侵袭性牙周炎龈沟液中白介素-8 的检测

目的：检测侵袭性牙周炎（AgP）龈沟液中白细胞介素（IL-8）的总量和浓度并探讨其与牙周临床指标的关系。方法：采用常规滤纸条法收集侵袭性牙周炎实验组患牙（T1）和健康牙（T2）各位点及正常对照组（C）各位点的龈沟液（GCF）样本,用ELISA法检测各样本中IL-8的总量和浓度。结果：3组受检牙龈沟液中IL-8的总量和浓度不同。侵袭性牙周炎患牙组GCF中IL-8总量高于健康牙位组（P〈0．05）及正常对照组;而3组中IL-8浓度差异也有显著性,侵袭性牙周炎患牙组GCF中IL-8的浓度高于健康牙位组（P〈0．05）和正常对照组;虽然GCF中IL-8浓度与牙周探诊深度（PD）、牙龈出血指数（BOP）、附着丧失（AL）无相关关系;但IL-8总量与以上牙周临床指标相关。结论：在侵袭性牙周炎患者龈沟液中IL-8是参与牙周炎症反应的重要调节因子。     

慢性牙周炎龈沟液中白细胞介素-8与硫化物的相关关系

目的：探讨慢性牙周炎龈沟液（gingival crevicular fluid，GCF）中白细胞介素-8（interleukin-8，IL-8）与硫化物（suleus sulphide level，SUL）的关系。方法：采用双抗体夹心ELISA法、金刚牙周诊断仪对龈沟液中IL-8和硫化物的含量和临床指标进行测定。23个牙周健康牙作正常对照组（C），12个慢性牙周炎健康牙作实验组1（T1），30个慢性牙周炎患牙作实验组2（T2）。用标准化滤纸条采集观察牙位GCF样本，记录相应位点30’硫化物浓度，同时记录龈沟出血指数（SBI）、牙周袋探诊深度（PPD）、牙周附着丧失水平（CAL）。结果：①受检位点龈沟液中IL-8总量存在显著性差别，其中慢性牙周炎炎症牙位组IL-8总量高于健康牙位组、正常对照组（p〈0.05），但龈沟液中IL-8浓度无显著性差别。龈沟液中IL-8总量与SBI、PPD、CAL之间有明显相关关系（P〈0.05），但IL-8的浓度与临床指标间相关关系不明显。②慢性牙周炎炎症牙位组的硫化物浓度与健康牙位组、正常牙位组之间均有显著性差别（P〈0.05），慢性牙周炎健康牙位组与正常牙位组之间无显著性差别。③慢性牙周炎炎症牙位组硫化物浓度与临床指标间具正相关关系（P〈0.05），而健康牙位组和正常对照组硫化物浓度与临床指标间无相关关系。GCF中慢性牙周炎炎症牙位组的硫化物浓度与IL-8总量具负相关关系（P〈0．05），而慢性牙周炎健康牙位组和正常对照组的硫化物浓度与IL-8总量之间无相关关系。结论：慢性牙周炎患牙龈沟液中IL-8和硫化物的含量与临床指标之间有相关性。龈沟液中细菌代谢产物所产生的硫化物对IL-8的含量存在一定抑制作用。     

慢性牙周炎龈沟液中硫离子水平与临床相关性研究

目的:分析慢性牙周炎(CP)患者龈沟液中硫离子(su lfides)水平的变化与临床牙周指数的相关关系及其对诊断预后的意义。方法:采用金刚牙周诊断仪进行龈沟液硫离子和牙周临床指标测定。选定实验组(T):36例慢性牙周炎患者,57颗牙位,共342个位点。其中健康牙位(T1)21颗,位点126个;炎症牙位(T2)36颗,位点216。对照组(C):全身及牙周健康者8例,16颗牙位,共96个位点。测定所选位点龈沟液(GCF)中硫化物水平(su lcussu lph ide level,SUL),牙周袋探诊深度(prob ing depth,PD),牙周临床附着丧失水平(c lin ical attachm ent level,CAL),龈沟出血指数(su lcus b leed ing index,SB I)。所有统计结果均采用SPSS11.0进行统计学分析。结果:1)牙周健康对照组(C)GCF中硫离子SUL的浓度均值为(0.0648±0.0169)pg/mL,明显低于慢性牙周炎炎症牙位组(T2)(0.3249±0.0489)pg/mL及慢性牙周炎健康牙位组(T1)(0.1160±0.0271)pg/mL;慢性牙周炎炎症牙位组(T2)GCF中硫离子(SUL)的浓度均值均高于正常对照组及慢性牙周炎健康牙位组(T1)。2)经相关性分析,慢性牙周炎炎症牙位组(T1)GCF中SUL的浓度均值与PD、SB I和CAL均呈正相关关系。而慢性牙周炎健康牙位组(T1)及正常对照组(C)GCF中SUL的浓度均值与PD、SB I及CAL间无相关性。结论:慢性牙周炎(CP)炎症牙位组龈沟液中硫离子(SUL)的浓度均值与牙周临床指标之间具有相关关系,其水平的高低变化可客观反映牙周组织的炎症状态。     

