has its own defence mechanisms to eliminate them as soon as they are formed. The aim of this review is to focus on the role of different free radicals, ROS, and antioxidants in the pathophysiology of periodontal tissue destruction.
活性氧和抗氧化剂在牙周病中的作用
最近的流行病学研究表明,世界上超过三分之二的人口患有一种慢性牙周病。这种炎症性疾病的主要病原体是一种多微生物复合物,主要是牙龈下生物膜内的革兰氏阴性厌氧或兼性细菌。这些细菌启动了各种细胞因子的产生,如白细胞介素-8和TNF-α,进一步导致多形核细胞(PMN)的数量和活性增加,同时这些细胞因子也通过呼吸爆发机制产生活性氧(ROS)超氧化物,作为对感染的防御反应的一部分。ROS就像白细胞介素一样,当过量产生时,对组织细胞有有害影响。为了对抗ROS的有害影响,人体有自己的防御机制,一旦ROS形成,就会将其清除。这篇综述的目的是关注不同自由基、ROS和抗氧化剂在牙周组织破坏的病理生理学中的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Journal of Cellular Biotechnology
Journal of Cellular Biotechnology Biochemistry, Genetics and Molecular Biology-Biotechnology
CiteScore
0.70
自引率
0.00%
发文量
13
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