不同fimA基因型牙龈卟啉单胞菌刺激上皮细胞表达细胞因子的比较

目的比较不同fimA基因型牙龈卟啉单胞菌（Porphyromonas gingivalis,P.gingivalis）刺激下口腔上皮细胞表达细胞因子的水平。方法P.gingivalis ATCC33277（IfimA）,W83（ⅣfimA）,47A-1（ⅣfimA）分别与KB细胞ATCCCCL17共同孵育6h,在3h和6h收集细胞和培养上清液。逆转录-聚合酶链式反应检测KB细胞IL-8,IL-6,IL-1βmRNA的表达,酶联免疫反应检测培养上清液中IL-8,IL-6,IL-1β的变化。结果3h时,ⅣfimA组IL-6蛋白水平低于IfimA组（P〈0.05）,6h时,ⅣfimA组IL-6和IL-8蛋白水平均低于ⅠfimA组（P〈0.05）;IL-8,IL-6mRNA和蛋白水平表达不一致,提示存在转录后水平的调节。3h,6h时,IL-1β对P.gingvalis刺激不敏感,mRNA和蛋白表达水平都很低。结论P.gingivalis fimA基因型与上皮细胞表达细胞因子的水平相关,提示P.gingivalis致病性与其fimA基因型相关。     

牙周炎伴COPD患者血清25-（OH）D、TNF-α和IL-6水平检测的研究

目的：探讨慢性牙周炎与慢性阻塞性肺疾病（chronic obstructive pulmonary disease,COPD）患者的血清25-（OH）D、TNF-α和IL-6水平变化及相互关系。方法：收集符合条件的COPD伴牙周炎患者[（C＋P）组]20例,单纯慢性牙周炎患者（P组）20例,同期门诊随诊的健康对照组（H组）20例。采集临床指标并采用ELISA法检测3组受试者血清25-（OH）D、TNF-α和IL-6的含量。结果：各组间牙周病指数有显著性差异。（C＋P）组与P组、H组相比,TNF-α和IL-6水平明显升高,差别有统计学意义（P〈0.05）;25-（OH）D水平较低,但差别无统计学意义。等级相关性分析结果显示H组血清25-（OH）D与IL-6呈负性相关关系（P〈0.05）,C＋P组血清25-（OH）D与Tnf-α呈负性相关关系（P〈0.05）。结论：25-（OH）D、TNF-α和IL-6可能与牙周炎和COPD病理机制相关,牙周炎和COPD之间存在一定的关联。     

Ⅱ型糖尿病合并牙周病患者龈沟液中细胞因子/趋化因子的表达水平

目的 探讨Ⅱ型糖尿病合并牙周病患者与单纯牙周病患者龈沟液（gingival crevicular fluid,GCF）中细胞因子/趋化因子的表达水平。 方法 选取伴Ⅱ型糖尿病的牙周病患者52例,单纯牙周病患者40例,用Luminex FLEXMAP3D仪和Human Cytokine/Chemokine试剂盒检测GCF中14种细胞因子/趋化因子的表达水平。 结果 牙周病部位：嗜酸性粒细胞趋化因子、巨噬细胞炎症蛋白-1α、粒细胞-巨噬细胞集落刺激、白介素-6、肿瘤坏死因子-α和白介素-12的浓度,糖尿病组受试者高于非糖尿病组受试者（P<0.0035）。 结论 糖尿病可影响牙周病部位细胞因子/趋化因子的表达,糖尿病可能是牙周病的促进因素。     

白介素-6与口腔鳞状细胞癌关系的研究进展

细胞因子是当代免疫学研究的重要领域。随着技术的进步及研究的深入,越来越多的新型细胞因子被发现,越来越多的细胞因子的新功能被证实。白介素6（IL-6）属于细胞因子家族,IL-6具有复杂的生物学功能,IL-6在机体免疫应答、血细胞生成、炎症反应以及促进肿瘤细胞生长中起重要作用。     