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目的探讨血清和龈沟液中白细胞介素(IL)-6含量与绝经妇女牙周炎的关系。方法选择2010年8月至2011年1月广东省深圳市龙岗中心医院耳鼻咽喉科分院口腔科牙周炎初诊绝经女性患者20例(患牙20颗),检查并记录治疗前和治疗后4周患牙的牙龈指数(GI)、牙周探诊深度(PD)、附着丧失(AL),采集治疗前和治疗后4周患者的血清和患牙龈沟液并用酶联免疫吸附法(ELISA)测定其IL-6质量浓度。结果牙周基础治疗后患牙龈沟液中IL-6质量浓度较治疗前明显降低,差异有统计学意义(t=3.015,P<0.01);患者血清中IL-6阳性率在治疗前后的差异无统计学意义(χ2=1.056,P>0.05)。治疗后各项牙周指标(GI、PD、AL)均较治疗前降低,差异有统计学意义(均P<0.05)。结论牙周基础治疗对患牙周炎的绝经妇女牙周局部IL-6含量有影响,而对其血液IL-6含量无影响。     

牙龈卟啉单胞菌与龈沟液中白细胞介素8关系的研究

目的:探讨龈沟液(GCF)中白细胞介素8(IL -8)在慢性牙周炎病程中的变化、IL- 8与牙周临床检测指标以及同龈下菌斑中细菌含量的相关关系。方法: 5名非牙周炎患者的10颗牙周健康牙和30名慢性牙周炎(CP)患者的70颗牙(其中10颗为健康牙, 60颗为牙周炎患牙)纳入本研究。采集观察牙的GCF样本、龈下菌斑样本,同时记录所有牙的牙龈指数(GI)、牙周袋探诊深度(PPD)、临床附着丧失水平(CAL)。用ELISA法检测样本中IL -8的水平,用厌氧菌培养技术培养菌斑标本,用PCR法检测菌斑中的牙龈卟啉单胞菌(Pg),结果:慢性牙周炎组的GCF中IL -8的总量高于临床牙周健康组,而IL -8的质量浓度在各组中无差异。GCF中IL- 8浓度与GI、PPD、CAL无相关关系,而IL -8的总量与GI、PPD、CAL呈正相关关系。龈下菌斑中Pg的检出量与GCF中IL- 8的含量间未发现有相关关系。结论:慢性牙周炎患者龈沟液中IL- -8量增加与龈沟液分泌增加有关而与牙龈卟啉单胞菌检出CFU无关。     

慢性牙周炎治疗前后龈沟液中PGE2、IL-6、IL-8的变化

目的检测慢性牙周炎患牙龈沟液(GCF)中PGE2、IL-6、IL-8在治疗前后的浓度,探讨评价牙周治疗效果的指标.方法选择20例牙周炎患牙,用超声波治疗仪进行龈下刮治,检查治疗前、治疗后4周龈沟出血指数(SBI),并收集治疗前后的GCF,用ELISA检测其中PGE2、IL-6、IL-8的浓度.结果治疗前后SBI分别为2.87±0.52和1.32±0.28,P＜0.01;PGE2 浓度为254.86±123.60和157.78±129.06 (ng/ml),P＜0.05;而IL-6、IL-8的浓度没有显著性差异.结论经过彻底的牙周治疗后,GCF中PGE2浓度明显降低,IL-6、IL-8降低没有统计学意义,提示作为牙周治疗效果评价的指标,PGE2较IL-6、IL-8等更为敏感.     

