类风湿关节炎伴牙周炎患者血清龈沟液中白介素18检测及意义

目的本研究通过观察白介素18(IL-18)在慢性牙周炎(CP)及类风湿关节炎(RA)患者血清及龈沟液中浓度的改变探讨类风湿性关节炎与牙周炎的关系。方法采用双免疫酶联法检测16例健康志愿者、20例牙周炎患者、21例类风湿关节炎患者、26例牙周炎伴类风湿关节炎患者血清及牙龈沟液中IL-18的含量。记录四组患者的牙龈出血指数(BI)、牙周探诊深度(PD)、临床附着丧失(CAL)水平。结果龈沟液中IL-18水平RA+CP组(221.83±43.38)pg/m L高于CP组(198.00±37.72)pg/m L,RA组(138.10±23.16)pg/m L和HP组(135.12±27.11)pg/m L且与各组之间差异均具有统计学意义(p<0.05);血清中IL-18水平在CP+RA组(321.02±260.57)pg/m L,CP组(220.60±228.37)pg/m L,RA组(186.29±253.03)pg/m L,HP组(169.56±143.82)pg/m L间呈现降低趋势,CP+RA组与HP组差异具有统计学意义。结论类风湿性关节炎与牙周炎之间可能存在相关性,而IL-18可能是联系两者的生物学基础之一。     

慢性牙周炎龈沟液中KGF-1含量检测及其意义

目的：检测慢性牙周炎患者牙周基础治疗前及治疗后不同时期龈沟液中角质细胞生长因子（keratinocytegrowth factor,KGF）-1的质量浓度,探讨KGF-1与牙周炎的关系及其在牙周炎发病机理、病情进展方面的作用。方法：用滤纸条浸润法采集牙周健康者和慢性牙周炎患者治疗前后不同时期的龈沟液样本,用酶联免疫吸附测定法检测样本中KGF-1的质量浓度。结果：慢性牙周炎患者龈沟液中KGF-1的质量浓度高于健康对照组（P〈0.05）,牙周基础治疗后第4、6、8周复查,KGF-1的质量浓度低于治疗前,且治疗后不同时期的复查结果与治疗前相比,均有统计学意义（P〈0.05）,KGF-1的质量浓度与牙周探诊深度（PD）、附着丧失（AL）、龈沟出血指数（SBI）存在正相关。结论：龈沟液中KGF-1水平与牙周炎症密切相关,KGF-1可作为反映牙周状态的客观指标。     

牙周炎患者非刺激性全唾液、龈沟液及血清中CD147的表达及意义

目的研究发现CD147可能参与调节牙周疾病的进展过程,因而评估牙周炎患者经牙周基础治疗前后和健康者的非刺激性全唾液、龈沟液及血清中CD147水平,探讨其与牙周炎的相关性以及作为牙周炎诊断及预后标志物的可能性。方法酶联免疫吸附试验(ELISA)检测20例牙周炎患者治疗前、后及20名健康人非刺激性全唾液、龈沟液及血清中CD147的水平,并记录牙周袋探诊深度(PD)、附着丧失(AL)和出血指数(BI)。结果经牙周基础治疗6周后,牙周炎患者的临床指标除AL外BI及PD均低于治疗前(P<0.05);治疗后非刺激性全唾液、龈沟液及血清中CD147水平明显降低,与治疗前相比差异具有统计学意义(P<0.05);除血清外,牙周炎患者治疗前、后的非刺激性全唾液和龈沟液中CD147水平仍高于健康对照组,其差异有统计学意义(P<0.05)。结论牙周炎患者、健康者的非刺激性全唾液及龈沟液中均有CD147表达,并随牙周炎症减轻CD147表达降低。     

牙周炎患者龈沟液中乳酸脱氢酶水平分析

目的：探讨龈沟液中乳酸脱氢酶（ＬＤＨ）水平对于慢性成人牙周炎患者诊断及预后观察的意义。方法：酶动力学方法。结果：患病部位和健康部位龈沟液中ＬＤＨ水平有非常显著差异（Ｐ〈０．００１）。探诊深度和龈沟液中ＬＤＨ水平呈正相关（Ｐ〈０．０５）。附着丧失水平和龈沟液中ＬＤＨ水平呈正相关（Ｐ〈０．０５）。结论：龈沟液中ＬＤＨ水平对于慢性成人牙周炎的诊断和疗效监测具有一定的临床意义。     

牙周炎患者龈沟液中的碱性磷酸酶水平

选择慢性期牙周炎患者２０人５５个牙，健康者５人１０个牙，用滤纸条采集龈沟液并以全自动生化分析仪测出碱性磷酸酶水平。同时记录牙龈指数、探诊深度和附着水平。结果表明ＡＬＰ活性水平与临床数呈正相关，提示牙周炎及齿沟中ＡＬＰ水平可能反映牙周组织的破坏程度。     

