补体5a及其受体和效应通路与牙周炎的关系

补体（C）5a与其受体（C5aR）结合后,可诱导中．性粒细胞、巨噬细胞等向炎症部位聚集,诱导炎性递质的生成。CD88和C5L2为目前已知的两种C5aR,在中性粒细胞、巨噬细胞和不成熟树突细胞上都有表达,可能促进炎症反应的发生。C5a可能通过细胞外信号调节激酶1、2以及P38促丝裂原激活蛋白激酶通路抑制中性粒细胞程序性死亡发挥促炎作用。抑制C5a与C5aR之间的相互作用,在一定程度上可以抑制中性粒细胞的活化、活性氧的释放以及那基质金属蛋白酶的生成,从而减轻炎症和组织损伤。进一步了解c5a及其受体在牙周炎发生发展中的作用机制可为牙周炎的治疗提供又一新途径。     

抗体,补体及白细胞介素和牙周炎的关系

牙周炎的主要致病因素——细菌及其产物侵入机体后,可引起宿主的免疫系统产生一系列免疫反应。这种防御性的应答反应,包括T细胞系统、B细胞系统及补体系统。人体存在一套完整的免疫系统,淋巴细胞是构成特异免     

细胞自噬在牙周炎中的作用与机制

牙周炎是由牙菌斑生物膜引起的牙周组织的慢性炎症性疾病。细胞自噬是宿主对抗细菌感染的有效武器。近年来研究发现,细胞自噬不仅可以促进感染细胞对细菌和毒素的清除,而且有助于抑制炎症反应,以维持细胞内环境稳态,与牙周炎的发生发展关系密切。本文从细胞自噬与牙周病原菌感染的相互作用,细胞自噬与免疫炎症反应的相互调控,以及细胞自噬与牙槽骨代谢的关系3个方面,对细胞自噬与牙周炎发生发展的关系进行综述,为深入地研究细胞自噬与牙周炎相关机制提供参考,为牙周炎防治的研究提供新的思路。     

细胞焦亡参与牙周炎发生发展的研究进展

牙周炎是一种慢性感染性炎症疾病,探究牙周炎发生发展过程中炎症调节机制是预防和治疗牙周炎的关键,但目前其尚不明确。细胞焦亡是一种新发现的炎症性细胞程序性死亡方式,以细胞裂解并释放大量促炎因子为主要特征。菌斑微生物、局部及全身促进因素等多种牙周炎相关因素可能通过细胞焦亡引起牙周组织损伤。文章就细胞焦亡参与牙周炎发生发展的相关研究进展做一综述。     

细胞自噬在牙周炎中的作用与机制

牙周炎是由牙菌斑生物膜引起的牙周组织的慢性炎症性疾病。细胞自噬是宿主对抗细菌感染的有效武器。近年来研究发现,细胞自噬不仅可以促进感染细胞对细菌和毒素的清除,而且有助于抑制炎症反应,以维持细胞内环境稳态,与牙周炎的发生发展关系密切。本文从细胞自噬与牙周病原菌感染的相互作用,细胞自噬与免疫炎症反应的相互调控,以及细胞自噬与牙槽骨代谢的关系3个方面,对细胞自噬与牙周炎发生发展的关系进行综述,为深入地研究细胞自噬与牙周炎相关机制提供参考,为牙周炎防治的研究提供新的思路。     

菌群失调在牙周炎促进结直肠癌发生发展中的作用

结直肠癌是一种常见的恶性肿瘤,其发生发展受饮食、遗传、环境和代谢等多种因素的影响。肠道微生物组成的变化是重要的内部环境之一,与结直肠癌的发生发展密切相关。而牙周炎患者的口腔菌群失调可影响肠道菌群的组成,降低肠道的屏障功能,促进炎症微环境的形成,进而促进结直肠癌的进展。本文从菌群失调入手,对牙周炎促进结直肠癌发生发展的作...     