侵袭性牙周炎龈沟液中硫化物的检测

目的:检测侵袭性牙周炎(AgP)龈沟液中硫化物浓度水平变化并探讨其与牙周临床指标的关系。方法:采用金刚牙周诊断仪进行龈沟液硫化物和牙周临床指标测定。选定实验组(T)16例侵袭性牙周炎病人,56个牙,共336个位点。其中健康牙(T1)16个,位点96个;炎症牙(T2)40个,位点240。对照组(C):全身、牙周健康者10例,20个牙,共120个位点。测定所选位点龈沟液(gingival crevicu lar flu id,GCF)中硫化物水平(su lcus su lph ide level,SUL),牙周袋探诊深度(pocket prob ing depth,PPD),牙周临床附着丧失水平(c lin i-cal attachm ent level,CAL),龈沟出血指数(su lcus b leed ing index,SB I)。结果:①3组受检牙龈沟液中硫化物浓度不同。侵袭性牙周炎炎症牙位组GCF中硫化物浓度(0.2210±0.0415)×10-6mol/L高于健康牙位组(P<0.05)、正常对照组;健康牙位组GCF中硫化物浓度(0.1025±0.0198)×10-6mol/L高于正常对照组(0.0523±0.0044)×10-6mol/L。②经相关性分析,侵袭性牙周炎炎症牙位组(T1)GCF中硫化物的浓度均值与PD、SB I和CAL均呈正相关关系,健康牙位组(T1)、正常对照组(C)GCF中硫化物浓度均值与PD、SB I及CAL无相关性。结论:侵袭性牙周炎病人龈沟液中的硫化物是参与牙周炎症反应的重要调节因子,其水平变化可反映牙周组织的炎症状态。     

牙周非手术治疗对重度慢性牙周炎患者龈沟液中C反应蛋白的影响

目的检测牙周基础治疗对慢性牙周炎患者龈沟液中C反应蛋白(CRP)的影响,为牙周病活动期诊断及判断牙周治疗的效果提供一定的客观依据。方法治疗前及治疗后1、3、6、12个月,用滤纸条收集30例重度慢性牙周炎患者的60个重度牙周炎牙位(探诊深度PD≥6 mm)和60个轻度牙周炎牙位(PD≤4 mm)的龈沟液并称重,用酶联免疫吸附测定法(ELISA)测定CRP的含量并记录牙周临床指标,15例牙周健康者的30个健康牙位作为对照。结果深牙周袋牙位的CRP在龈沟液中的浓度((968.06±360.54)pg/m L)显著高于浅牙周袋牙位((291.65±65.62)pg/m L),且疾病牙位的CRP浓度均显著高于健康牙位((33.47±24.53)pg/m L),龈沟液中CRP浓度与探诊深度(r=0.825,P<0.05)、附着丧失(r=0.833,P<0.05)、菌斑指数(r=0.741,P<0.05)呈正相关关系。同时,牙周基础治疗后沟液中CRP浓度明显降低,并且与口腔卫生情况有关。结论龈沟液中CRP浓度与牙周破坏程度有关,非手术治疗后龈沟液中CRP浓度下降。     

2型糖尿病合并慢性牙周炎患者血清与龈沟液瘦素水平的研究

目的 探讨2型糖尿病合并慢性牙周炎患者血清、龈沟液瘦素水平与临床指标的相关性。方法将60名受试者分成三组：DMCP组：2型糖尿病合并慢性牙周炎患者20人;CP组：慢性牙周炎患者20人;HC组：健康对照者20人。对所有受试者进行健康体检,同时用酶联免疫吸附测定法分别对所有受试者血清及龈沟液中的瘦素水平进行检测。结果 血清瘦素水平DMCP组最高[(4946.42±244.82) pg/ml],HC组最低[(3731.62±166.39) pg/ml],但三组之间血清的瘦素水平无显著差异（P> 0.05）。龈沟液瘦素水平DMCP组水平最低[(1554.37±161.28) pg/ml],HC组最高[(3868.87±128.99) pg/ml],同时三组龈沟液瘦素水平有显著差异（P<0.01）。血清瘦素水平与性别、BMI密切相关,龈沟液瘦素水平与多个牙周临床指标显著相关。结论 2型糖尿病合并慢性牙周炎患者血清瘦素水平与龈沟液瘦素水平呈现相反的变化趋势。血清瘦素水平与性别、BMI密切相关,龈沟液中的瘦素水平与牙周临床指标密切相关。     

