慢性牙周炎与前列腺疾病相关性的研究进展

近年来,慢性牙周炎与前列腺疾病的相关性研究受到广泛关注,衰老、肥胖、吸烟和精神心理等是这两种疾病的共同危险因素,但关键的相关性机制目前尚未明确。该文就慢性牙周炎与前列腺疾病的相关研究及可能的生物学机制作一综述,为今后的疾病管理和临床研究提供依据。     

糖尿病前期与牙周炎关系的研究进展

糖尿病前期(pre-diabetes mellitus, Pre-DM)是介于正常血糖稳态和2型糖尿病之间的中间高血糖状态, 我国一半以上的成年人处于Pre-DM。牙周炎主要是由菌斑微生物引起的慢性炎症性疾病, 与糖尿病等非传染性疾病的发生具有共同的危险因素, 且互相影响。Pre-DM可能增加罹患牙周炎的风险, 牙周炎也可能影响糖尿病的发生和发展。氧化应激、系统性炎症、肠道菌群是目前牙周炎与Pre-DM互相联系的主要机制。本文主要对Pre-DM与牙周炎的关系及潜在的相关机制进行综述, 为两者的防治提供新的依据。     

慢性牙周炎是影响全身健康的危险因素

近年来,人们的兴趣越来越多地转向于牙周感染和全身性疾病之间的可能关联。事实上,慢性牙周炎致病菌和它们的产物,以及在牙周组织产生的炎症介质,可能会进入血液,影响全身或者造成全身性疾病,包括心血管疾病、呼吸道疾病、糖尿病、不良妊娠等,慢性牙周炎是影响全身健康的危险因素。     

Ⅱ型糖尿病牙周炎及牙周基础治疗对其影响的现状研究

Ⅱ型糖尿病是引起慢性牙周炎的主要危险因素之一,慢性牙周炎增加了Ⅱ型糖尿病的患病风险,但至今为止糖尿病牙周炎的发病机制尚未明确。牙周基础治疗不仅可以改善牙周炎患者的牙周状况,而且在一定程度上改善了糖尿病牙周炎患者的血糖状况。随着分子生物学技术的不断发展,研究人员对糖尿病牙周炎疾病在微生物、免疫及炎症因子方面的研究不断深入,该文对糖尿病牙周炎的微生物指标,免疫、炎症因子指标,临床指标及牙周基础治疗对疾病的影响做一综述。     

牙周炎与慢性肾脏病相关性研究现状

牙周炎与慢性肾脏病均为慢性炎症性疾病,患者伴有全身的炎症负担及机体的免疫异常。血糖、血压、血脂等异常以及炎症的刺激对疾病有显著影响。该文主要对牙周炎与慢性肾脏病相关性的流行病学研究情况,共同的影响因素,以及可能相关的生物学机制等进行综述。旨在实现早期预防,控制危险因素,降低二者互相影响的可能性,同时指导治疗,进而达到良好的预后。     

牙周炎对糖尿病的影响——基于队列研究的综述

牙周炎是以菌斑生物膜为始动因素的发生于牙齿支持组织的炎症,与众多全身系统性疾病息息相关,其中对于牙周炎和糖尿病关系的报道最为广泛。队列研究是探讨疾病病因的重要临床研究方法,大规模、规范设计的前瞻性队列研究证据强度较高,可为牙周炎对糖尿病患者血糖控制、发病情况以及并发症的发生率的影响提供临床证据。牙周炎与血糖控制恶化存在关联,目前有中等强度的证据表明,与不进行牙周治疗相比,牙周非手术治疗可以显著改善伴牙周炎的糖尿病患者的血糖水平;牙周炎的存在对糖尿病的发病情况在不同人口背景的研究中缺乏一致性结论,而牙周炎对糖尿病并发症的发生率的影响的证据相对有限,需要良好设计的队列研究以提供高质量的循证医学证据。     

糖尿病前期和牙周炎的相互关系

糖尿病前期是从早期代谢异常到糖尿病的过渡期,牙周炎是发生在牙周组织的慢性感染性疾病.糖尿病前期和牙周炎之间存在着相关性,即糖尿病前期增加牙周炎的发病率及其严重程度,牙周炎亦加重糖尿病前期的严重程度,牙周炎治疗可以有效改善糖尿病前期患者的糖代谢.氧化应激和细胞因子,包括肿瘤坏死因子-α以及白细胞介素-1β和6,可能是影响这两种疾病发生发展的关键环节.肥胖和年龄是这两种疾病的共同危险因素,可促进这两种疾病同时发生发展.本文主要就糖尿病前期与牙周炎相关性及可能作用机制进行阐述.     