补肾固齿丸对人牙周膜成纤维细胞分泌白细胞介素-6的影响

牙周病是在致病菌和宿主免疫反应失衡情况下发生的感染性疾病。多种炎性介质和细胞因子参与了牙周病的发生发展过程,其中白细胞介素-6（interleukin-6,IL-6）是一种重要的细胞因子,其分泌增多时会产生明显的致炎作用。牙周膜成纤维细胞（periodontal ligament cell,PDLC）是牙周组织中合成分泌IL-6的重要细胞,在受到细菌刺激时,合成分泌IL-6的能力增强。     

3种牙科合金对龈沟液中IL-6和TNF-α表达的影响

目的：探讨3种牙科合金对局部龈沟液中肿瘤坏死因子（TNF-α）以及白介素-6（IL-6）表达的影响.方法：制作全冠（钴铬合金、镍铬合金、金合金）,在修复后第一个月和第六个月,用WhatmanⅠ号滤纸采集龈沟液（gingival crevicular fluid,GCF）样本.用ELISA法测定GCF中Interleukin-6（IL-6）和Tumeo Necrosis factor-α（TNF-α）的含量.结果：对TNF-α的影响,修复后1个月3种材料之间相比,没有显著性差别;修复后6个月钴铬合金相对于镍铬合金、金合金引起TNF-α分泌量增加.而3种全冠都没有引起IL-6分泌量的显著增加.结论：不同的牙科合金材料对龈沟液中某些细胞因子的含量有影响.     

IL-6、IL-33、IL-10在牙周炎和类风湿关节炎中的表达和相关性分析

目的: 检测牙周炎和类风湿关节炎患者龈沟液中白介素6（interleukin-6,IL-6）、白介素33（interleukin-33,IL-33）、白介素10（interleukin-10,IL-10）的含量,并探讨IL-6、IL-33、IL-10与牙周炎和类风湿关节炎2种疾病的相关关系。方法: 按纳入标准,选取就诊于中国医科大学附属盛京医院口腔科及风湿免疫科的患者,其中牙周炎组21例（PD组）,类风湿关节炎组21例（RA组）,类风湿关节炎合并牙周炎组24例（PD + RA组）,健康对照者24例（H组）。记录4组受试者一般信息、牙周探诊深度（periodontal probing depth,PPD）、临床附着丧失（clinical attachment loss,CAL）、龈沟出血指数（sulcus bleeding index, SBI）。收集各组受试者龈沟液样本,应用酶联免疫吸附试验测定IL-6、IL-33、IL-10的含量,并对4组受试者IL-6、IL-33、IL-10含量与牙周指标进行相关性分析。采用SPSS 20.0 软件包对数据进行统计学分析。结果: IL-6在PD+RA组的表达水平显著高于H组、PD组和RA组（P<0.05）; PD组、RA组、PD+RA组IL-33的含量显著高于H组（P<0.05）,PD+RA组IL-33的含量显著高于RA组(P<0.05);RA组IL-10的表达水平显著高于H组、PD组和PD+RA组(P<0.05)。PD组PPD与IL-6、IL-33的含量呈正相关（r=0.62, 0.43）,PD+RA组SBI、PPD、CAL与IL-33含量呈正相关（r=0.69,0.58,0.55）。结论: 牙周炎伴发类风湿关节炎患者龈沟液中IL-6、IL-33水平显著升高,IL-10含量显著降低,推测IL-6、IL-33和IL-10在牙周炎和类风湿关节炎的发生、发展中具有重要作用。     

牙周病与慢性阻塞性肺病的联系

牙周病作为一种慢性感染性疾病与许多全身性疾病有着密切的联系。对于慢性阻塞性肺病（chronic obstractive pulmonarg discases，COPD），牙周病作为局部病灶可以促进其发生与发展。本文就牙周病对COPD的影响途径、两者间的流行病学调查，以及一些细胞因子对两者的作用机制做一综述。     