活动期与静止期牙周炎患牙龈沟液中IL-10和IFN-Y的含量测定

目的：探讨IFN-γ和白细胞介素10（IL-10）与牙周炎活动期和静止期的关系。方法：应用ELISA免疫夹心法检测牙周炎活动期30个患牙和静止期30个患牙龈沟液（GCF）中IFN—γ和IL-10的含量。结果：活动期忠牙组龈沟液中IFN-γ的浓度（14．25±2．35ng／ml）显著高于静止期患牙组（4．36±0．41ng／ml,p〈0．05）,活动期患牙组龈沟液中IL-10的浓度（3．64±0．56ng／ml）显著低于静止期患牙组（11．26±3．05ng／ml,p〈0．05）。结论：作为Th1家族的细胞因子IFN-γ在牙周病灶区是占优势的,而Th2的代表性细胞因子IL-10则和牙周炎的缓解有关,IL-10／IFN-γ的高比值意味着牙周状况的改善。     

Biomarker levels in gingival crevicular fluid of subjects with different periodontal conditions: A cross-sectional study

ObjectiveTo compare five biomarker levels in gingival crevicular fluid (GCF) in different tooth-sites of subjects with healthy periodontium, aggressive periodontitis and severe chronic periodontitis, and to evaluate the value of these biomarker levels for diagnosis of the type and activity of periodontitis.Materials and methodsPrior to therapy, GCF samples were collected using filter paper strip at different tooth-sites of 10 subjects with healthy periodontium (H), 15 with severe chronic periodontitis (CP) and 15 with aggressive periodontitis (AgP). The strips were weighed and the periodontal clinical parameters were recorded. Levels of interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor-alpha (TNF-α), C-reactive protein (CRP), and alkaline phosphatase (ALP) in GCF were assessed by enzyme-linked immunosorbent assay (ELISA).ResultsThe volumes of the GCF samples obtained in CP and AgP subjects were significantly higher than those from subjects with healthy periodontium (P < 0.05). Levels of IL-6, TNF-α, CRP and ALP were significantly higher in the untreated disease sites in the CP and AgP groups compared to those in control sites in the H group, while IL-10 levels were lower in the CP and AgP groups than those in the control sites in the H group. However, the levels of all five biomarker levels showed significant correlation with the clinical parameters.ConclusionThe measurement of five biomarker levels in GCF may facilitate overall screening of periodontitis patients in epidemiological studies and allow estimation of periodontitis activity.     

Levels of interleukin-1 beta, -8, and -10 and RANTES in gingival crevicular fluid and cell populations in adult periodontitis patients and the effect of periodontal treatment

BACKGROUND: Various cytokines have been identified at sites of chronic inflammation such as periodontitis. Cytokines are synthesized in response to bacteria and their products, inducing and maintaining an inflammatory response in the periodontium. The purpose of the present study was to investigate the involvement of interleukin-1 beta (IL-1 beta), IL-8, and IL-10 and RANTES (regulated on activation, normally T cell expressed and secreted) and the cell populations associated with the immune response in destructive periodontitis, as well as the effect of periodontal therapy on cytokine levels in gingival crevicular fluid (GCF). METHODS: Data were obtained from 12 patients with moderate to advanced periodontitis and 6 healthy controls. Patients presenting at least 2 sites with > or =2 mm clinical attachment loss were included in the destructive periodontitis group. After monitoring for 4 months, only 6 patients showed destructive periodontitis and GCF samples and soft tissues biopsies were collected from these patients. GCF samples and biopsies were collected both from active (12 CGF samples and 6 biopsies) and inactive (12 CGF samples and 6 biopsies) sites. The comparison with healthy controls was carried out by collecting GCF samples from 6 healthy volunteers (12 samples) and biopsies during the surgical removal of wisdom teeth. In periodontal patients, clinical data and GCF samples were obtained prior to periodontal treatment (72 samples) and 2 months after periodontal therapy (72 samples). GCF was collected using a paper strip; eluted and enzyme-linked immunoabsorbent assays (ELISA) were performed to determine cytokine levels. The inflammatory infiltrate was analyzed by immunohistochemistry of gingival biopsy samples with monoclonal antibodies against CD3, CD8, CD4, CD11c, and CD19 antigens. RESULTS: Cellular components of the inflammatory infiltrate include B and T lymphocytes and monocyte/macrophages. Active sites contained a higher number of B lymphocytes and macrophages. IL-8 and IL-1 beta and RANTES in GCF were detected in the majority of sites from periodontal patients (100%, 94% and 87%, respectively); IL-10 was found in only 43%. IL-8 was the only cytokine detected in the GCF (75%) of the control group. Moreover, IL-1 beta levels were significantly higher in active sites versus inactive sites (P <0.05). IL-8 and IL-10 and RANTES were increased in active sites; however, differences were not significant (P>0.05). A positive correlation between the IL-8 and RANTES (r = 0.677, P<0.05) was observed in periodontitis patients. Periodontal therapy reduced the total amount of IL-1 beta, IL-8, and IL-10 and RANTES. Data showed a weak correlation between the clinical parameters and the total amount of cytokines in periodontitis. CONCLUSIONS: These data suggest that the amount of crevicular IL-1 beta, IL-8, and IL-10 and RANTES is associated with periodontal status. Removal of the bacterial plaque reduces the antigenic stimuli and consequently could modulate the chemokines present in GCF. We propose that the dynamic interactions between cytokines, their production rates, and their quantity could represent factors controlling the induction, perpetuation, and collapse of the cytokine network present in the periodontal disease.     