牙周炎与低体重早产儿

近来研究表明牙周炎可作为多种系统性疾病的病原因素。本义试述孕妇牙周炎与低体重早产儿之间的相关关系及其可能机制。以有助于发挥牙周临床医生在预防低体重早产儿发生方面的作用，为预防其发生提供了新的思路和途径。     

糖尿病与牙周炎的关系

糖尿病与牙周炎关系密切，糖尿病患者伴发重度牙周炎的风险比非糖尿病患者增高２￣３倍，而牙周慢性炎症又会促进患者血糖升高。二者有共同的遗传学基础，糖尿病还通过对牙周菌群、中性粒细胞功能，炎症反应强度，胶原代谢及组织愈合能力的影响促进牙周炎的发生。本文探讨了糖尿病和牙周炎的相互影响及糖尿病患者的牙周治疗有关注意事项。     

The complement system and its role in the pathogenesis of periodontitis: current concepts

Periodontitis is a highly prevalent inflammatory disease in tooth supporting tissues, induced by bacteria growing in a biofilm on tooth surfaces. Components of the complement system are present in the periodontal tissue and the system is activated in periodontitis. Continuous complement activation and modulation by bacteria within the biofilm in periodontal pockets, however, may enhance local tissue destruction, providing the biofilm with both essential nutrients and space to grow. A more profound understanding of the mechanisms involved in complement‐derived tissue degradation may facilitate the development of new treatment concepts for periodontitis. Further studies on the role of complement in periodontitis pathogenesis may also contribute to the understanding of why some individuals fail to resolve periodontitis. Here, we review evidence that links complement to the pathogenesis of periodontitis with an emphasis on interaction of complement with bacteria from periodontitis‐associated biofilm.     

中性粒细胞在牙周炎发生发展中的作用的研究进展

龈沟内的中性粒细胞是抵御牙周致病菌入侵的第一道防线。炎症感染时,中性粒细胞最早被募集到炎症部位,通过吞噬、脱颗粒、呼吸爆发等方式杀灭细菌。本文拟就中性粒细胞在牙周炎发生发展中的作用进行综述。     

Single nucleotide polymorphisms of complement component 5 and periodontitis

Chai L, Song Y‐Q, Zee K‐Y, Leung WK. Single nucleotide polymorphisms of complement component 5 and periodontitis. J Periodont Res 2010; 45: 301–308. © 2009 John Wiley & Sons A/S Background and Objective: Polymorphisms of host defence genes might increase one’s risks for periodontitis. This study investigated whether tagging single nucleotide polymorphisms (SNPs) of the gene encoding complement component 5 (C5) are associated with periodontitis in a Hong Kong Chinese population. Material and Methods: Eleven tagging SNPs of 229 patients with at least moderate periodontitis and 207 control subjects without periodontitis were genotyped using an i‐plexGOLD MassARRAY mass‐spectrometry system. Results: Genotype AG of SNP rs17611 was more prevalent in the group of periodontitis patients than in the controls (54.6% vs. 41.7%, p = 0.007). The haplotype CGCA of the haplotype block consisting of rs1035029, rs17611, rs25681 and rs992670 was significantly associated with periodontitis in a dominant model (p = 0.001). The SNP rs17611 showed high linkage disequilibrium with rs1035029, rs25681 and rs992670. Smoking was also significantly associated with periodontitis (p = 0.006). Conclusion: The tagging SNP rs17611 of the C5 gene and smoking may be associated with periodontitis among the Hong Kong Chinese population.     

