龈沟液中的炎症调节因子——白细胞介素8

为研究白细胞介素８（ｉｎｔｅｒｌｅｕｋｉｎ－８，ＩＬ－８）在牙周炎中的作用，作者应用ＥＬＩＳＡ法检测了５４例（１０５个牙）成人牙周炎和２４名（５４个牙）健康对照者龈沟液中ＩＬ－８的水平。结果显示：龈沟液中ＩＬ－８的浓度低于３０μｇ／Ｌ时，ＩＬ－８与龈沟出血指数呈正相关（Ｐ＜０．０１）。龈沟液中ＩＬ－８的浓度高于３０μｇ／Ｌ时，ＩＬ－８与出血指数和探诊深度呈负相关（Ｐ值均小于０．０１）。９１％的牙周炎患牙龈沟液中ＩＬ－８低于３０μｇ／Ｌ。结果提示：ＩＬ－８可能具有抗炎和致炎的双重调节作用；其抗炎和致炎作用的分界值约为３０μｇ／Ｌ。高浓度的ＩＬ－８具有抗炎作用，低浓度的ＩＬ－８具有致炎作用。牙周炎时，龈沟液中的ＩＬ－８主要起致炎作用。     

牙周炎患者血清,龈沟中的IL—8检测及其局部病变组织的免疫组？…

目的：探讨龈沟液中白细胞介素８（ＩＬ－８）的来源及ＩＬ－８与成人牙周炎的关系。方法：用ＥＬＩＳＡ法检测了３０份血清样本（１３例牙周健康者,１７全成人牙周炎患者血清）和２７份龈沟液样本（９例牙周健康者,１８例成人牙周炎患者）中ＩＬ－８的水平。用免疫组织化学的方法检查了ＩＬ－８分泌细胞在牙龈组织的分布（７例健康牙龈组织,１８例成人牙周炎牙龈组织）。结果：成人牙周炎患者中血清ＩＬ－８的检出率（４７％,８     

固齿膏对牙周炎龈沟液中IL—8的影响

通过观察服用固齿膏后龈沟液（ｇｉｎｇｉｖａｌｃｒｅｖｉｃｕｌａｒｆｌｕｉｄ，ＧＣＦ）中白细胞介素８（ＩＬ８）的变化，目的为探讨中药固齿膏与细胞因子间的关系。选成人牙周炎患者２４人，每人口中选患牙１个，龈上洁治后随机分为两组，一组服用固齿膏，另一组不服用任何药物，１个月后复诊。用酶联免疫检测（ＥＬＩＳＡ）法检测龈沟液中ＩＬ８水平。结果表明，服药组１个月后龈沟液中ＩＬ８水平和龈沟液量显著下降，而未服药组的ＩＬ８水平和龈沟液量与治疗前无显著差别。提示固齿膏对ＩＬ８和龈沟液的产生有抑制作用。     

龈沟液中TNFα的检测及其与IL—8的关系

目的：对牙周炎患者龈沟液（ＧＣＦ）中ＴＮＦα进行定量分析，初步探讨ＴＮＦα与牙周炎临床指标及ＧＣＦ中ＩＬ－８的关系。方法：采集２３例成人牙周炎患者ＧＣＦ，并记录临床指标：菌斑指数，牙龈指数，牙周袋深和附着水平。用Ｗｈａｔ－ｍａｎⅠ号滤纸条采集ＧＣＦ，通过ＥＬＩＳＡ法对ＧＣＦ中ＴＮＦα进行检测。结果：牙周炎ＧＣＦ中ＴＮＦα的检出率为４４．１２％，含量范围为０．００１～０．０２４ｍｇ／Ｌ，ＧＣＦ中ＴＮＦα含量与牙周附着水平，ＧＣＦ中ＩＬ－８水平相关显著；而健康组ＧＣＦ中ＴＮＦα检出率为０。结论：ＴＮＦα参与牙周炎症反应，并与细胞因子ＩＬ－８有一定的联系。     

低量强力霉素对牙周炎患者龈沟液胶原酶等活性的影响

为探讨低剂量强力霉素对牙周炎患者龈沟液中多种酶活性的抑制作用，作者对５例慢性成人牙周炎患者，经分别口服空白剂，强力霉素４０ｍｇ／ｄ，强力霉素２０ｍｇ／ｄ及停药共４个阶段，测量各自龈沟液量及龈沟液胶原酶、弹性蛋白酶、β－葡萄糖醛酸酶活性。结果：在口服强力霉素４０ｍｇ／ｄ时，其龈沟液量及活性均较用药前明显下降（Ｐ〈０．０１），且连续服用２周无明显副作用，可间隔１个月后重新用药。     

