牙周致病菌在动脉粥样硬化发生发展中的作用研究

牙周炎与全身健康特别是心血管疾病关系密切,牙周致病菌积极参与了动脉粥样硬化的形成与发展。目前已有研究证据表明,牙周致病菌感染是心血管事件的独立危险因素,其通过多种免疫炎症以及代谢相关分子机制促进动脉粥样硬化病变的发生发展。本文从牙周炎及牙周致病菌与心血管疾病的相关性、牙周致病菌影响动脉粥样硬化的机制等方面,对这一主题进...     

牙龈卟啉单胞菌与动脉粥样硬化发病的关系

慢性牙周炎是心血管疾病特别是冠心病的危险因素之一,然而其相关的生物学基础目前尚不清楚.笔者下面就与慢性牙周炎关系最为密切的牙龈卟啉单胞菌与动脉粥样硬化的相关性和牙龈卟啉单胞菌致动脉粥样硬化的可能机制以及Toll样受体在牙龈卟啉单胞菌与动脉粥样硬化相关性中的作用作一综述.     

牙周炎与代谢综合征关系的研究进展

代谢综合征是一组以腹型肥胖、胰岛素抵抗、高血压、致动脉粥样硬化性血脂异常为主要表现的临床综合征, 是心血管疾病和糖尿病的危险因素。牙周炎是由菌斑微生物引起的慢性炎症性疾病, 与心脏病、糖尿病、慢性呼吸系统疾病等非传染性疾病具有共同的危险因素。多项横断面研究表明牙周炎与代谢综合征之间存在不同程度的关联, 个体患牙周炎的概率随着代谢综合征组分数量的增加而增加, 但二者的因果关系尚不明确。本文主要对牙周炎和代谢综合征主要组分之间的关系及相关机制进行综述, 为代谢综合征及牙周炎的防治提供新的依据。     

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.     

牙龈卟啉单胞菌促进心血管疾病的研究进展

慢性牙周炎和心血管疾病为当今社会两大常见的慢性炎症性疾病,受多种危险因素影响.流行病学调查发现,慢性牙周炎与心血管疾病风险增加密切相关.慢性牙周炎患者龈沟内的牙龈卟啉单胞菌可以通过血液和吞噬细胞介导途径侵入心血管组织,分泌毒力因子.通过引发内毒素血症、内皮功能障碍、氧化应激、泡沫细胞形成与脂质蓄积、血管重塑以及斑块破裂...     

慢性牙周炎与心血管疾病

慢性牙周炎已成为心血管疾病的独立危险诱因，其危害可能比血清胆固醇水平、健康质量指标、糖尿病和吸烟等因素更为重要。慢性牙周炎促心血管疾病最可能的致病机制是细菌产物与各种凝血机制间的相互作用。LPS可导致TNF—α、IL-1B和血栓因子A2的释放。这些细胞因子可引起血小板的黏附和积聚，提高载脂泡沫细胞的形成和血管内膜胆固醇的沉积，使平滑肌异常增生，从而导致血管壁的增厚。     

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。     

牙周炎与全身性疾病相关性研究的新进展

牙周炎可能是引起或加重一些全身性疾病的潜在危险因素,根据近年来有关牙周炎与全身性疾病相关性的研究新进展,笔者重点从牙周炎与妊娠不良、心血管疾病及糖尿病的关系3个方面进行综述。     

牙周炎与动脉粥样硬化相关性研究进展

牙周炎是菌斑微生物引起的慢性多因子炎症性疾病,其造成了局部和全身的炎症反应.动脉粥样硬化是心血管疾病的病理基础,其发生发展与氧化应激、炎症和血脂紊乱均密切相关.近年来大量研究在作用机制、动物实验和临床病例中阐释了二者的相关性,且牙周炎是动脉粥样硬化的独立危险因素.但因两种疾病的多方面和长期性使得很难建立明确的因果关系,...     