Levels of interleukin-17 in gingival crevicular fluid and in supernatants of cellular cultures of gingival tissue from patients with chronic periodontitis

BACKGROUND AND AIMS: Interleukin-17 (IL-17) is a T-cell-derived cytokine that may play an important role in the initiation or maintenance of the pro-inflammatory response and has recently been found to stimulate osteoclastic resorption. The purpose of the present study was to determine the presence of IL-17 in gingival crevicular fluid (GCF) samples and in the culture supernatants of gingival cells from patients with chronic periodontitis. METHOD: GCF samples were collected during 30 s from two sites in 16 patients from periodontally affected sites (probing depth > or =5 mm, attachment loss > or =3 mm). The comparison with healthy controls was carried out by collecting GCF samples from eight healthy volunteers. GCF was collected using a paper strip and ELISA was performed to determine the total amount of IL-17. Supernatant cellular cultures of gingival cells were obtained from periodontal biopsies taken from 12 periodontitis patients and from eight healthy control subjects during the surgical removal of wisdom teeth. Spontaneous and phytohaemagglutinin (PHA)-stimulated levels of IL-17 were determined by ELISA. RESULTS: The total amount of cytokine IL-17 was significantly higher in the periodontitis group than the control group (45.9 versus 35.6 pg, p=0.005). Significantly higher GCF volume and amount of total proteins were obtained from periodontitis patients as compared with control subjects (0.98 versus 0.36 microl, p=0.0005; 0.12 versus 0.05 microg, p=0.0005, respectively). A higher concentration of IL-17 was detected in culture supernatants from periodontitis patients compared with healthy subjects, either without stimulation (36.28+/-8.39 versus 28.81+/-1.50 microg/ml, p=0.011) or with PHA stimulation (52.12+/-14.56 versus 39.00+/-4.90 microg/ml, p=0.012). Treatment with PHA induced a significant increase in the production of IL-17 in healthy subjects and periodontitis patients (p=0.001 and 0.003). CONCLUSIONS: The total amount of cytokine IL-17 in GCF samples and in the culture supernatants of gingival cells are significantly increased in periodontal disease.     

Identification of the osteoprotegerin/receptor activator of nuclear factor-kappa B ligand system in gingival crevicular fluid and tissue of patients with chronic periodontitis

