正常及炎症牙髓组织中IL-6的表达

目的：通过检测ＩＬ－６在人牙髓组织中的表达,探讨ＩＬ－６与正常及炎症牙髓组织的关系。方法：采用免疫组化（ＡＢＣ）法,检测正常组８个牙及炎症牙髓组１０个牙中ＩＬ－６的表达。结果：正常人牙髓组织ＩＬ－６染色为阴性,炎症牙髓组织中ＩＬ－６染色均呈阳性,主要表达细胞为单核－巨噬细胞,少量血管内皮细胞和成纤维细胞。结论：ＩＬ－６与牙髓组织的炎症反应密切相关,是重要的炎症介质之一。     

成人正常、炎症牙髓组织匀浆中IL-8含量的测定

目的:研究成人正常、炎症牙髓组织中IL-8(Interleuk in-8)的含量,同时探讨IL-8在牙髓炎症机制中的作用和意义。方法:采用ELISA法分别对成人正常、慢性牙髓炎、急性牙髓炎牙髓组织中IL-8的含量进行测定。结果:3组成人牙髓标本中均能检测到IL-8,其中正常组IL-8含量最低,为0.0026±0.0011 ng/mg;慢性牙髓炎组IL-8的含量升高为0.0120±0.0032 ng/mg;而急性牙髓炎组IL-8含量最高,为0.0224±0.0097 ng/mg;各组间均有显著性差异。结论:成人炎症牙髓组织中IL-8的含量高于正常牙髓,IL-8可能参与并调节成人牙髓炎的病理形成过程。     

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。     

牙髓,尖周炎症组织渗出液中白细胞介素—6含量的检测

目的：通过检测炎症牙髓、尖周组织渗出液中白细胞介素－６（ＩＬ－６）的含量，探讨ＩＬ－６与牙髓、尖周炎症的关系。方法：采用ＥＬＩＳＡ免疫夹心法进行ＩＬ－６含量检测。结果：正常牙髓组织渗出液中未检测到ＩＬ－６，炎症牙髓、尖周组织渗出液中均有不同含量ＩＬ－６检出，急性炎症组高于慢性炎症组，急性尖周炎组高于急性牙髓炎组。结论：ＩＬ－６与牙髓、尖周炎症密切相关，主要参与急性期炎症反应，在牙髓、尖周炎症病变过程中起着重要作用。     

根尖周炎渗出液中IL-1β、PGE2的检测及临床相关性

目的：比较急，慢性根尖周炎根管渗出液出液中白细胞介素－1β（interleukin-1β,IL-1β）和前列腺素E2（prostaglandin E2,PGE2）的浓度；确定IL-1β，PGE2浓度与临床，X线结果的相关性，方法：标准纸尖法用于测量根管渗出液体积；ELISA法和RIA法分别用于检测根管渗出液中的IL-1β，PGE2浓度。结果：急性根尖周炎组IL-1β，PGE2浓度，渗出液体积明显高于慢性根尖周炎组（P＜0．0001），IL-1β浓度与临床自发痛，根尖区肿胀，脓性渗出，渗出液臭味和阴影面积密切相关。结论：IL-1β，PGE2主要参与根尖周炎急性期炎期反应，并在其病变过程中发挥重要作用。     

急性不可逆性牙髓炎患者牙髓组织和龈沟液中炎症介质水平变化研究

目的:分析急性不可逆性牙髓炎患者牙髓组织和龈沟液中炎症介质水平变化.方法:选择56例急性不可逆性牙髓炎患者为观察组,50例行正畸牙拔除的健康受试者为对照组.检测牙髓组织和龈沟液中NKA、SP、IL-8、MMP-8、TIMP-1水平.评估疼痛评分(VAS)、牙龈指数(GI)、龈沟出血指数(SBI)、探诊深度(PD).结果...     

正常人、龋病和牙髓炎患者牙髓组织中一氧化氮含量的检测分析

目的：对正常人、龋病和牙髓炎患者牙髓组织中一氧化氮（Ｎｉｔｒｉｃｏｘｉｄｅ，ＮＯ）含量进行检测，初步探讨ＮＯ在牙髓组织自身修复中的作用。方法：采用荧光分光光度法检测其中亚硝酸根（ＮＯ２－）含量，以间接确定ＮＯ含量。结果：正常牙髓组织中ＮＯ无性别差异（Ｐ＞０．０５），浅龋组与对照组ＮＯ无显著性差异（Ｐ＞０．０５），而深龋伴慢性牙髓炎组ＮＯ含量则显著高于对照组（Ｐ＜０．０５）。结论：牙髓组织中ＮＯ含量的变化与其炎症反应有一定的联系，ＮＯ可能在牙髓炎症和自身修复过程中起到一定的作用。     