糖尿病性牙周炎与细胞凋亡

目前,世界卫生组织已将糖尿病列为严重影响人类健康的第三大疾病.而牙周炎作为口腔常见病和多发病,其发病率也有逐渐曾高的趋势.现已明确,糖尿病与牙周炎相互影响,互为高危因素.糖尿病可增加牙周炎的发病风险及严重程度,牙周炎亦是糖尿病的易感和促进因素.     

慢性牙周炎与心血管疾病关系的研究进展

牙周炎与心血管疾病具有共同的危险因素,如吸烟、精神压力和糖尿病等.已有较充分的证据表明,慢性牙周炎是心血管疾病发生的独立危险因素,但两者相互作用的内在机制尚不十分明确.本文从牙周炎与心血管疾病的相关性、牙周治疗对心血管疾病的影响以及牙周炎与常见心血管疾病相关机制等方面,对牙周炎与心血管疾病关系的研究进展进行阐述.     

激光在糖尿病患者牙周炎非手术治疗中的应用

与糖尿病相伴随的牙周炎是一种易造成牙周支持组织显著破坏的疾病,在中老年人群具有较高发病率,常规治疗效果欠佳。激光是一种单光子的人造光,具有杀菌消毒、降低促炎症因子水平以及减少牙槽骨吸收的作用,对以炎症为联系基础的糖尿病伴牙周炎患者的治疗效果较显著。因此,本文主要从糖尿病患者牙周炎的诊疗特点,激光治疗在其中应用的原理、类型、疗效以及存在的问题和发展方向等作一综述。     

内质网应激在牙周炎影响全身疾病过程 中的作用

牙周炎是发生在牙周组织的慢性感染性疾病,其发病机制及对全身系统疾病的影响一直是学术界关注的热点问题。许多学者认为,牙周炎不仅是一种常见的口腔疾病,更是全身疾病的潜在危险因素之一,但是目前关于牙周炎诱发全身系统疾病的具体机制尚不明确,可能与牙周致病菌、炎症因子及内质网应激等有关。近年来的研究发现,内质网应激是介导细胞凋亡的重要通路之一,并且与全身疾病密切相关。有研究显示,内质网应激在牙周炎诱导全身疾病过程中存在调控作用,但是目前关于内质网应激在牙周炎影响全身疾病过程中的作用研究较少,需要进一步探索。本文就内质网应激在牙周炎影响全身系统疾病中的研究进展进行综述,旨在探究牙周炎和全身系统疾病的内在联系,以期为牙周炎与其相关全身系统疾病的防治提供新的思路。     

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.     

牙周炎与阿尔兹海默症相关性研究进展

阿尔兹海默症是一种最常见的老年痴呆症,与环境因素密切相关。牙周炎是发生在牙周支持组织的一种慢性感染性疾病。研究表明,牙周炎与阿尔兹海默症的发生发展密切相关,但作用机制尚未完全明确,炎症反应及血管结构的改变可能是两种疾病的中介,共同的危险因素促进两种疾病的发生发展。文章就近年来牙周炎与阿尔兹海默症相关性的研究进展做一综述。     

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??Alzheimer's disease is the most common form of dementia associated with environmental factors. Periodontitis is a chronic infectious disease that occurs in periodontal supporting tissues. Studies have found a close association between periodontitis and Alzheimer′s disease??but the potential mechanism linking periodontitis with Alzheimer′s disease is not fully clear. It might be that the inflammatory response and vascular changes are the two mediators of the disease??and the common risk factors promote the development of both diseases. The recent findings of the association between periodontitis and Alzheimer′s disease were discussed in this paper.     

