慢性牙周炎患者唾液中miR-146a的表达及其与龈沟炎症、MMP-8/TIMP-1水平的关系

目的： 探讨慢性牙周炎患者唾液中miR-146a的表达及其与龈沟炎症、基质金属蛋白酶8（MMP-8）、基质金属蛋白酶抑制剂1（TIMP-1）水平的关系。方法： 选择2015年3月—2017年1月间收治的慢性牙周炎患者68例作为慢性牙周炎组,同期在本院进行体检的健康志愿者50例作为正常对照组。检测2组研究对象唾液中miR-146a的表达量,龈沟液中炎症因子、MMP-8/TIMP-1的水平及牙周临床症状指标。采用SPSS24.软件中的Pearson检验评估慢性牙周炎患者唾液中miR-146a的表达量与病情严重程度的相关关系。结果： 慢性牙周炎患者唾液中miR-146a的表达量显著高于正常对照组（P<0.05）,龈沟液中炎症因子（IL-1β、IL-6、IL-35、TNF-α）水平、牙周临床症状指标（PD、AL、PLI、BI）以及龈沟液中MMP-8、TIMP-1的水平显著高于正常对照组（P<0.05）。Pearson检验发现,慢性牙周炎患者唾液中miR-146a表达量与龈沟炎症程度、牙周临床症状严重程度及MMP-8/TIMP-1水平呈正相关。结论： 慢性牙周炎患者唾液中miR-146a表达量异常增高,且与龈沟炎症程度、牙周损伤程度一致。     

牙周炎患者外周血miRNA表达谱分析评价

目的:分析牙周炎患者外周血微小RNA(microRNA,miRNA)表达谱,筛选出具有潜在牙周炎诊断价值的外周血miRNA,为牙周炎特异性诊断方式的探寻提供参考.方法:从基因表达综合数据库(Gene Expression Om-nibus,GEO)获取受试者外周血miRNA表达谱数据集(GSE61741),并进行GEO2R在线工具分析.Logistic回归分析进行差异表达miRNA自变量筛选,依据接受者操作特征(receiver operating characteristic,ROC)曲线下面积(area under the curve,AUC)确定miRNA的诊断价值.结果:与健康对照组相比,牙周炎患者外周血123个miRNA表达水平显著下调,109个miRNA表达水平显著上调;Logistic回归分析筛选出3个与牙周炎发病相关的外周血miRNA,即hsa-miR-361-5p、hsa-miR-663和hsa-miR-744;ROC曲线显示,hsa-miR-361-5p、hsa-miR-663、hsa-miR-744以及三者联合诊断牙周炎的AUC值分别为0.871、0.899、0.925和0.981,均具有统计学意义(P<0.01).结论:牙周炎患者外周血miRNA表达谱与健康对照组存在明显差异,hsa-miR-361-5p、hsa-miR-744和hsa-miR-663与牙周炎发病风险相关,对于牙周炎的诊疗具有一定价值.     

慢性牙周炎患者治疗前后血清CRP、sICAM-1水平的变化

目的：了解慢性牙周炎患者经过牙周非手术治疗前后血清C反应蛋白（c-reactive protein,CRP）、可溶性细胞间黏附分子1（soluble intercellular adhesion molecule-1,sICAM-1）的水平的变化.方法：选择22例中重度慢性牙周炎患者,治疗前后分别收集患者的血清,用酶联免疫吸附反应法（ELISA）方法测定CRP、sICAM-1水平,并和16例无其它系统疾病的临床牙周健康的对照组比较.结果：慢性牙周炎患者血清CRP、sICAM-1水平显著高于临床牙周健康的对照组.治疗后血清CRP、sICAM-1水平下降,接近牙周正常者水平.结论：慢性牙周炎影响血清CRP、sICAM-1的水平.牙周非手术治疗可以明显控制牙周局部炎症,降低血液中CRP、sICAM-1的水平.     