Oral treatment with complement factor C5a receptor (CD88) antagonists inhibits experimental periodontitis in rats

Breivik T, Gundersen Y, Gjermo P, Taylor SM, Woodruff TM, Opstad PK. Oral treatment with complement factor C5a receptor (CD88) antagonists inhibits experimental periodontitis in rats. J Periodont Res 2011; 46: 643–647. © 2011 John Wiley & Sons A/S Background and Objective: The complement activation product 5a (C5a) is a potent mediator of the innate immune response to infection, and may thus also importantly determine the development of periodontitis. The present study was designed to explore the effect of several novel, potent and orally active C5a receptor (CD88) antagonists (C5aRAs) on the development of ligature‐induced periodontitis in an animal model. Material and Methods: Three different cyclic peptide C5aRAs, termed PMX205, PMX218 and PMX273, were investigated. Four groups of Wistar rats (n = 10 in each group) were used. Starting 3 d before induction of experimental periodontitis, rats either received one of the C5aRas (1–2 mg/kg) in the drinking water or received drinking water only. Periodontitis was assessed when the ligatures had been in place for 14 d. Results: Compared with control rats, PMX205‐ and PMX218‐treated rats had significantly reduced periodontal bone loss. Conclusion: The findings suggest that complement activation, and particularly C5a generation, may play a significant role in the development and progression of periodontitis. Blockade of the major C5a receptor, CD88, with specific inhibitors such as PMX205, may offer novel treatment options for periodontitis.     

辅助性T细胞及其平衡与牙周炎

CD4阳性T细胞在细菌或病毒等外部信号的刺激下分化为辅助性T(Th)1、2和17细胞。Th1细胞主要分泌干扰素-γ、白细胞介素(IL)-2和肿瘤坏死因子-β等,这些细胞及细胞因子可导致炎症和组织破坏。Th2细胞主要分泌IL-4、5、6和10等,这些细胞及细胞因子是负性调节者或保护因子。Th17细胞可产生IL-6、1以及转化生长因子-β等,表达IL-23受体,介导前炎症反应。研究显示:Th1细胞可加重牙周组织炎症和牙槽骨的破坏程度;Th2细胞则可有效地减轻病变程度,对牙周组织起到保护作用;Th17细胞在慢性牙周炎炎症反应和骨质破坏中起重要作用。由于Th2细胞主导保护作用,因此对这些目的因子的产生及其生物学效应进行有效的调控,阻断异常的免疫过程,可能是临床评估和控制牙周炎慢性炎症的一条新方向,可为采用细胞因子制剂治疗牙周炎提供理论依据。     

牙周炎和趋化因子的研究新进展

趋化因子(chemokines)是一类一级结构相似,对白细胞具有化学趋化作用等多种生物学效应的小分子蛋白,在机体的防御和炎症反应等方面起着重要的调节作用.近年来许多研究发现,趋化因子在牙周炎的免疫发病机制中发挥着重要作用.深入研究趋化因子和牙周炎的关系,对牙周炎的预防、诊断、治疗以及治疗后疗效监测有重要意义.     

Sequence divergence in the Treponema denticola FhbB protein and its impact on factor H binding

Treponema denticola is an anaerobic spirochete whose abundance in the subgingival crevice correlates with the development and severity of periodontal disease. The ability of T. denticola to survive and thrive in the hostile environment of the periodontal pocket is due, at least in part, to its ability to bind factor H (FH), a negative regulator of the alternative complement pathway. The FH binding protein of T. denticola has been identified as FhbB and its atomic structure has been determined. The interaction of FH with T. denticola is unique in that FH bound to the cell surface is cleaved by the T. denticola protease, dentilisin. It has been postulated that FH cleavage by T. denticola leads to immune dysregulation in periodontal pockets. In this study, we conduct a comparative assessment of the sequence, properties, structure and ligand binding kinetics of the FhbB proteins of strains 33521 and 35405. The biological outcome of the interaction of these strains with FH could differ significantly as 33521 lacks dentilisin activity. The data presented here offer insight into our understanding of the interactions of T. denticola with the host and its potential to influence disease progression.     

牙龈卟啉单胞菌在牙周病防治中的应用

牙周病是口腔两大类主要疾病之一,具有较高的发病率,因此,探索预防牙周病的有效途径十分重要。本文介绍了国外学者以牙龈卟啉单胞菌不同形式的抗原进行免疫学防治牙周炎的试验,其中包括对牙龈卟啉单胞菌菌毛、血凝素、牙龈素和外膜蛋白的研究。