快速进展性牙周炎患者龈沟液中的弹性蛋白酶活性

目的探讨中性多形核白细胞与快速进展性牙周炎的关系。方法检测２例快速进展性牙周炎患者共１０２个位点（其中２８个位点进行治疗前后的对比）的龈沟液弹性蛋白酶活性,将人多形核白细胞弹性蛋白酶特异底物———Ｓ２４８４与龈沟液反应,测吸光度值,以反映龈沟液弹性蛋白酶活性。结果快速进展性牙周炎龈沟液中的弹性蛋白酶活性［（０．６３±０．３８）Ａｂｓ／位点］明显高于健康对照组［（０．０７±０．０５）Ａｂｓ／位点］,差异有显著性;弹性蛋白酶活性的高低与龈沟液体积、探诊深度、附着丧失和出血指数呈正相关关系;治疗后龈沟液体积和各临床指数显著降低,弹性蛋白酶活性也从治疗前的（０．７３±０．３６）Ａｂｓ／位点下降为（０．１±０．１７）Ａｂｓ／位点,差异有显著性。结论快速进展性牙周炎患者的中性多形核白细胞并不是趋化反应不足,而是过度浸润与释放溶酶体酶,起协同致炎作用。     

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。     

炎症人牙髓组织渗出液中IL-8含量的检测

目的：检测人正常和炎症牙髓组织渗出液中ＩＬ－８的含量,揭示ＩＬ－８与牙髓炎的关系。方法：用滤纸条浸润法采集正常和临床诊断为急性或慢性牙髓炎患牙牙髓组织渗出液。用ＥＬＩＳＡ方法检测其ＩＬ－８含量。结果：正常牙髓组织渗出液中检测不到ＩＬ－８,而炎症牙髓组织渗出液中均有较高水平的ＩＬ－８（０．３３～１．０μｇ／Ｌ）,且在急性牙髓炎中的水平高于慢性牙髓炎（Ｐ〈０．０１）。结论：ＩＬ－８参与了牙髓炎的发生和     

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。     

人重组白细胞介素1和氟美松对髁突软骨细胞合成前列腺素的影响

目的研究人重组白细胞介素１（ｒｅｃｏｍｂｉｎａｎｔｈｕｍａｎｉｎｔｅｒｌｅｕｋｉｎ１，ｒｈＩＬ１）和氟美松对髁突软骨细胞合成６酮前列腺素Ｆ１α的影响。方法在加入ｒｈＩＬ１及氟美松后４、８、１２、２４和７２ｈ，应用放射免疫方法检测髁突软骨细胞培养液内６酮前列腺素Ｆ１α的浓度。结果空白对照组在４、８、１２、２４和７２ｈ时，髁突软骨细胞培养液内６酮前列腺素Ｆ１α的浓度分别为１５１６．４９ｎｇ／Ｌ、１５１３．２２ｎｇ／Ｌ、１５０６．７６ｎｇ／Ｌ、１５２６．７９ｎｇ／Ｌ和２１１４．３６ｎｇ／Ｌ；加入ｒｈＩＬ１组，４ｈ时为１６６４．３２ｎｇ／Ｌ，显著高于空白对照组（Ｐ＜０．０１），８、１２、２４和７２ｈ时分别为１１４６．１１ｎｇ／Ｌ、９４９．２４ｎｇ／Ｌ、１３９２．３３ｎｇ／Ｌ和１４８１．９８ｎｇ／Ｌ，均显著低于空白对照组（Ｐ＜０．０１）。同时加入ｒｈＩＬ１和氟美松及单纯加入氟美松组，所有时间点均比空白对照组显著降低（Ｐ＜０．０１）。结论白细胞介素１使髁突软骨细胞合成前列腺素增加；氟美松使之合成减少，并可抑制白细胞介素１的活性     

龈沟液中的IL—8抑制因子及其生物活性

In order to confirm the existence of Interleukin-8 (IL-8) inhibitor and its biological activity in gingival crevicular fluid (GCF), this study examined the GCF taken from 7 adult periodontitis (AP) patients. In neutralization test of IL-8, the results showed that the mean level of IL-8 was less than 1 ng/ml, which had been added into the GCF before ELESAs was performed to measure the amount of IL-8 in GCF. The mean level of IL-8 in the GCF of AP group was significantly lower than that of healthy group (P < 0.001). In biological activity test of IL-8 inhibitor, using pooled GCF taken from 8 AP patients (23 teeth), the results showed that the GCF (without recombinant human IL-8, rhIL-8) caused more white blood cell (WBC) migration than blank control group (physiological saline) did. When the amount of rhIL-8 increased in GCF from 0.1 microgram to 1 microgram, the WBC count increased by 18.6% which was less than the increase rate (49.1%) in control group with same dose of IL-8. In the saline group containing rhIL-8, the WBC chemotactic response appeared as an inverted "V"-shape curve. All these data suggested that 1. Certain kinds of IL-8 inhibitor exist in GCF which can "cleave" IL-8. 2. The level of IL-8 inhibitor(s) increases significantly in the GCF from periodontitis sites. 3. The GCF of adult periodontitis patient has strong chemotactic effects on WBC. IL-8 inhibitor(s) in GCF can slightly suppress the chemotactic effect induced by IL-8. When assessing the role of IL-8 in pathophysiology, the high and low dose of IL-8 might have different sense.     