唾液中一氧化氮含量与牙周炎的相关性研究

目的:研究牙周炎患者唾液中一氧化氮(NO)含量与牙周炎各种临床指标的相关性,探讨一氧化氮在牙周炎发展过程中可能发挥的作用.方法:选择牙周健康者28人(对照组),慢性牙周炎32人(实验组),用Griess反应测定牙周基础治疗前后唾液中亚硝酸盐含量,间接反映NO水平,分析牙周临床指标与NO含量的关系.结果:实验组唾液中NO含量较对照组显著增加,牙周炎患者唾液NO含量与牙周探诊深度,附着水平之间有显著正相关.结论:NO的产生与牙周炎症过程有关.牙周基础治疗后,随着局部炎症逐渐减轻,唾液NO含量呈下降趋势.     

实验性牙周炎动物模型的微生物研究

目的 利用Beagle犬建立一种近似人类临床牙周炎的牙周炎动物模型.方法 在6只Beagle犬牙颈部龈缘水平结扎丝线并配以形成牙周炎食谱饲养,分别于实验的第0、1、3、7、14 d,1、2、3个月检查实验动物的临床牙周状况和提取颊侧牙周龈下微生物标本,并用多聚酶链反应(polymerase chain reaction,PCR)技术检测龈下标本8种常见牙周炎致病菌,记录结果.结果 所有动物实验侧牙齿的牙周均形成近似人类临床牙周炎的实验性牙周炎,但严重程度和龈下致病菌种类不一.结论 在Beagle犬建立的牙周炎模型是较近似于人类临床牙周炎的实验性牙周炎动物模型.     

牙周炎症对冠心病患者CRP水平影响的初探

目的通过横向研究初步探讨牙周炎症对冠心病患者CRP水平的影响。方法受检者共60人,包括冠心病＋牙周炎组、单纯牙周炎组和健康对照组,每组20人。检测超敏C反应蛋白（hs—CRP）,牙周临床指标包括牙周探诊深度、附着丧失、出血指数、菌斑指数,并检测血脂水平（HDL、LDL、TG、CHO）和白细胞计数。采用ANOVA法分析以上指标在各组间的差别,Pearson法分析hs—CRP与牙周指标间的相关性。结果牙周炎＋冠心病组hs．CRP显著高于单纯牙周炎组和健康组（P〈0．05）,单纯牙周炎组的hs—CRP水平又显著高于健康组（P〈0．05）。牙周炎＋冠心病组牙周指标均高于单纯牙周炎组和健康组。受检者的血清hs—CRP水平与牙周指数显著相关（P〈0．05）。结论牙周感染和炎症可能是牙周炎＋冠心病患者hs—CRP水平升高的原因之一。     

小鼠牙周炎模型牙周组织中MicroRNA表达谱研究

目的：建立小鼠牙周炎模型牙周组织和正常小鼠牙龈组织microRNA表达差异谱,为探讨microRNA在牙周炎发病过程中是否起到可能的调控作用提供前期研究基础。方法：小鼠牙周炎牙周组织和正常小鼠牙龈组织各3例,Trizol法抽提细胞总RNA。采用基因芯片技术,将总RNA与microRNA芯片杂交,GenePixProV6．0软件进行数据分析。结果：与正常小鼠牙龈组织相比,牙周炎小鼠牙周组织中表达上调超过2倍的microRNA有4个,分别为mmu—miR-126,mmu—miR-32,mmu—miR-147,mmu—miR-155。其中牙周炎小鼠牙周组织中mmu—miR-155表达量明显提高,是正常小鼠牙龈组织的5．2倍。结论：筛选出的差异表达microRNA可能参与了牙周炎的发病过程,为探讨microRNA分子在牙周炎中的可能作用提供了途径。     

