牙周病与心血管疾病的相关性研究

近年来牙周病和心血管疾病的关系日益受到医学界的重视。根据现有的流行病学、分子生物学和动物实验证据表明,牙周病和心血管疾病有一定相关性,但不能证明二者的因果关系。牙周病可能是一个重要的危险因素,与先天遗传特性和传统危险因素相互作用,可导致心血管疾病。本文就其可能的相关机制和动物实验作一综述。     

牙周病与心血管疾病的相关性研究

近年来牙周病和心血管疾病的关系日益受到医学界的重视。根据现有的流行病学、分子生物学和动物实验证据表明，牙周病和心血管疾病有一定相关性，但不能证明二者的因果关系。牙周病可能是一个重要的危险因素，与先天遗传特性和传统危险因素相互作用，可导致心血管疾病。本文就其可能的相关机制和动物实验作一综述。     

牙周病与心血管疾病的相关性及其可能机制

近年来,牙周疾病与心血管疾病的关系逐渐受到人们的重视,大量研究表明牙周病可能是动脉粥样硬化的危险因素之一.本文就近年来有关牙周病与心血管疾病相关性的流行病学调查和可能的机制予以综述.     

牙周病与高脂血症关系的研究进展

牙周病和高脂血症都是影响人类健康的高发性慢性疾病。近年来的研究表明,牙周病与心血管疾病之间存在密切的联系,而心血管疾病特别是动脉粥样硬化的重要危险因素之一便是高脂血症。研究显示,牙周病和高脂血症二者之间存在紧密的双向关系。本文就牙周病与高脂血症的相关性、牙周病与高脂血症相互影响的生物学机制等做一综述。     

牙周病与冠心病的相关性研究

牙周病是一种常见的口腔慢性感染性疾病,是成年人牙齿缺失的主要原因之一,近年来的研究显示牙周病还是冠心病的一个重要危险因素。本文着重对这两种疾病相关的流行病学资料和可能机制进行综述。     

对氧磷酶与牙周炎相关性研究

研究发现对氧磷酶可以保护低密度脂蛋白的氧化。目前国内外对对氧磷酶的研究主要停留在对其与心血管疾病、糖尿病相关性的研究,其活性与基因多态性被认为是动脉粥样硬化、冠心病的独立危险因素,然而对对氧磷酶与牙周病的相关性研究较少。现就对氧磷酶的生物学特征与牙周病相关性进行综述。     

牙周病与冠心病的相关性研究

牙周病是一种常见的口腔慢性感染性疾病，是成年人牙齿缺失的主要原因之一。近年来的研究显示牙周病还是冠心病的一个重要危险因素。本文着重对这两种疾病相关的流行病学资料和可能机制进行综述。     

牙周病与心血管疾病

牙周炎是一种由微生物引起的慢性多因子炎症性疾病,以渐进性牙周支持组织破坏导致牙齿脱落为特征。牙周炎患者因长期存在大面积溃疡面的低度感染而被视为是心血管疾病的高危因素。现对牙周炎与心血管疾病之间相关性的可能机制及二者之间相关联的4个方面的研究证据做一阐述,并将美国牙周病学会和欧洲牙周病学会联盟对牙周炎与心血管疾病二者关系研讨后达成的最新共识提供给大家做参考。     

牙龈卟啉单胞菌与冠心病

牙周病是引起冠心病的危险因素之一,牙龈卟啉单胞菌是引起牙周病的主要致病菌,它可以侵入血管内膜导致血管壁增厚及释放内毒素,释放细胞因子促进血小板的聚集,血栓形成,从而导致心血管疾病的发生。     

牙龈卟啉单胞菌与冠心病之间的关系

牙龈卟啉单胞菌既是牙周病主要的可疑致病菌，亦是冠心病潜在的危险因素，因此牙周病是否为引起冠心病的危险因素之一引起了诸多研究者的兴趣。本文就牙龈卟啉单胞菌，牙龈卟啉单胞菌可能引起冠心病的致病过程和机制等研究进展作一综述。     

怀化地区侗族和汉族冠心病伴牙周炎的危险因素研究

目的：调查怀化地区侗族、汉族冠心病患者的牙周状况,并对其危险因素进行单因素和多因素分析。方法：采用随机整群抽样的方法选择2012年1月～2012年12月怀化地区通道县、麻阳县和溆浦县人民医院明确诊断为冠心病患者246人作为研究对象,采用SOSERVER2000软件建立数据库,分别对性别、年龄、吸烟、饮酒、口腔卫生习惯和民族等与冠心病伴牙厨炎的相关性进行单因素和多因素分析。结果：冠心病伴牙周炎总患病率为54．2％,单因素分析结果显示年龄、吸烟、口腔卫生习惯和民族是冠心病伴牙周炎的危险因素（OR值分别为2．30、1．65、3．67、2．06,P〈O．05）。以民族分层进行多因素分析结果显示,吸烟和口腔卫生习惯（OR值分别为2．03、1．60,P〈O．05）为侗族冠心病伴牙周炎的危险因素,同时,吸烟也是汉族冠心病伴牙周炎的危险因素（OR=1．69,P〈O．05）。结论：冠心病伴牙周炎的危险因素较多,不同民族之间存在一定的差异,吸烟和口腔卫生不良可增加怀化地区侗族冠心病并发牙周炎的风险。     

