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牙周炎发病机制中的炎症介质。

Inflammatory mediators in the pathogenesis of periodontitis.

机构信息

Department of Dental Medicine, Division of Periodontology, Karolinska Institutet, SE-141 04 Huddinge, Sweden.

出版信息

Expert Rev Mol Med. 2013 Aug 5;15:e7. doi: 10.1017/erm.2013.8.

Abstract

Periodontitis is a chronic inflammatory condition of the periodontium involving interactions between bacterial products, numerous cell populations and inflammatory mediators. It is generally accepted that periodontitis is initiated by complex and diverse microbial biofilms which form on the teeth, i.e. dental plaque. Substances released from this biofilm such as lipopolysaccharides, antigens and other virulence factors, gain access to the gingival tissue and initiate an inflammatory and immune response, leading to the activation of host defence cells. As a result of cellular activation, inflammatory mediators, including cytokines, chemokines, arachidonic acid metabolites and proteolytic enzymes collectively contribute to tissue destruction and bone resorption. This review summarises recent studies on the pathogenesis of periodontitis, with the main focus on inflammatory mediators and their role in periodontal disease.

摘要

牙周炎是一种涉及细菌产物、多种细胞群和炎症介质相互作用的慢性炎症性疾病。人们普遍认为,牙周炎是由牙齿上形成的复杂多样的微生物生物膜(即牙菌斑)引发的。生物膜释放的物质,如脂多糖、抗原和其他毒力因子,进入牙龈组织并引发炎症和免疫反应,导致宿主防御细胞被激活。由于细胞激活,炎症介质,包括细胞因子、趋化因子、花生四烯酸代谢物和蛋白水解酶,共同导致组织破坏和骨质吸收。本文综述了牙周炎发病机制的最新研究进展,主要关注炎症介质及其在牙周病中的作用。

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