慢性牙周炎患者治疗前后龈沟液中IL-23、IL-17表达水平的变化

目的研究慢性牙周炎患者牙周基础治疗前后龈沟液(gingival crevicular fluid,GCF)中IL-17、IL-23表达水平的变化,探讨IL-23/IL-17轴在慢性牙周炎发生、发展过程中的作用。方法选取来我科就诊的慢性牙周炎患者50例为研究对象。于牙周基础治疗前后,采集龈沟液并测量体积,运用夹心酶联免疫吸附试验测定IL-17和IL-23的质量浓度以及测量两者之间的关系。结果牙周基础治疗后龈沟液中的IL-17、IL-23表达水平均较治疗前显著下降,差异均有统计学意义(P<0.05)。牙周基础治疗前后龈沟液中的IL-17、IL-23表达水平与牙周临床指标呈正相关。结论 IL-17、IL-23在慢性牙周炎发生发展过程中起重要作用。     

IL-35在牙周炎及口腔扁平苔藓中的表达及相关性分析

目的:探讨IL-35在牙周炎及口腔扁平苔藓免疫机制中的作用及相关影响,以及牙周炎与口腔扁平苔藓之间的相互关系.方法:按纳入标准选择单纯口腔扁平苔藓患者20例,单纯牙周炎患者20例,牙周炎伴口腔扁平苔藓患者20例和健康者12例;记录患者的一般信息及牙周探诊深度、临床附着丧失、牙龈指数、龈沟出血指数,并收集静脉血清及龈沟液样本,采用酶联免疫吸附测定血清及龈沟液中IL-35的表达水平.采用SPSS19.0软件包对数据进行统计学分析.结果:单纯口腔扁平苔藓组、单纯牙周炎组、牙周炎伴口腔扁平苔藓组龈沟液及血清中IL-35浓度显著高于健康对照组(P＜0.01),牙周炎伴口腔扁平苔藓组龈沟液及血清中IL-35浓度显著高于单纯口腔扁平苔藓组及牙周炎组(P＜0.05);各组牙周临床指标与龈沟液及血清中IL-35表达水平呈正相关关系.结论:牙周炎及口腔扁平苔藓中IL-35表达水平显著升高,其升高程度与两者呈正相关.     

慢性牙周炎患者牙龈组织内诱导型一氧化氮合酶表达的研究

目的:研究牙周健康者和慢性牙周炎患者牙龈组织中诱导型一氧化氮合酶的表达强度,探讨一氧化氮在牙周病发病过程中的作用.方法:选择牙周健康组、慢性牙周炎活动期组,慢性牙周炎静止期组各20例,采取免疫组织化学的方法染色,光镜下观察牙龈组织内诱导型一氧化氮合酶的表达强度.结果:慢性牙周炎时牙龈组织中诱导型一氧化氮合酶主要在鳞状上皮和间质组织的细胞胞浆中阳性表达,正常组表达强度弱于慢性牙周炎静止期组和活动期组,慢性牙周炎静止期组表达强度弱于慢性牙周炎活动期组.结论:一氧化氮参与了慢性牙周炎的发生和发展过程,牙龈组织中诱导型一氧化氮合酶的表达强度与慢性牙周炎的炎症程度密切相关.     

Localized juvenile periodontitis or localized aggressive periodontitis

In general, the new term "localized aggressive periodontitis" replaces what was previously known as "localized juvenile periodontitis." Similarly, "generalized aggressive periodontitis" replaces what used to be called "generalized juvenile periodontitis." Aggressive periodontitis is a specific type of periodontitis with clearly identifiable clinical and laboratory findings, making it sufficiently different from chronic periodontitis and warranting separate classification. Not all the characteristics must be present to assign a diagnosis or classify the disease. The diagnosis may be based on clinical, radiographic, and historical data, and laboratory testing may not be essential for assigning a diagnosis.     