IL-1β对人牙龈成纤维细胞在不同钛板表面表达炎性因子的影响

目的 :探讨白介素1β对不同钛板表面牙龈成纤维细胞分泌炎性因子的影响。方法 :将牙龈成纤维细胞接种在3种不同表面结构组分的钛板上,在白介素1β的刺激下,在3、6、24 h分别用聚合酶链反应(PCR)检测炎性因子白介素6及白介素8的表达量。采用SPSS13.0软件包对数据进行统计学分析。结果:在白介素1β的诱导下,牙龈成纤维细胞对炎性因子(IL-6、IL-8)的表达量明显增加;纯钛与钛合金的钛板比表面氮化处理的钛板产生炎性因子(IL-6、IL-8)的表达量较少。结论 :白介素1β能刺激炎性因子的高表达;纯钛和钛合金IL-6、IL-8表达量较少。采用纯钛和钛合金种植体,可减少种植体周围炎的发生率,提高种植成功率。     

炎症因子白介素-6对骨细胞表达RANKL的影响

目的 :通过研究炎症因子白介素-6对骨细胞表达核因子-κB受体活化因子配基(RANKL)的影响,为更好地理解炎症因子在骨细胞参与骨重塑中的作用,提供理论基础。方法:体外培养MLO-Y4细胞系细胞,并应用不同浓度的人工合成白介素-6(IL-6)和白介素-6受体(IL-6R),共同作用刺激骨细胞24 h后,采用实时荧光定量PCR、免疫印迹试验、免疫荧光等方法,检测RANKL以及酪氨酸激酶2(JAK2)的磷酸化蛋白的表达变化。结果:应用不同浓度人工合成的IL-6和IL-6R,共同作用刺激骨细胞后,RANKL的表达水平随着IL-6的浓度增加而增加,并且IL-6通路中的JAK2蛋白磷酸化亦增加,提示IL-6及其受体可以促进骨细胞表达RANKL,并且与JAK2的活化密切相关。结论 :炎症因子IL-6可以通过增加JAK2蛋白的磷酸化,来促进骨细胞表达RANKL。     

Cigarette smoking, periodontal disease: and chronic obstructive pulmonary disease

BACKGROUND: Cigarette smoking is a significant risk factor for both chronic obstructive pulmonary disease (COPD) and periodontal disease. The goal of this study was to better understand the role of smoking in a possible relationship between periodontal disease and COPD. METHODS: The study population consisted of 7,625 participants in the Third National Health and Nutrition Examination Survey (NHANES III) during 1988-1994 who were aged 30 years or older when examined and who received a spirometric examination. The data analysis employed logistic regression models and accounted for the complex sampling design used in NHANES III. RESULTS: After adjustment for potential confounders, there was no statistically significant association between periodontal disease and COPD among former or non-smokers. Current smokers with > or = 4 mm mean loss of attachment had an odds ratio of 3.71 (95% confidence interval: 1.74, 7.89). CONCLUSIONS: These results suggest that cigarette smoking may be a cofactor in the relationship between periodontal disease and chronic obstructive pulmonary disease. The key role played by smoking in the etiology of both periodontal disease and chronic obstructive pulmonary disease suggests that much of the observed increase in risk may actually reflect the exposure to smoking. Additional research into smoking-related effect modification is needed to clarify the role of periodontal disease in the etiology of smoking-related systemic diseases.     

The immunopathogenic and immunomodulatory effects of interleukin‐12 in periodontal disease

Interleukin 12 (IL‐12) is an inflammatory cytokine that promotes the response of the immune system. This cytokine has been implicated as a potent stimulator of several diseases characterized by inflammatory‐induced bone destruction, such as rheumatoid arthritis and periodontitis. Yet, the exact role of IL‐12 in the development and progress of periodontitis has not been clarified. Several studies have demonstrated a positive correlation between the level of IL‐12 and the severity of periodontal destruction. Deletion of IL‐12 in mice with periodontitis significantly suppressed the level of bone destruction. Interestingly, next to a role in modulating the pathogenesis, IL‐12 also has immunological‐regulatory properties. This cytokine induces expression of immunosuppressive molecules, such as indoleamine‐pyrrole 2,3‐dioxygenase (IDO). Thus, these findings suggest both negative and positive influences of IL‐12 in periodontal disease. It is currently proposed that the diversity of action of cytokines is a molecular key which regulates biological development and homeostasis. Accordingly, the actions of IL‐12 might be one of the mechanisms that regulate homeostasis of periodontal tissue during and following inflammation. Therefore, this article aims to review both destructive and protective functionalities of IL‐12 with an emphasis on periodontal disease.     