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。     

口腔扁平苔藓与牙周炎关系的研究进展

牙周炎为发生在牙周组织的慢性感染性疾病,同时口腔扁平苔藓也是口腔粘膜的常见疾病。临床上大多数口腔扁平苔藓患者牙周状态差,并且牙周基础治疗对其有一定疗效;在发病机制上二者都与免疫、遗传及心理精神因素等有关。牙周炎与口腔扁平苔藓这两种慢性炎症疾病可同时存在或伴随患者终身,维护好牙周健康已成为口腔医学必须面对的现实。本文对近年来牙周炎与口腔扁平苔藓的关系进行回顾总结,为牙周病和口腔扁平苔藓的进一步研究奠定基础。     

妊娠期糖尿病伴牙周炎治疗研究进展

牙周炎和妊娠期糖尿病（gestational diabetes mellitus,GDM）都是十分常见的慢性病。研究发现,GDM与牙周炎之间可能存在相关性,GDM影响牙周炎发展的严重程度,牙周炎对GDM的发展亦有着推动作用。GDM伴牙周炎的发病机制复杂,可能对正常妊娠及胎儿生长发育产生不良影响,因此,对GDM伴牙周炎患者的综合治疗需持谨慎的态度。迄今为止,对于GDM合并牙周炎的治疗尚存在争议,主要以降血糖、降低炎症反应的治疗为主,但并无统一的治疗方案。文章回顾了近年来国内外相关研究,就GDM伴牙周炎患者的治疗研究进展做一综述,为其临床诊疗及科学研究提供新的思路。     

牙周基础治疗调节2型糖尿病患者代谢的研究进展

牙周炎与糖尿病密切相关,糖尿病是牙周炎的全身促进因素之一,牙周炎会加重糖尿病的病情和代谢紊乱程度。牙周基础治疗在这个双向关系中意义重大,能显著改善牙周支持组织状态、降低血清和龈沟液中炎症因子的表达,研究发现这与牙龈卟啉单胞菌fimA II型减少和内皮祖细胞免疫炎症基因等体内相关炎症基因表达降低有关。一些研究还表明牙周基础治疗能减少胰岛素拮抗脂肪因子释放、增加胰岛素敏感脂肪因子生成,缓解胰岛素抵抗;或因加强脂肪组织代谢相关基因和炎症标志物基因的表达,而对患者的糖脂代谢有益。因此,明确牙周基础治疗对2型糖尿病伴牙周炎患者的影响及相关机制,可为防治2型糖尿病及其并发症提供新的理论依据。     

The pathogenesis of periodontal disease: a paradigm shift

Periodontitis is a family of related diseases that differ in etiology, natural history, disease progression and response to therapy, but have a common underlying chain of events, thatareinfluenced by disease modifiers. The clinical manifestations observed are a result of the complex interplay of these factors. The pathogenesis of human periodontitis was placed on a rational footing for the first time by Page & Schroeder in 1976 and the general principles and the overall conclusions reached in that article are still largely acceptable today. Still, an enormous amount has been learned about all aspects of human periodontitis, including its pathogenesis, since 1976. A critical evaluation of the literature regarding the complex relationship between the microbial factor, the host factor and the occurrence of a disease, might be leading us over a surge of a paradigm shift in our understanding the pathogenesis of the disease. It is well acknowledged that while the etiology of periodontitis is bacterial, the pathogenesis is inflammatory. The understanding of regulation of inflammation in periodontitis is far from complete; however, as the understanding of periodontal inflammation increases, the current understanding of the microbiology of periodontitis becomes less clear. While we think we know that bacteria initiate the disease, the role of specific bacteria is still unknown. The current knowledge of the microbiology of periodontitis is based on large cross-sectional and association studies. Periodontitis is seen as the direct consequence of bacterial invasion and is regarded as an infectious disease. It is however, not possible to draw cause and- effect inferences from these studies. One might state that the inflammation precedes the overgrowth of the bacteria. In this scenario, the initiator of the disease might be early, gram-positive colonizers that elicit a profound inflammatory response in the susceptible host. The implication of that paradigm shift outlined above is that periodontitis is an inflammatory disease, and in that case the primary target of pharmacotherapy should be the inflammation, rather than the bacteria. Still, the question to be asked and investigated is whether dampening of the inflammatory response in certain individuals susceptible to periodontitis might prevent development of disease. This is a question yet to be answered.