Pathogenesis of periodontitis

Periodontitis is an inflammatory disease of the periodontium which is characterized by a progressive destruction of the tissues supporting the tooth. Its primary etiology is an ill-defined series of microbial infections which may be composed of only some of the more than 300 species of bacteria currently recognized in the oral cavity. The disease is currently considered to progress as periodic, relatively short episodes of rapid tissue destruction followed by some repair, and prolonged intervening periods of disease remission. Despite the apparent random distribution of episodes of disease activity, the resulting tissue breakdown exhibits a symmetrical pattern of alveolar bone loss and pocket formation which is common to several forms of periodontitis, although the distribution of the most affected teeth and surfaces may vary among diseases (e.g., juvenile periodontitis versus adult periodontitis or rapidly progressive periodontitis). Several reports have indicated that bacterial cells can be found in the pocket wall of periodontitis lesions. The translocation of bacteria into the tissues from the pocket environment is quite common, as evidenced by the common occurrence of bacteremias in patients with periodontitis following relatively minor events such as chewing and oral hygiene procedures. However, it is important to distinguish between the passive introduction of bacteria into periodontal tissues and frank invasion as might occur in an acute infection, since the pathological implications may be quite different.     

侵袭性牙周炎和慢性牙周炎的龈下优势菌分析

目的 :分析侵袭性牙周炎 (aggressiveperiodontitis ,AgP)与慢性牙周炎 (chronicperiodontitis ,CP)的龈下优势菌群 ,为探讨牙周炎分类、病因和诊断提供实验依据。方法 :将中学生流调筛选 (16例 )及牙周病专科就诊(2 4例 )的AgP和CP患者 ,采集龈下菌斑样本 ,在厌氧菌基础培养基 (CDC)和选择性培养基 (TSBV)上培养分析。结果 :局限型AgP患者的伴放线放线杆菌 (Actinobacillusactinomycetemcomitans ,Aa)及兼性厌氧菌的检出率显著高于中度CP患者 (P <0 .0 5 ,P <0 .0 1) ,而广泛型AgP和重度CP患者的厌氧菌总数较局限型AgP和中度CP患者显著增加 (P <0 .0 5 )。结论 :局限型AgP和中度CP的龈下优势菌有明显差别 ,Aa是一个重要的危险因子。     

Juvenile periodontitis

Juvenile periodontitis occurs in children and young adults and can be classified into: periodontitis which occurs in otherwise healthy individuals, and periodontitis which occurs in juveniles with systemic disease. The periodontitis which occurs in otherwise healthy individuals consists of two major forms: juvenile periodontitis, also called periodontosis or localized juvenile periodontitis (LJP), and generalized juvenile periodontitis which includes early onset adult periodontitis, recurrent necrotizing ulcerative periodontitis and the true generalized form of juvenile periodontitis. Periodontitis in systemically diseased individuals can be divided into three subgroups: juvenile periodontitis associated with primary neutrophil disorders, juvenile periodontal disease in which neutrophils are secondarily abnormal, and juvenile periodontitis associated with other diseases. Juvenile periodontitis is perhaps the best understood form of periodontal disease. A major infecting organism, Actinobacillus actinomycetemcomitans, is strongly associated with the disease, and may be an exogenous pathogen since it is not found in healthy individuals or in healthy sites in LJP patients. It is virulent with marked leukaggressive properties and it induces a marked antibody response in infected patients. Eradication of Actinobacillus actinomycetemcomitans requires attention to the fact that it invades the tissue and hence systemic antimicrobials or surgical excision of the tissues is necessary for eradication. Marked suppression of the organism from subgingival sites is associated with healing. Host responses in LJP have also been well described and most immune functions studied appear to be normal. The notable exception is neutrophil chemotaxis which is depressed. Associated with depressed neutrophil chemotaxis is a reduction of neutrophil receptors for several chemotactic factors including C5a, the fifth component of complement.(ABSTRACT TRUNCATED AT 250 WORDS)     

Adult periodontitis

The etiology and the pathogenesis, the diagnosis and the therapy of adult periodontitis (AP) are reviewed. Data from epidemiologic studies performed in recent years give a better knowledge of AP-progression. Successful long-term maintenance care give the proof that individual tooth preservation is life-long possible.