Epidemiologic associations between periodontal disease and chronic obstructive pulmonary disease

The nature of the relationship of periodontal disease to a number of systemic health outcomes, including chronic obstructive pulmonary disease (COPD), remains unclear. Various causal mechanisms have been proposed to explain the observed epidemiologic associations between periodontal diseases and respiratory diseases. We have reviewed the epidemiologic and clinical evidence for this association. The methodologic approach we have taken is based on a structured systematic review of the indexed biomedical literature on these subjects. The primary focus of this review was on the analysis of periodontal health status measures and their association with COPD, which includes chronic bronchitis and emphysema. We found that a paucity of published results exist on this specific relationship and those which do exist typically represent secondary analyses of existing data sets. Nevertheless, the epidemiologic evidence identified in this systematic review indicates that worse periodontal health status is associated with an increased risk of COPD, with odds ratios ranging from 1.45 to 4.50 (significant at the 95% confidence interval). However, it is possible that residual confounding by tobacco smoking may account in part for the observations. A causal association between periodontal health status and risk of COPD, although biologically plausible, remains speculative. Randomized controlled trials will be required in order to address the question of causality and to better understand the biological basis of these epidemiologic associations.     

Diabetes and periodontal disease

Epidemiological data demonstrate a clear link between periodontal disease and diabetes, and individuals with diabetes, particularly if poorly controlled, are at risk for advanced periodontitis. Diabetes is increasingly viewed as an inflammatory condition and dysregulated immune‐inflammatory responses in diabetes may increase susceptibility to periodontal disease by disrupting local cytokine networks in the periodontium. Inflammatory cytokines such as interleukin‐6 (IL‐6) and tumour necrosis factor‐α (TNF‐α) are important in the pathogenesis of both diseases, and together with other pro‐inflammatory cytokines and adipokines, may provide a mechanistic link between the two diseases. Altered neutrophil function and deposition of advanced glycation end‐products (AGEs) are also likely to be important in the increased susceptibility to periodontal disease seen in people with diabetes. Emerging data suggest that treating periodontal disease may have a beneficial effect on glycaemic control, and highlight the need to incorporate a full periodontal examination into management strategies for patients with diabetes. It is clear that the dental team must become increasingly involved in the management of patients with diabetes, and it is recommended that periodontal screening of all patients diagnosed with diabetes is undertaken as a matter of routine.     

牙周病与肺部感染的关系

牙周病不仅破坏局部牙齿支持组织，亦可影响许多全身性疾病。近年来，牙周病与肺感染的关系逐渐引起人们的重视。本文就牙周病与肺炎(尤其是重症卧床老年人的院内获得性肺炎)及慢性阻塞性肺病(COPD)之间的潜在联系作一综述。     

The contribution of interleukin-1 and tumor necrosis factor to periodontal tissue destruction

Interleukin (IL)-1 and tumor necrosis factor (TNF) represent proinflammatory cytokines that stimulate a number of events which occur during periodontal disease. These include the induction of adhesion molecules and other mediators that facilitate and amplify the inflammatory response, the stimulation of matrix metalloproteinase, and bone resorption. The activity of these cytokines coincides with the critical events that occur during periodontal disease, namely, loss of attachment and bone resorption. The use of antagonists to IL-1 and TNF in experimental periodontitis have demonstrated a cause-and-effect relationship between the activity of these cytokines and the spread of an inflammatory front to deeper areas in the connective tissue, loss of connective tissue attachment, osteoclast formation, and loss of alveolar bone. In addition, the loss of fibroblasts that occurs during infection with periodontal pathogens is, in part, mediated by TNF. Thus, much of the damage that occurs during periodontal tissue destruction can be attributed to IL-1 and TNF activity. This destruction may very well represent an overreaction of the host response to periodontal pathogens caused by excessive production of IL-1 and TNF.     