BACKGROUND AND OBJECTIVE: Recent findings have suggested that osteoclastogenesis is directly regulated by receptor activator of nuclear factor-kappa B ligand (RANKL) and its decoy receptor, osteoprotegerin (OPG). However, no studies have described interactions of OPG/RANKL and the gp130 cytokine family in periodontal disease. This study aimed to identify and quantify OPG/RANKL in the gingival crevicular fluid (GCF) and connective tissue of patients with periodontitis, and to clarify possible correlations with disease severity and interleukin-6 (IL-6) cytokines. MATERIAL AND METHODS: Ninety-five sites in 20 patients with generalized chronic periodontitis were divided into four groups by site based on probing depth (PD) and bleeding on probing (BOP). In periodontitis patients, GCF was obtained using sterile paper strips from clinically healthy sites (PD 6 mm with BOP, n = 27). Fourteen clinically healthy sites from four periodontally healthy individuals were used as the control group. The levels of OPG, RANKL and two gp130 cytokines - IL-6 and oncostatin M (OSM) - in the GCF were determined by an enzyme-linked immunosorbent assay (ELISA) and are expressed as total amounts (pg/site). Immunohistochemical localization of OPG- and RANKL-positive cells was also performed on gingival connective tissues harvested from patients with periodontitis (inflammatory group, n = 8 biopsies) and from non-diseased individuals (healthy group, n = 8 biopsies). RESULTS: GCF RANKL, but not OPG, was elevated in diseased sites of patients with periodontitis. However, the expressions of OPG and RANKL showed no correlation with disease severity (r = 0.174 and 0.056, respectively), but the content of RANKL in the GCF was significantly positively correlated with those of IL-6 (r = 0.207) and OSM (r = 0.231) (p < 0.01). Immunohistochemical staining showed that RANKL-positive cells were significantly distributed in the inflammatory connective tissue zone of diseased gingiva, compared with those of samples from non-diseased persons (p < 0.01). However, few OPG-positive cells were found in connective tissue zones of either the diseased gingiva or healthy biopsies. CONCLUSION: These findings imply that in this cross-sectional study of GCF, RANKL, IL-6 and OSM were all prominent in periodontitis sites, whereas OPG was inconsistently found in a few samples of diseased sites but was undetectable in any of the control sites. The results also imply that the expression of RANKL was positively correlated with IL-6 and OSM in the GCF.     

Soluble interleukin-1 receptor type II levels in gingival crevicular fluid in aggressive and chronic periodontitis

Background: Interleukin (IL)-1 is closely related to the initiation and progression of periodontal disease. IL-1 levels in the gingival crevicular fluid (GCF) of subjects with periodontitis are higher than those in periodontally healthy controls, and the levels of IL-1 correlate with disease severity. However, soluble IL-1 receptor type II (sIL-1RII), which acts as a decoy receptor for IL-1s, has not been investigated in detail in periodontal disease. The purpose of this study was to measure sIL-1RII levels in the GCF of subjects with chronic or aggressive periodontitis; the correlation between the sIL-1RII levels in GCF and clinical parameters also was examined. Methods: IL-1beta and sIL-1RII were measured in 64 GCF samples collected from 47 subjects with chronic periodontitis (CP) and 17 subjects with aggressive periodontitis (AgP). The clinical characteristics of each site were recorded at the time of GCF sampling. IL-1beta and sIL-1RII were measured by specific non-cross-reactive enzyme-linked immunosorbent assay. Results: The disease severity was comparable in CP and AgP. IL-1beta was detected in 98% of CP GCF samples and 88% of AgP GCF samples. sIL-1RII was detected in 55% of CP GCF samples and 35% of AgP GCF samples. However, the concentrations of IL-beta and sIL-1RII detected in GCF from subjects with CP or AgP were similar. Conclusion: sIL-1RII was detected more often in CP GCF than in AgP GCF, and there was no correlation between GCF sIL-1RII concentration and clinical parameters.     

Interleukin-1 and IL-1 receptor antagonist in gingival crevicular fluid

BACKGROUND/AIMS: This study aimed to investigate the cytokine IL-1beta and its receptor antagonist IL-1ra in gingival crevicular fluid (GCF), in patients with adult periodontitis. METHOD: A total of 40 GCF samples were harvested from 10 subjects with moderate to severe adult periodontitis and 10 healthy controls. Subjects were selected from both genders, with all the upper anterior teeth present, and with no relevant systemic illness, pregnancy or recent medication. All subjects were non-smokers and had not received any periodontal therapy within the preceding 3 months. Deep bleeding sites, deep non-bleeding sites and healthy sites were investigated in relation to upper anterior teeth. Clinical measurements were recorded for each site, after obtaining a GCF sample. IL-1beta and IL-1ra were quantified using new commercially available ELISA kits (Quantikine), and could be detected in all samples. RESULTS: The mean concentration for IL-1beta was 0.11 (SD 0.14) pg/microl for bleeding periodontitis sites, 0.04 (0.05) pg/microl for non-bleeding periodontitis sites, and 0.01 (0.03) pg/microl for healthy sites (p<0.001). In contrast, the mean concentration for IL-1ra was 6.99 (9.78) pg/microl for healthy sites, 0.59 (0.44) pg/microl for non-bleeding periodontitis sites, and 0.44 (0.36) pg/microl for bleeding periodontitis sites (p<0.001, except for comparisons between bleeding and non-bleeding periodontitis sites, p>0.05). For healthy sites, a strong inverse relationship was found between IL-1beta and IL-1ra levels in GCE. CONCLUSIONS: The results suggest a strong relationship between the severity of adult periodontitis and the increasing GCF levels of IL-1beta and decreasing levels of IL-1ra.     

