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牙周疾病的病理生物学可能影响全身疾病:一种范式的转变。

The pathobiology of periodontal diseases may affect systemic diseases: inversion of a paradigm.

作者信息

Page R C

机构信息

Department of Periodontics, School of Medicine, University of Washington, Seattle, USA.

出版信息

Ann Periodontol. 1998 Jul;3(1):108-20. doi: 10.1902/annals.1998.3.1.108.

DOI:10.1902/annals.1998.3.1.108
PMID:9722695
Abstract

A new paradigm for the pathobiology of periodontitis is presented, and the manner in which periodontitis may relate to susceptibility for certain systemic diseases such as cardiovascular disease and preterm labor is described. Periodontitis is caused by a small group of Gram-negative bacteria present on the tooth root surfaces as bioffilms. Lipopolysaccharide (LPS) and other substances gain access to the gingival tissues, initiate and perpetuate immunoinflammation, resulting in production of high levels of proinflammatory cytokines. These induce production of matrix metalloproteinases which destroy the connective tissues of the gingiva and periodontal ligament, and prostaglandins which mediate alveolar bone destruction. Periodontitis may enhance susceptibility to systemic diseases in several ways. LPS and viable Gram-negative bacteria from the biofilms and proinflammatory cytokines from the inflamed periodontal tissues may enter the circulation in pathogenic quantities. In addition, periodontitis and certain systemic diseases, such as cardiovascular disease, share risk factors including tobacco smoking, male gender, race/ethnicity, stress, and aging.

摘要

本文提出了一种牙周炎病理生物学的新范式,并描述了牙周炎与某些全身性疾病(如心血管疾病和早产)易感性之间的关联方式。牙周炎是由一小群以生物膜形式存在于牙根表面的革兰氏阴性菌引起的。脂多糖(LPS)和其他物质进入牙龈组织,引发并持续免疫炎症,导致产生高水平的促炎细胞因子。这些因子诱导基质金属蛋白酶的产生,破坏牙龈和牙周韧带的结缔组织,以及介导牙槽骨破坏的前列腺素。牙周炎可能通过多种方式增强对全身性疾病的易感性。生物膜中的LPS和活的革兰氏阴性菌以及发炎牙周组织中的促炎细胞因子可能以致病量进入循环。此外,牙周炎和某些全身性疾病,如心血管疾病,有共同的风险因素,包括吸烟、男性、种族/族裔、压力和衰老。

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