慢性牙周炎患者龈沟液中白细胞介素-4的检测和意义

目的检测慢性牙周炎患者牙周基础治疗前后龈沟液中白细胞介素-4(IL-4)的质量浓度,探讨IL-4与牙周炎的关系及其在牙周炎发病机制、病情进展等方面所起的作用。方法用滤纸条浸润法采集成年健康者和牙周炎患者治疗前后的龈沟液样本,用酶联免疫吸附测定检测样本中IL-4的质量浓度。结果慢性牙周炎患者龈沟液中IL-4的质量浓度低于健康对照组(P<0.05)。经牙周基础治疗1个月后,IL-4的质量浓度无明显变化,治疗前后的差异无统计意义(P>0.05);IL-4的质量浓度与探诊深度呈显著负相关,与牙龈指数和附着丧失无明显相关性。结论IL-4缺乏可能会导致牙周病的发生,IL-4可作为早期诊断牙周病和检测易患人群的敏感性指标。     

牙周炎患者龈沟液中IL—8的含量测定

目的：研究IL－8在牙周炎病程中的变化及与临床指标的关系,方法：采用双抗夹心ABC－ELISA法测定慢性牙周炎（CP）患者,健康对照者以及CP治疗前后患者的龈沟液中IL－8含量,IL－8总量,同时检测临床指标并作相关性检验。结果：CP患者龈沟液中IL－8检出率显著高于健康对照者（P＜0．025）,在CP患者和健康者之间以及CP治疗前后患者的龈沟液中IL－8总量,龈沟液（GCF）量均存在统计学差异（分别为P＜0．01,P＜0．05）,而IL－8含量无统计学差异（P＞0．05）,IL－8总量,GCF量与临床指标存在正相关性（P＜0．01）,结论：IL－8总量在牙周炎病程中呈动态性改变,检测GCF中IL－8的水平对评价牙周炎的程度及指导临床治疗有一定价值。     

牙周炎大鼠龈沟液中β防御素浓度的检测

目的：通过建立大鼠的牙周炎模型,检测β防御素在牙周健康大鼠和慢性牙周炎大鼠龈沟液中浓度的变化,探讨β防御素与牙周炎的关系.方法：结扎法建立慢性牙周炎大鼠（20只）模型,分别采集结扎前,结扎后第2,4,6周末4组龈沟液（gingival crevicular fluid,GCF）样本,首先用ELISA方法检测β防御素总蛋白的浓度,然后应用蛋白质印迹法分别检测β防御素1,2的蛋白表达,并傲半定量分析.利用SPSS 16.0统计软件进行单因素方差分析,P＜0.05为差异有统计学意义.结果：临床观察慢性牙周炎大鼠模型的形成过程,在第2周末牙龈炎形成期龈沟液β防御素蛋白与β-防御素2浓度与结扎前均明显上升（P＜0.05）;在第4,6周末牙周炎期,两者的表达强度又明显降低（P＜0.01）;β-防御素1浓度随时间未见明显改变（P＞0.05）.结论：β防御素总蛋白与β-防御素2浓度在牙周炎大鼠的龈沟液（GCF）中两者的浓度显著上升后又降低,提示两者可与慢性牙周炎的病程和致病机制密切相关.     

三种牙周炎患者龈沟液中IL—8的检测

目的：探讨ＩＬ－８与不同种类牙周炎的关系，比较三种牙周炎，即青少年牙周炎（ｊｕｖｅｎｉｌｅｐｅｒｉ－ｏｄｏｎｔｉｔｉｓ，ＪＰ），快速进展型牙周炎（ｒａｐｉｄｐｒｏｇｒｅｓｓｉｖｅｐｅｒｉｏｄｏｎｔｉｔｉｓ，ＲＰＰ）和成人牙周炎（ａｄｕｌｔｐｅｒｉｏｄｏｎｔｉｔｉｓ，ＡＰ）龈沟液（ｇｉｎｇｉｖａｌｃｒｅｖｉｃｕｌａｒｆｌｕｉｄ，ＧＣＦ）中ＩＬ－８浓度和检出率。方法：采集ＪＰ、ＲＰＰ和ＡＰ患者ＧＣＦ，用ＥＬＩＳＡ法对ＧＣＦ中ＩＬ－８进行检测。结果：ＡＰ患者ＧＣＦ中ＩＬ－８检出率为６７．８５％，明显高于ＪＰ组、ＲＰＰ组的检出率（分别为３４．４８％、２５％）；ＧＣＦ中ＩＬ－８浓度无明显差别。结论：ＪＰ、ＲＰＰ患牙ＧＣＦ中ＩＬ－８检出率低可能是造成此种牙周炎局部中性粒细胞趋化异常的原因之一。     