牙周致病菌促进心血管疾病发生发展的分子机制研究进展

牙周炎是发生于牙支持组织的一种多因素感染性疾病。牙周炎和心血管疾病之间关系密切,牙周致病菌是联系牙周炎与心血管疾病的重要因子。本文综述了最新的临床研究和疾病分子机制的研究进展,为牙周炎及牙周致病菌与心血管疾病的相关性研究提供依据。牙周致病菌影响心血管疾病的可能机制,包括牙周致病菌通过直接或间接的方式进入血液循环引起菌血症,牙周致病菌对心血管系统的直接侵袭;牙周致病菌相关毒力因子导致的内毒素血症,继而引发全身炎症状态、脂代谢异常及氧化应激状态,进一步影响心血管系统局部炎症环境;而分子拟态学说以及载脂蛋白E在牙周炎与心血管疾病的内在相关性还需要进一步的研究去探讨。结合现有的研究,合理猜测积极的牙周治疗和口腔卫生措施能够降低牙周炎患者罹患心血管疾病的风险。希望有更多的研究能够关注牙周致病菌和心血管疾病联系的分子机制,尤其是牙周致病菌直接入侵心血管系统或间接入侵宿主细胞,从病变区域组织中分离培养细菌的直接证据;以及局部炎症状态、牙周致病菌及其产物对心血管疾病相关生物标志物（C反应蛋白、血管内皮生长因子、热休克蛋白等）的影响机制,为今后对牙周炎和心血管疾病的有效防治提供参考。     

Cardiovascular disease and periodontitis: an update on the associations and risk

Background: Associations between periodontitis and cardiovascular diseases have been recognized.
Material and Methods: New literature since the last European Workshop on Periodontology has been reviewed.
Results: The lack of reliable epidemiological data on disease prevalence makes an assessment of the associations and risks between periodontitis and cardiovascular diseases difficult. Two recent meta-analysis reports have identified associations between periodontitis and cardiovascular diseases (odds ratios: 1.1–2.2). Different surrogate markers for both disease entities, including serum biomarkers, have been investigated. Brachial artery flow-mediated dilatation, and carotid intima media thickness have in some studies been linked to periodontitis. Studies are needed to confirm early results of improvements of such surrogate markers following periodontal therapy. While intensive periodontal therapy may enhance inflammatory responses and impair vascular functions, studies are needed to assess the outcome of periodontal therapies in subjects with confirmed cardiovascular conditions. Tooth eradication may also reduce the systemic inflammatory burden of individuals with severe periodontitis. The role of confounders remain unclear.
Conclusions: Periodontitis may contribute to cardiovascular disease and stroke in susceptible subjects. Properly powered longitudinal case–control and intervention trials are needed to identify how periodontitis and periodontal interventions may have an impact on cardiovascular diseases.     

Periodontal therapy and cardiovascular risk

Cardiovascular diseases are the worldwide leading cause of mortality. Cardiovascular diseases are noncommunicable conditions with a complex pathogenesis, and their clinical manifestations include major cardiovascular events such as myocardial infarction and stroke. Epidemiologic evidence suggests a consistent association between periodontitis and increased risk of cardiovascular diseases. Some evidence supports a beneficial effect of the treatment of periodontitis on both surrogate and hard cardiovascular outcomes. This narrative review has been conducted as an update of the most recent evidence on the effects of periodontitis treatment on cardiovascular outcomes since the last commissioned review of the European Federation of Periodontology-American Academy of Periodontology World Workshop in 2012. Newer evidence originating from published randomized controlled trials confirms a positive effect of periodontal treatment on surrogate measures of cardiovascular diseases, whereas there have been no randomized controlled trials investigating the effect of periodontal treatment on the incidence of cardiovascular disease events such as myocardial infarction and stroke. In conclusion, there is sufficient evidence from observational and experimental studies on surrogate cardiovascular measures to justify the design and conduct of appropriately powered randomized controlled trials investigating the effect of effective periodontal interventions on cardiovascular disease outcomes (ie, myocardial infarction and stroke) with adequate control of traditional cardiovascular risk factors.     

慢性口腔感染性疾病与心血管疾病的关系

慢性口腔感染性疾病和心血管疾病的关系日渐受到人们的关注。流行病学、分子生物学和动物实验等方面的证据表明,慢性口腔感染性疾病是导致心血管疾病发生的危险因素之一。本文从牙周炎、龋病、牙髓病这3种慢性口腔感染性疾病和心血管疾病之间的相互关系作一综述。     

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.     