Effect of non-surgical periodontal therapy on C-telopeptide pyridinoline cross-links (ICTP) and interleukin-1 levels

BACKGROUND: Biochemical markers harvested from gingival crevicular fluid (GCF) may be useful to identify and predict periodontal disease progression and to monitor the response to treatment. C-telopeptide pyridinoline cross-links (ICTP), a host-derived breakdown product specific for bone, and interleukin-1beta (IL-1), a potent bone-resorptive cytokine, have been associated with periodontal tissue destruction. The aim of this study was to examine the effect of non-surgical periodontal therapy on GCF levels of ICTP and IL-1. METHODS: Twenty-five chronic periodontitis subjects were monitored at 8 sites per subject at baseline prior to scaling and root planing and 1, 3, and 6 months after therapy. Four shallow (probing depths < 4 mm) and 4 deep (probing depths > or = 5 mm) sites were monitored for both marker levels and clinical parameters. GCF was collected for 30 seconds on paper strips, and levels of ICTP and IL-1 were determined using radioimmunoassay (RIA) and enzyme-linked immunosorbent assay (ELISA) techniques, respectively. Clinical measurements included probing depth (PD), clinical attachment level (CAL), and bleeding on probing (BOP). RESULTS: Deep sites exhibited significantly (P<0.001) higher ICTP and IL-1 levels compared to shallow sites at all time intervals. ICTP demonstrated a stronger association to clinical parameters than IL-1 including a modest correlation (r = 0.40, P<0.001) between ICTP and attachment loss. Significant improvements in PD, CAL, and BOP were observed at 1, 3, and 6 months in all sites (P<0.01). However, non-surgical mechanical therapy did not significantly reduce ICTP and IL-1 levels over the 6-month period. Further examination of subjects based on smoking status revealed that ICTP levels were significantly reduced at 3 and 6 months and IL-1 levels reduced at 3 months among non-smokers only. CONCLUSIONS: A single episode of non-surgical mechanical therapy did not significantly reduce biochemical markers associated with bone resorption in patients exhibiting chronic periodontitis. Future longitudinal studies are warranted to specifically evaluate the relationship between C-telopeptide pyridinoline cross-links and periodontal disease progression.     

Correlations between pentraxin 3 or cytokine levels in gingival crevicular fluid and clinical parameters of chronic periodontitis

The gingival crevicular fluid (GCF) contains various biomarkers, such as interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor-α (TNF-α), and IL-10, among others. These cytokines have been reported to correlate with gingival inflammation and periodontal status. Therefore, the analysis of GCF may be useful for the diagnosis of periodontal status. Pentraxin 3 (PTX3) is the first identified long pentraxin, and is released by several cell types in response to proinflammatory signals. The aim of this study was to determine the levels of IL-1β, IL-6, IL-8, TNF-α, IL-10 and PTX3 in GCF from diseased and healthy sites in patients with chronic periodontitis. Cross-sectional clinical data were obtained from 50 patients with chronic periodontitis. GCF samples were collected with paper strips from one periodontal diseased site and one periodontally healthy site per subject. The levels of IL-1β, IL-6, IL-8, IL-10 and TNF-α were determined using a multiplexed bead immunoassay, and the PTX3 level was measured using an enzyme-linked immunosorbent assay. Mean clinical parameters were significantly higher at diseased sites (P < 0.01) as compared to healthy sites, and the mean levels of PTX3, IL-1β, IL-6, IL-8, IL-10 and TNF-α were higher in diseased sites (P < 0.01) than in healthy sites. There were strong correlations between PTX3 or IL-1β and periodontal status. These results suggest that GCF PTX3 levels might be useful as a diagnostic marker for periodontal disease.     

