Van Dyke T E, Serhan C N
Department of Periodontology and Oral Biology, Boston University, Goldman School of Dental Medicine, 100 East Newton Street, Boston, MA 02118, USA.
J Dent Res. 2003 Feb;82(2):82-90. doi: 10.1177/154405910308200202.
The periodontal diseases are infectious diseases caused by predominantly Gram-negative bacteria. However, as our understanding of the pathogenesis of the periodontal diseases grows, it is becoming clear that most of the tissue damage that characterizes periodontal disease is caused by the host response to infection, not by the infectious agent directly. Investigation into the mechanism of action of host-mediated tissue injury has revealed that the neutrophil plays an important role in destruction of host tissues. In this paper, we review the biochemical pathways and molecular mediators that are responsible for regulation of the inflammatory response in diseases such as periodontitis, with a focus on lipid mediators of inflammation. Pro-inflammatory mediators, such as prostaglandins and leukotrienes, are balanced by counter-regulatory signals provided by a class of molecules called lipoxins. The role of lipoxins in the control and resolution of inflammation is discussed, as is the possibility of the development of new therapeutic strategies for the control and prevention of neutrophil-mediated tissue injury in inflammatory diseases like periodontitis.
牙周疾病是主要由革兰氏阴性菌引起的感染性疾病。然而,随着我们对牙周疾病发病机制的认识不断深入,越来越清楚的是,构成牙周疾病特征的大多数组织损伤是由宿主对感染的反应引起的,而非直接由感染因子导致。对宿主介导的组织损伤作用机制的研究表明,中性粒细胞在破坏宿主组织中发挥着重要作用。在本文中,我们综述了负责调节诸如牙周炎等疾病中炎症反应的生化途径和分子介质,重点关注炎症的脂质介质。促炎介质,如前列腺素和白三烯,由一类称为脂氧素的分子提供的反调节信号来平衡。本文讨论了脂氧素在控制和消退炎症中的作用,以及开发新治疗策略以控制和预防诸如牙周炎等炎症性疾病中中性粒细胞介导的组织损伤的可能性。