Cardiovascular and oral disease interactions: what is the evidence?
Cardiovascular and oral disease interactions: what is the evidence?
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DOI：
10.1308/135576107780556806
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发表时间：
2007-04-01
期刊：
影响因子：
--
通讯作者：
Seymour, Gregory J
中科院分区：
文献类型：
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作者：
Ford, Pauline J;Yamazaki, Kazuhisa;Seymour, Gregory J
本文回顾了口腔疾病（更具体地说，牙周感染）与心血管疾病相互作用的证据。心血管疾病是全世界死亡的主要原因，其中动脉粥样硬化是绝大多数病例的根本病因。感染和炎症在动脉粥样硬化中的作用的重要性现已被广泛接受，并且人们越来越认识到免疫反应是动脉粥样硬化形成的核心。慢性炎症性牙周病是最常见的慢性感染之一，许多研究表明牙周病与中风和冠心病风险增加之间存在关联。尽管人们认识到需要大规模的干预研究，但仍然需要进行致病机制研究以建立生物学原理。在此背景下，提出了一些假设；这些包括常见的易感性、循环细胞因子和炎症介质增加引起的炎症、血管的直接感染以及细菌和自身抗原之间交叉反应或分子模拟的可能性。在后一种假设中，动脉粥样硬化的进展可以用对细菌热休克蛋白（HSP）的免疫反应来解释。由于免疫系统可能无法区分自身 HSP 和细菌 HSP，因此宿主针对致病性 HSP 产生的免疫反应可能会导致对宿主中相似序列的自身免疫反应。此外，动脉粥样硬化中内皮细胞表达HSP，动脉粥样硬化患者的动脉和外周血中存在交叉反应性T细胞。这些假设中的每一个都根据当前的研究进行了审查。结论是，虽然动脉粥样硬化性心血管疾病几乎肯定是一种多因素疾病，但现在有强有力的证据表明感染和炎症是重要的危险因素。由于口腔是潜在的感染源之一，因此明智的做法是尽量确保最大限度地减少任何口腔疾病。这可能对心血管健康有显着益处，并使口腔健康团队的成员能够为患者的整体健康做出贡献。
This paper reviews the evidence for the interaction of oral disease (more specifically, periodontal infections) with cardiovascular disease. Cardiovascular disease is a major cause of death worldwide, with atherosclerosis as the underlying aetiology in the vast majority of cases. The importance of the role of infection and inflammation in atherosclerosis is now widely accepted, and there has been increasing awareness that immune responses are central to atherogenesis. Chronic inflammatory periodontal diseases are among the most common chronic infections, and a number of studies have shown an association between periodontal disease and an increased risk of stroke and coronary heart disease. Although it is recognised that large-scale intervention studies are required, pathogenic mechanism studies are nevertheless required so as to establish the biological rationale. In this context, a number of hypotheses have been put forward; these include common susceptibility, inflammation via increased circulating cytokines and inflammatory mediators, direct infection of the blood vessels, and the possibility of cross-reactivity or molecular mimicry between bacterial and self-antigens. In this latter hypothesis, the progression of atherosclerosis can be explained in terms of the immune response to bacterial heat shock proteins (HSPs). Because the immune system may not be able to differentiate between self-HSP and bacterial HSP, an immune response generated by the host directed at pathogenic HSP may result in an autoimmune response to similar sequences in the host. Furthermore, endothelial cells express HSPs in atherosclerosis, and cross-reactive T cells exist in the arteries and peripheral blood of patients with atherosclerosis. Each of these hypotheses is reviewed in light of current research. It is concluded that although atherosclerotic cardiovascular disease is almost certainly a multifactorial disease, there is now strong evidence that infection and inflammation are important risk factors. As the oral cavity is one potential source of infection, it is wise to try to ensure that any oral disease is minimised. This may be of significant benefit to cardiovascular health and enables members of the oral health team to contribute to their patients' general health.