牙周炎与冠心病相关性的研究进展

大量的研究表明,牙周炎与冠心病存在一定的相关性.牙周炎对冠心病的影响,可能是通过牙周细菌直接激发冠状动脉粥样硬化或影响冠心病的危险因素来实现的.下面就近年来牙周炎与冠心病相关性的流行病学研究进展,可能相关的发病机制以及在临床实践中对冠心病的预防作一综述.     

Does dental disease hurt your heart?

Recent research has yielded conflicting data regarding the relationship between dental disease, particularly periodontitis, and cardiovascular disease. A causative relationship would have major ramifications for health care. There is a plausible theoretical basis for such a link, as increased levels of inflammatory mediators may increase the risk of atherosclerotic plaque formation. Nevertheless, a clinical confirmation of a causative relationship has been difficult, in part because cardiovascular disease and periodontal disease share common risk factors such as increasing age and tobacco use, and because cardiovascular medications may increase the risk of periodontitis. Patients should be encouraged to control documented risk factors for cardiovascular disease and to maintain oral health for its well-known health benefits.     

Periodontal diseases and association with atherosclerotic disease

Cardiovascular diseases still account for the majority of deaths worldwide, although significant improvements in survival, after being affected by cardiovascular disease, have been achieved in the last decades. Periodontal diseases are also a common global burden. Several studies have shown a link between cardiovascular disease and periodontitis, although evidence is still lacking regarding the direct cause-effect relation. During the 2012 “Periodontitis and systemic diseases” workshop, the available evidence on the association between cardiovascular and periodontal diseases was discussed, covering biologic plausibility and clinical studies. The objective of the present narrative review was to update the previous reviews presented at the 2012 workshop, following similar methodological approaches, aiming to critically assess the available evidence. With regard to biologic plausibility, two aspects were reviewed: (a) for microbiologic mechanisms, assessing periodontal bacteria as a contributing factor to atherosclerosis based on seven “proofs,” substantial evidence was found for Proofs 1 through 6, but not for Proof 7 (periodontal bacteria obtained from human atheromas can cause atherosclerosis in animal models), concluding that periodontal pathogens can contribute to atherosclerosis; (b) mechanistic studies, addressing five different inflammatory pathways that could explain the links between periodontitis and cardiovascular disease with the addition of some extra pathways , suggest an association between both entities, based on the presence of higher levels of these inflammatory markers in patients with periodontitis and cardiovascular disease, vs healthy controls, as well as on the evidence that periodontal treatment reduces serum levels of these mediators. When evidence from clinical studies was analyzed, two aspects were covered: (a) epidemiologic studies support the estimation that the incidence of atherosclerotic disease is higher in individuals with periodontitis than in individuals with no reported periodontitis, irrespective of many common risk factors, but with a substantial variability in the definitions used in reporting of exposure to periodontal diseases in different studies; (b) intervention trials have shown that periodontal therapy can reduce serum inflammatory mediators, improve the lipids profile, and induce positive changes in other cardiovascular disease surrogate measures, but no evidence is available to support that adequate periodontal therapy is able to reduce the risk for cardiovascular diseases, or the incidence of cardiovascular disease events in periodontitis patients.     

Relationship between periodontitis and cardiovascular diseases: A literature review

Periodontitis and cardiovascular disease have a complex etiology and genetics and share some common risk factors (i.e., smoking, age, diabetes, etc.). In recent years, the relationship between periodontal disease and cardiovascular disease has been investigated extensively. This research mostly focused on the fact that periodontitis is an independent risk factor for cardiovascular disease. Our aim in this article is to investigate the etiological relationship between periodontal disease and cardiovascular disease and the mechanisms involved in this association. According to the current literature, it is concluded that there is a strong relationship between these chronic disorders.     

牙周炎和前列腺疾病相关性研究现状

牙周炎是常见的口腔炎症性疾病,有大量文献报告牙周炎与全身系统性疾病存在密切联系,如心血管疾病、2型糖尿病、早产低出生体重儿等.牙周炎与前列腺疾病有相似的风险因素,年龄、吸烟、肥胖和糖尿病以及炎症的刺激对疾病有显著影响.该文主要对牙周炎和前列腺疾病的相关性的研究情况,共同的影响因素,以及相关的生物学机制等进行综述.     