Clinical and public health implications of periodontal and systemic diseases: An overview

Severe periodontitis is defined by extensive loss of the tooth attachment apparatus. It is the sixth most common human disease and is estimated to affect 11.2% of the global adult population, hence representing a significant healthcare, social, and economic burden. Since the 1990s, multiple epidemiologic, experimental, and interventional studies have evidenced how periodontitis may also impact systemic health and it has been independently associated with the majority of chronic noncommunicable diseases. The evidence supporting these associations, mainly focusing on diabetes, pregnancy complications, and cardiovascular disease, was thoroughly reviewed in 2012 by an international consensus workshop. In the last 5 years, however, important advances have been made, not only in our understanding of the etiopathogenesis of periodontitis, or concerning the mounting evidence regarding the independent associations between periodontitis, diabetes, and cardiovascular disease, but also with many other systemic diseases including metabolic disease and obesity, rheumatoid arthritis, certain cancers, respiratory diseases, and cognitive disorders including Alzheimer's disease. This review describes these scientific advances by gathering together the existing evidence on the importance and relevance of the associations between periodontitis and many systemic diseases.     

Obesity, inflammation, and periodontal disease

The prevalence of obesity has increased substantially over the past decades in most industrialized countries. Obesity is a systemic disease that predisposes to a variety of co-morbidities and complications that affect overall health. Cross-sectional studies suggest that obesity is also associated with oral diseases, particularly periodontal disease, and prospective studies suggest that periodontitis may be related to cardiovascular disease. The possible causal relationship between obesity and periodontitis and potential underlying biological mechanisms remain to be established; however, the adipose tissue actively secretes a variety of cytokines and hormones that are involved in inflammatory processes, pointing toward similar pathways involved in the pathophysiology of obesity, periodontitis, and related inflammatory diseases. We provide an overview of the definition and assessment of obesity and of related chronic diseases and complications that may be important in the periodontist's office. Studies that have examined the association between obesity and periodontitis are reviewed, and adipose-tissue-derived hormones and cytokines that are involved in inflammatory processes and their relationship to periodontitis are discussed. Our aim is to raise the periodontist's awareness when treating obese individuals.     

Relationship between upper body obesity and periodontitis

Upper body obesity, related to visceral fat accumulation, is known to increase the risk of various adult diseases, especially type 2 diabetes and cardiovascular disease. This study was conducted to clarify the relationship between upper body obesity and periodontitis. We studied 643 apparently healthy, dentulous Japanese adults who attended programs at Fukuoka Health Promotion Center. Waist-hip ratio, body-mass index (BMI), and body fat were significant risk indicators for periodontitis after adjustment for known risk factors (p < 0.002). Subjects were divided into four BMI (or body fat) categories. In only the subjects with high waist-hip ratio, higher categories of BMI (or body fat) significantly increased the adjusted risk of periodontitis, compared with subjects with low waist-hip ratios and the lowest category of BMI (or body fat). The reported relationship between cardiovascular disease and periodontitis should be reconsidered, since abdominal adiposity or visceral fat can be related to both diseases.     

Periodontal diseases and cardiovascular events: meta‐analysis of observational studies

Objective : Many studies have investigated the relationship between periodontal and cardiovascular diseases but their results are heterogeneous. Meta‐analyses were conducted to examine the association between exposure to periodontitis and cardiovascular diseases. Material and methods : Studies published between 1989 and 2007 were retrieved from seven databases. The included articles reported the results from observational studies (cohort, cross‐sectional and case‐control studies) and assessed the link between periodontal exposure and cardiovascular diseases as confirmed by one of the following criteria: diagnosed coronary artery disease, angina pectoris, acute myocardial infarction, mortality caused by cardiac pathology. The study characteristics were abstracted by independent researchers following a standardised protocol. The MOOSE guidelines for meta‐analysis of observational studies were followed. Results : From 215 epidemiological studies, 47 were observational, of which 29 articles could be combined by the meta‐analysis methodology. The pooled odds ratio calculated from the 22 case‐control and cross‐sectional studies was 2.35 (95% CI [1.87; 2.96], p< 0.0001). The risk of developing cardiovascular disease was found to be significantly (34%) higher in subjects with periodontal disease compared to those without periodontal disease (pooled relative risk from the 7 cohort studies was 1.34 (95% CI [1.27; 1.42], p< 0.0001). Conclusions : It seems from observational studies that subjects with periodontal diseases have higher odds and higher risks of developing cardiovascular diseases but the reduction in the risk of cardiovascular events associated with the treatment of periodontitis remains to be investigated.     

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.