牙周治疗前后龈沟液中白细胞介素-6水平的变化

目的：探讨牙周洁利治对患牙龈沟液中IL-6水平的影响。方法：选取12例成人牙周炎患者的重度牙周炎换牙12颗,采集治疗前患牙的龈沟液并记录相关的临床指标。然后对患牙进行龈上洁治和龈下刮治,两周后,再次采集患牙的龈沟液并记录相关的临床指标。采用双抗体夹心ELISA法对牙周炎患牙龈沟液中IL-6水平进行检测。比较牙周洁刮治前后龈沟液中IL-6水平的差异。结果：经过牙周洁刮治,患牙龈沟中IL-6的水平明显降低,同时患牙的牙周临床指标也有明显的改善。结论：牙周基础治疗在缓解牙周炎患牙局部炎症的同时,也对患牙局部的IL-6水平产生明显影响。     

Interleukin 1 and receptor antagonist levels in gingival crevicular fluid in heavy smokers versus non-smokers

BACKGROUND/AIMS: This study aimed to investigate the concentration of the cytokine interleukin (IL)-1beta and its receptor antagonist IL-1ra in gingival crevicular fluid (GCF) in patients with adult periodontitis who were heavy smokers compared with non-smokers. METHOD: GCF samples were collected from two groups of subjects: smokers and non-smokers. Thirty-nine GCF samples were harvested from 13 subjects with moderate to severe adult periodontitis who were heavy smokers. A further 30 GCF samples were harvested from 10 subjects with moderate to severe adult periodontitis who were non-smokers. Subjects were selected from both genders and none had any relevant systemic illness, were pregnant, had recent medication or had received any periodontal therapy in the preceding 3 months. One deep bleeding site, one deep non-bleeding site and one healthy site were investigated in each subject. Clinical measurements were recorded for each site, after obtaining a GCF sample using a Periopaper strip. IL-1beta and IL-1ra were quantified using new commercially available ELISA kits (Quantikine), and could be detected in all samples. RESULTS: For smokers, the mean concentrations for IL-1beta were 2714.5 (SD 4416.2) pg/ micro L for healthy sites, 37.0 (SD 57.2) pg/ micro L for non-bleeding periodontitis sites and 24.5 (SD 29.2) pg/ micro L for bleeding periodontitis sites. The concentrations of IL-1beta for non-smokers for the same category of sites were 393.8 (SD 867.1), 74.2 (SD 107.0) and 73.1 (SD 61.0) pg/ micro L, respectively. The mean concentrations of IL-1ra for smokers were 5.8 x 10(5) (SD 9.7) pg/ micro L for healthy sites, 2.2 x 10(5) (SD 0.15) pg/ micro L for deep non-bleeding sites and 0.19 x 10(5) (SD 0.07) pg/ micro L for deep bleeding sites. The concentrations for non-smokers were: 4.1 x 10(10) (SD 3.8), 18.1 x 10(5) (SD 20.4) and 3.2 x 10(5) (SD 2.3) pg/ micro L, respectively. Significance levels of P < 0.05 were found for comparisons of healthy vs. deep bleeding and deep non-bleeding sites for IL-1beta and IL-1ra in smokers, before adjustments for multiple testing. However, none of these comparisons reached statistical significance following adjustments for multiple testing. P < 0.05 for the correlation between IL-1beta and IL-1ra at healthy sites in smokers only. Differences in GCF concentrations for IL-1beta in smokers vs. non-smokers were significant for deep bleeding sites only (P < 0.05), the mean concentration of IL-1beta being lower in GCF from smokers vs. non-smokers. All differences in GCF concentrations of IL-1ra reached statistical significance for smokers vs. non-smokers. The mean concentrations of IL-1ra in GCF were lower in smokers compared with non-smokers for all categories of sites. CONCLUSIONS: A decreased concentration of IL-1beta and also IL-1ra was found in GCF from periodontitis sites compared to healthy sites in smokers and in non-smokers, although this did not reach statistical significance following adjustments for multiple testing. For comparisons between heavy smokers and non-smokers, statistically significant differences were found in the GCF concentrations of IL-1beta from deep bleeding sites only. Statistically significant differences were found in the IL-1ra concentrations for smokers vs. non-smokers for all categories of sites.