Expression of periodontal interleukin‐6 protein is increased across patients with neither periodontal disease nor diabetes,patients with periodontal disease alone and patients with both diseases

Ross JH, Hardy DC, Schuyler CA, Slate EH, Mize TW, Huang Y. Expression of periodontal interleukin‐6 protein is increased across patients with neither periodontal disease nor diabetes, patients with periodontal disease alone and patients with both diseases. J Periodont Res 2010; 45: 688–694. © 2010 John Wiley & Sons A/S Background and Objective: Epidemiological studies have established that patients with diabetes have an increased prevalence and severity of periodontal disease. Interleukin (IL)‐6, a multifunctional cytokine, plays a role in the tissue inflammation that characterizes periodontal disease. Our recent study has shown a trend of increase in periodontal IL‐6 expression at the mRNA level across patients with neither periodontal disease nor diabetes, patients with periodontal disease alone and patients with both diseases. However, the periodontal IL‐6 expression at the protein level in these patients has not been investigated. Material and Methods: Periodontal tissue specimens were collected from eight patients without periodontal disease and diabetes (group 1), from 17 patients with periodontal disease alone (group 2) and from 10 patients with both periodontal disease and diabetes (group 3). The frozen sections were prepared from these tissue specimens and IL‐6 protein expression was detected and quantified. Results: The nonparametric Kruskal–Wallis test showed that the difference in IL‐6 protein levels among the three groups was statistically significant (p = 0.035). Nonparametric analysis using the Jonckheere–Terpstra test showed a tendency of increase in periodontal IL‐6 protein levels across group 1 to group 2 to group 3 (p = 0.006). Parametric analysis of variance (ANOVA) on IL‐6 protein levels showed that neither age nor gender significantly affected the difference of IL‐6 levels among the groups. Conclusion: Periodontal IL‐6 expression at the protein level is increased across patients with neither periodontal disease nor diabetes, patients with periodontal disease alone and patients with both diseases.     

Potential associations between chronic respiratory disease and periodontal disease: analysis of National Health and Nutrition Examination Survey III

BACKGROUND: Associations between poor oral health and chronic lung disease have recently been reported. The present study evaluated these potential associations by analyzing data from the National Health and Nutrition Examination Survey III (NHANES III), which documents the general health and nutritional status of randomly selected United States subjects from 1988 to 1994. METHODS: This cross-sectional, retrospective study of the NHANES III database included a study population of 13,792 subjects > or = 20 years of age with at least 6 natural teeth. A history of bronchitis and/or emphysema was recorded from the medical questionnaire, and a dichotomized variable combined those with either chronic bronchitis and/or emphysema, together considered as chronic obstructive pulmonary disease (COPD). Subject lung function was estimated by calculating the ratio of forced expiratory volume (FEV) after 1 second (FEV1)/forced vital capacity (FVC). Oral health status was assessed from the DMFS/T index (summary of cumulative caries experience), gingival bleeding, gingival recession, gingival probing depth, and periodontal attachment level. Unweighted analyses were used for initial examination of the data, and a weighted analysis was performed in a final logistic regression model adjusting for age, gender, race and ethnicity, education, income, frequency of dental visits, diabetes mellitus, smoking, and alcohol use. RESULTS: The mean age of all subjects was 44.4 +/- 17.8 years (mean +/- SD): COPD = 51.2 +/- 17.9 years and subjects without COPD = 43.9 +/- 17.7 years. Subjects with a history of COPD had more periodontal attachment loss than subjects without COPD (1.48 +/- 1.35 mm versus 1.17 +/- 1.09 mm, P = 0.0001). Subjects with mean attachment loss (MAL) > or = 3.0 mm had a higher risk of COPD than those having MAL < 3.0 mm (odds ratio, 1.45; 95% CI, 1.02 to 2.05). A trend was noted in that lung function appeared to diminish with increasing periodontal attachment loss. CONCLUSIONS: The findings of the present analysis support recently published reports that suggest an association between periodontal disease and COPD.