洁治和根面平整术对冠心病合并牙周炎患者血清及龈沟液中白介素-1β的影响

目的：探讨洁治和根面平整术对冠心病伴牙周炎患者血清及龈沟液中白介素-1β的影响。方法：选取50名患有冠心病并伴发中、重度慢性牙周炎的中老年患者（CHD组）、40名单纯中、重度慢性牙周炎患者（CP组）及50名健康者（H组）,对CHD组和CP组实施洁治和根面平整治疗,进行基线及治疗后1个月的牙周专科检查、采集血清及龈沟液;采用酶联免疫吸附法测定IL-1β。结果：基线时血清IL-1β在CHD组高于CP组和H组,且CP组高于H组,差异有统计学意义（P〈0.01）;CHD组和CP组的临床指标及龈沟液中IL-1β显著高于H组（P〈0.01）,而CHD组和CP组无显著性差异;CHD组和CP组经过治疗后所有病人的牙周临床指标及血清和龈沟液中IL-1β水平均明显降低（P〈0.01）。结论：洁治和根面平整术可降低冠心病伴牙周炎患者血清中IL-1β水平,有利于冠心病的预防和治疗。     

Platelet-activating factor levels of serum and gingival crevicular fluid in nonsmoking patients with periodontitis and/or coronary heart disease

The purpose of the present study was to investigate systemic and local levels of platelet-activating factor (PAF), a potent proinflammatory mediator implicated in cardiovascular pathophysiology in adult nonsmoking patients with periodontitis with or without coronary heart disease (CHD). Eighty-seven volunteers, 25 periodontitis patients, 19 periodontitis with CHD patients, 19 CHD patients, and 24 healthy controls were included, and periodontal conditions were assessed. Gingival crevicular fluid (GCF) and venous blood were collected, and PAF levels were measured by enzyme-linked immunosorbent assay. PAF levels in serum (303.3 ± 204 pg/ml) and in GCF (26.3 ± 6 pg/μl) of the periodontitis group with CHD, the periodontitis group (serum, 302.4 ± 241 pg/ml and GCF, 26.3 ± 8 pg/μl) and the CHD group (serum, 284.7 ± 192 pg/ml and GCF, 20.8 ± 6 pg/μl) were significantly higher than the healthy control group (serum, 65.4 ± 35 pg/ml and GCF, 7.7 ± 3 pg/μl; p < 0.05). In summary, the present study could demonstrate that in patients with periodontitis, the inflammatory mediator PAF is released into serum at least in the same range as for patients with coronary heart disease. However, no additive effects were seen when both conditions were present.     

Matrix metalloproteinases and their inhibitors in gingival crevicular fluid and saliva of periodontitis patients

Abstract Matrix metalloproteinases (MMPs) and serine proteinases seem to be related to tissue destruction in periodontitis. The presence of MMPs in gingival crevicular fluid (GCF) and saliva, however, has not been studied comprehensively with the enzyme-linked immunosorbent assay (ELISA)-technique, We therefore examined the levels of MMP-1,-3.-8 and -9, and their endogenous inhibitor, tissue inhibitor of matrix metalloproteinases (TIMP-1). in GCF and saliva of patients with adult periodontitiss (AP) and localized juvenile periodontitis (LJP). Elevated levels of MMP-1 were detected in LJP GCF compared to AP and control GCF. Elevated levels of TIMP-1 were also detected in LJP GCF in comparison to AP and control GCF Higher MMP-8 levels were detected in AP GCF compared to LJP and control GCF. The relative low levels of MMP-3 were present in all studied GCF samples. Elevated levels of MMP-8 were further detected in saliva of AP compared to LJP and the controls. Both MMP-1 and TIMP-1 were detected in all studied saliva samples, but not significant differences were detected between the studied groups. Our ELISA-results confirm that (i) PMN MMP-8 and MMP-9 are the main collagenase and gelatinase in AP GCF, whereas GCF collagenase in LJP seems to be of the MMP-1-type; (ii) only low levels of TIMP-1. endogenous MMP-inhibitor. are present in AP GCF. which emphasises the importance of doxycycline as a possible adjunctive drug in the treatment of AP patients; (iii) tests based on specific antibodies against PMN MMPs. especially MMP-8, might serve as a reliable method of measuring and monitoring enzyme levels in GCF from different periodontitis patients.     

Cotinine in saliva and gingival crevicular fluid of smokers with periodontal disease

A study was undertaken to determine the presence of cotinine, a metabolite of nicotine, in the saliva and gingival crevicular fluid of smokers with periodontal disease. Saliva and crevicular fluid samples were obtained from 16 habitual cigarette smokers and analyzed by High Performance Liquid Chromatography (HPLC) for the presence of cotinine. Thirteen non-smokers with periodontal disease served as controls. There was no evidence of cotinine (within our detection levels) in either the saliva or crevicular fluid of any of the nonsmokers. Cotinine, in a wide range of concentrations, was detected in the saliva and crevicular fluid in all of the 16 cigarette smokers. The presence of a nicotine metabolite in the saliva and gingival crevicular fluid reflects the extent of the systemic distribution of nicotine in smokers. The vasoactive properties of nicotine are well known and may possibly affect the pathogenesis of periodontal disease.     