Interleukin-1 genotypes and the association between periodontitis and cardiovascular disease

An epidemiological association between periodontitis and cardiovascular disease has been reported in multiple studies. Various mechanisms have been proposed as potential explanations for this association, including a common factor that predisposes certain individuals to a hyper-responsive inflammatory response. Variations in the genes that regulate the interleukin-1 (IL-1) response have been associated with both periodontal disease and cardiovascular disease. New data indicate that one pattern of IL-1 genetic polymorphisms, characterized by the IL-1A (+4845) and IL-1B (+3954) markers, is associated with periodontitis but not certain measures of atherosclerosis. Another IL-1 genetic pattern, characterized by the IL-1B (-511) and IL-1RN (+2018) markers, is associated with atherosclerotic plaque formation, as measured by angiography and arterial wall thickness, but not periodontitis. These two patterns also have different functional implications relative to IL-1 biological activity. Studies of IL-1 gene polymorphisms, atherosclerotic plaque instability and cardiovascular clinical events are in progress. Hypothetical models are presented to explain how IL-1 genetic factors may be involved in cardiovascular disease.     

牙周炎与高血压关系的研究进展

高血压是与遗传和环境因素有关的最常见的一种心血管疾病。牙周炎是发生在牙齿支持组织(牙龈、牙周膜、牙槽骨)的一种破坏性疾病。研究表明:高血压与牙周炎之间相互关联,牙周炎增加高血压病的患病率,高血压亦增加牙周炎的发病风险和严重程度。但是,两者相互作用的机制尚未完全明确,炎症可能是2种疾病的中介,共同的危险因素促进2种疾病的同时发生发展。本文主要就牙周炎与高血压相关性及其相互作用机制进行综述。     

Are cardiac transplant patients more likely to have periodontitis? A case record study

In several large epidemiological studies chronic periodontitis has been implicated as an additional risk factor, independent of other risk factors, for the development of ischaemic heart disease. The underlying mechanism is thought to be a localised infection giving rise to an inflammatory host response, and some experimental data agree with this hypothesis. Recently, however, some studies have questioned the post dated relationship between the two diseases. The current case-record study was undertaken to evaluate the prevalence of chronic periodontitis and the severity of such periodontal disease in a heart transplant population, assuming the latter represented a relatively severely compromised cardiovascular patient population. The study demonstrated that 76% of the patients had various degrees of periodontal disease prior to undergoing a heart transplant. Thus, it is possible that a relationship between cardiovascular disease and periodontal disease exists, but further, large intervention studies will be needed to confirm such a conclusion.     

Periodontal manifestations of systemic disease

Periodontitis is a chronic bacterial infection of the supporting structures of the teeth. The host response to infection is an important factor in determining the extent and severity of periodontal disease. Systemic factors modify periodontitis principally through their effects on the normal immune and inflammatory mechanisms. Several conditions may give rise to an increased prevalence, incidence or severity of gingivitis and periodontitis. The effects of a significant number of systemic diseases upon periodontitis are unclear and often it is difficult to causally link such diseases to periodontitis. In many cases the literature is insufficient to make definite statements on links between certain systemic factors and periodontitis and for several conditions only case reports exist whereas in other areas an extensive literature is present. A reduction in number or function of polymorphonuclear leukocytes (PMNs) can result in an increased rate and severity of periodontal destruction. Medications such as phenytoin, nifedipine, and cyclosporin predispose to gingival overgrowth in response to plaque and changes in hormone levels may increase severity of plaque-induced gingival inflammation. Immuno-suppressive drug therapy and any disease resulting in suppression of the normal inflammatory and immune mechanisms (such as HIV infection) may predispose the individual to periodontal destruction. There is convincing evidence that smoking has a detrimental effect on periodontal health. The histiocytoses diseases may present as necrotizing ulcerative periodontitis and numerous genetic polymorphisms relevant to inflammatory and immune processes are being evaluated as modifying factors in periodontal disease. Periodontitis severity and prevalence are increased in diabetics and worse in poorly controlled diabetics. Periodontitis may exacerbate diabetes by decreasing glycaemic control. This indicates a degree of synergism between the two diseases. The relative risk of cardiovascular disease is doubled in subjects with periodontal disease. Periodontal and cardiovascular disease share many common risk and socio-economic factors, particularly smoking, which is a powerful risk factor for both diseases. The actual underlying aetiology of both diseases is complex as are the potential mechanisms whereby the diseases may be causally linked. It is thought that the chronic inflammatory and microbial burden in periodontal disease may predispose to cardiovascular disease in ways proposed for other infections such as with Chlamydia pneumoniae. To move from the current association status of both diseases to causality requires much additional evidence. Determining the role a systemic disease plays in the pathogenesis of periodontal disease is very difficult as several obstacles affect the design of the necessary studies. Control groups need to be carefully matched in respect of age, gender, oral hygiene and socio-economic status. Many studies, particularly before the aetiological importance of dental plaque was recognised, failed to include such controls. Longitudinal studies spanning several years are preferable in individuals both with and without systemic disease, due to the time period in which periodontitis will develop.