牙周炎龈沟液免疫球蛋白含量的测定

用改良刻度毛细管收集龈沟液(GCF)，用单扩法测定了50名健康人(H)和32名成人型牙周炎CAP)龈沟液和血清中的IgG、IgA含量．结果：H组GCF中IgG为1．96g／L，是血清的19％。IgA未能测出．AP组GCF中IgG、IgA分别为7．21g／L和0．83g／L．是血清的71％和61％．AP组GCF中IgG与牙龈指数(GI)有正相关．提示GCF中IgG含量与局部炎症程度有关．本研究首次报道了健康人GCF中IgG含量．为研究GCF中Ig含量提供了一个正常值参数。     

The influence of diabetes on gingival crevicular fluid beta-glucuronidase and interleukin-8

OBJECTIVES: Polymorphonuclear neutrophil (PMN) dysfunction is associated with diabetes. We examined the gingival crevicular fluid (GCF) beta-glucuronidase (BG) and interleukin-8 (IL-8) levels of periodontitis patients with and without type 2 diabetes mellitus (DM). MATERIAL AND METHODS: Forty five adults with type 2 DM and 32 adults without DM, both with chronic periodontitis were enrolled. GCF was collected from eight posterior sites in each quadrant, and periodontal parameters were recorded. GCF was assayed for IL-8 by ELISA and BG by a fluorometric assay. RESULTS: GCF IL-8 was positively correlated with probing depth (PD), and GCF BG but not clinical attachment level (CAL), bleeding on probing (BOP), or plaque index (PI). In contrast, GCF BG was strongly correlated with each of the clinical measures of periodontal disease. Subjects with DM significantly lower levels of both BG (73.0+/-44.8 versus 121.9+/-84.6 pg/sample; p=0.002) and IL-8 (32.1+/-33.1 versus 90.8+/-83.2 pg/sample; p<0.0001) even after adjustments for age, gender, PD, CAL, BOP, and PI. Neither BG nor IL-8 was correlated with HbA1c levels in subjects with DM. CONCLUSION: These data suggest that an inadequate local response by PMN, partially explained by an altered chemokine gradient, may contribute to periodontal disease in patients with type 2 DM.     

The effects of Gu Chi Gao on IL-8 in GCF of periodontitis]

In order to find a new treatment of periodontitis, this paper studied the effects of Gu Chi Gao on IL-8 in gingival crevicular fluid (GCF) of periodontitis. One tooth was selected from every patient in 24 patients with adult periodontitis. After supragingival scaling, the patients were divided into two groups randomly. One group was treated with Gu Chi Gao, while the other group was untreated as control group. All patients were examined after one month. GCF samples were collected with 2 mm x 20 mm Whatman I filter paper stripes and IL-8 in the GCF samples were detected by the method of ELISA. The result demonstrated that the levels of GCF and IL-8 in the treated group were lower than that of control group (P < 0.01), it suggests that Gu Chi Gao may inhibit the production of IL-8 and GCF.     

Interleukin-8 and β-glucuronidase in gingival crevicular fluid

Abstract Polymorphonuclear leukocytes (PMN) play a critical role in the host's response to the subgingival microflora. Interleukin-8 (IL-8) is a potent chemotactic and activating factor for PMN. In this study, the presence of IL-8 in gingival crevicular fluid (GCF) was examined in relation to the PMN indicator β-glucuronidase (βG), as well as clinical parameters of chronic inflammatory periodontal disease. Data was obtained from 30 patients with periodontitis and 14 healthy controls. For the control group, GCF and clinical data were obtained only once. For the periodontitis patients, clinical data and GCF samples were collected prior to treatment, and GCF samples were again collected 2 weeks after scaling and root planing. Comparing control and periodontitis patients prior to treatment, IL-8 concentration was lower in the patients with periodontitis. Scaling and root planing resulted in either an increase or a decrease in total IL-8 and IL-8 concentration GCF. A reduction in total IL-8 or IL–8 concentration was accompanied by a corresponding reduction in βG activity. An increase in total IL-8 or IL-8 concentration after scaling and root planing was associated with an increase in βG activity in some patients and a reduction in βG activity in other patients. The periodontitis patients who did not demonstrate a linkage between IL-8 and βG activity in GCF were those individuals with the highest βG activity prior to treatment. As elevated βG activity in GCF has been associated with an increased risk for probing attachment loss, the absence of a direct relationship between IL-8 in GCF and PMN recruitment into the gingival crevice may characterize individuals at risk for progression of periodontitis.     

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.     

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.     

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.