Protein carbonyl levels in serum,saliva and gingival crevicular fluid in patients with chronic and aggressive periodontitis

Objective

This study aims at evaluating the degree of protein carbonyl (PC) levels in serum, gingival crevicular fluid (GCF) and saliva in patients who suffer from chronic periodontitis (CP) and generalized aggressive periodontitis (GAP).

Expression of cathepsin-K in gingival crevicular fluid of patients with periodontitis

Cathepsin-K is a highly expressed cysteine protease, and it plays a key role in bone remodeling and cartilage breakdown in bone. Cathepsin-K is used as a well-known marker of osteoclast activity, because this enzyme is mainly derived from osteoclasts. The receptor activator for NF-kappaB ligand (RANKL) plays an important role in osteoclast formation. Although a recent study suggests the involvement of RANKL in the pathogenesis of periodontal disease, no one has previously examined the level of cathepsin-K in the body fluid of human subjects. If the presence of cathepsin-K, as well as RANKL, can be detected in body fluids, it would be indirect proof of the differentiation and/or activation of osteoclasts in the tissues bathed by these fluids. This communication reports on the in vivo concentrations of cathepsin-K and RANKL in the gingival crevicular fluid (GCF) of normal subjects and those patients with severe, moderate, and mild forms of the disease. Increased concentrations of cathepsin-K and RANKL were detected in the GCF from patients with periodontitis (P<0.005 versus control subjects). Also, there was a positive correlation between cathepsin-K and RANKL levels (r=0.726), suggesting that both of them contribute to osteoclastic bone destruction in periodontal disease.     

Collagenase activity in gingival crevicular fluid of patients with juvenile periodontitis

The nature and origin of collagenases in gingival crevicular fluid of juvenile periodontitis patients was investigated. Gingival crevicular fluid collected from deep untreated periodontal pockets of juvenile periodontitis patients was found to contain only vertebrate collagenase (EC 3.4.24.7) activity that cleaved soluble type-I and -III collagens into 3/4 and 1/4 length fragments, as analyzed by SDS-polyacrylamide gel electrophoresis. Type II collagen was degraded at a markedly slower rate. This substrate specificity is indicative of collagenases produced by fibroblasts, epithelial cells and macrophages. We have previously found that collagenase in gingival crevicular fluid of adult periodontics patients appears to be mainly derived from polymorphonuclear leukocytes (PMN). The reasons for the apparent difference in collagenase source between the groups were investigated. We examined whether the pathogen characteristic for juvenile periodontitis, Actinobacillus actinomycetemcomitans, can release collagenase from normal human PMNs. All 10 A. actinomycetemcomitans strains tested, freshly isolated from the subgingival plaque of juvenile periodontitis patients, caused release of collagenase from PMNs in vitro. These results suggest that the lack of normally functioning PMNs in the periodontium of juvenile periodontitis patients may result in a colonization of bacteria that activate the resident periodontal cells to produce increased amounts of collagenase.     

Chemokine RANTES in gingival crevicular fluid of adult patients with periodontitis

Background, aims: This study presents the first evidence on the presence of the chemokine RANTES in the gingival fluid crevicular (GCF) of patients with periodontitis. RANTES is a chemokine that selectively attracts and activates macrophages and lymphocytes. Leucocytes play a critical rôle in the host response to the subgingival microflora. Method: In this study, the presence de RANTES in GCF was determined in samples obtained from adult patients with periodontitis and from control subjects with clinically healthy gingiva. GCF was collected from different probing depths (<3 mm, 4–6 mm, >6 mm) (n=72); and active (n=12) and inactive sites (n=12). An active site was defined as attachment loss >2 mm, as determined by sequential probing and the tolerance method. GFC was collected for 30 s using Periopaper^® strips, and RANTES was quantified by ELISA. Results: The presence of RANTES was detected exclusively in the group of patients with periodontitis, presenting a total amount of 40.43±16 pg and a concentration 67.80±41 pg/μl. RANTES concentration was significantly higher in probing depth <3 mm than in probing depth >6 mm (87.24 versus 51.87, p=0.014). Total amount and concentration in the GCF samples from active sites were higher that in inactive sites (p>0.05). Conclusions: The finding that RANTES is found only in patients with periodontitis, may represent a general feature of chronic inflammatory in periodontal diseases. Finally, RANTES may be implicated in the biological mechanisms underlying the pathogenesis and progression of periodontal disease.