根尖周炎渗出液中IL-1α的检测及其临床相关性

目的 :①比较Phoenix脓肿和慢性根尖周炎渗出液中的IL -1α浓度 ;②确定IL -1α浓度与临床、X线结果的相关性。方法 :选择临床诊断为Phoenix脓肿和慢性根尖周炎的单根管恒牙各 3 5颗 ,记录症状和体征 ,拍摄X线片 ,用AutoCAD软件测量X线片根尖阴影面积 ;用标准纸尖法收集根管渗出液并计算其体积 ;渗出液中IL -1α浓度用ELISA双抗体夹心法检测。所得数据用SPSS 10 .0软件分析。结果 :①Phoenix脓肿组渗出液中IL -1α浓度均值较慢性根尖周炎组低 ,但X线片根尖阴影面积均值较慢性组大 ,差异均有极显著性 (P <0 .0 0 1) ;②IL -1α浓度与渗出液体积、根尖阴影面积之间有高度负相关性 (P <0 .0 1)。结论 :IL -1α主要参与人慢性根尖周炎的发病过程 ,并可能与其骨改建有关     

正常及炎症牙髓组织中IL—6的表达

目的：通过检测ＩＬ－６在人牙髓组织中的表达,探讨ＩＬ－６与正常及炎症牙髓组织的关系,方法：采用免疫组化（ＡＢＣ）法,检测正常组８个牙及炎症牙髓组１０个牙中ＩＬ－６的表达。结果：正常人牙髓组织ＩＬ－６染色为阴性,炎症牙髓组织中ＩＬ－６染色 呈阳性表达细胞为单核－巨噬细胞,少量血管内皮细胞和成纤维细胞。结论：ＩＬ－６与牙髓组织的炎症反应密切相关,是重要的炎症介质之一。     

牙周炎治疗对患者龈沟液IL-8水平的影响

目的　研究牙周炎基础治疗前后IL 8水平的变化。方法　采用双抗夹心ABC ELISA法测定成人牙周炎患者 (AP)、健康对照以及牙周炎治疗前后患者的龈沟液中IL 8浓度和总量。结果　在疾病组和健康组之间以及牙周病治疗前后对照 ,IL 8浓度无统计学差异 (P >0 0 5 ) ,而IL 8总量、GCF量均存在着统计学差异 (P <0 0 5 ,P <0 0 0 1) ,并且发现治疗对IL 8水平有着明显影响。结论　IL 8总量在成人牙周炎病程中显示动态性改变 ,检验GCF中IL 8的水平对评价牙周炎的治疗是有价值的。?     

Intracellular complex carbohydrates in the normal and inflamed dental pulp

abstract — Forty-four inflamed pulps from human and monkey teeth were studied using histochemical staining methods. In pulps from carious human teeth, mast cells and many fibroblasts containing glycogen-like granules were regularly observed. In monkey pulps, where pulpitis was induced experimentally, mast cells were found only occasionally, and glycogen-like granules were absent. However, some fibroblasts in normal and inflamed monkey pulps contained periodic acid-Schiff (PAS) positive granules, which were resistant to amylase. Such granules were not found in human pulp fibroblasts.     

人正常或炎症牙髓组织中炎症信号细胞间黏附分子-1表达的研究

目的：研究人正常、慢性牙髓炎、急性牙髓炎牙髓组织中细胞间黏附分子-1免疫定位，探讨其在牙髓炎症机制中的作用和意义。方法：采用免疫组化（ABC）法对成人正常牙髓、慢性牙髓炎、急性牙髓炎牙髓中的细胞间黏附分子-1进行免疫定位。结果：细胞间黏附分子-1在3组牙髓组织中均有表达。其分布为：正常牙髓组织中少许血管内皮细胞呈较弱的阳性反应；慢性牙髓炎牙髓组织中较多的血管内皮有较强的阳性染色；急性牙髓炎牙髓组织中很多血管内皮染色呈强阳性。其中急性牙髓炎组染色强度与慢性牙髓炎组、正常组之间细胞间黏附分子-1的表达有显著差异；慢性牙髓炎组与正常组之间细胞间黏附分子-1的表达也有显著差异。结论：①人牙髓组织中血管内皮细胞膜表达细胞间黏附分子-1。②炎症组与正常组之间细胞间黏附分子-1的表达有显著性差异。③细胞间黏附分子-1可能参与介导牙髓炎症过程，在炎症机制中发挥重要作用。     

Ability of healthy and inflamed human dental pulp to reduce hydrogen peroxide

This study examined the defensive ability of human dental pulp against H2O2 in healthy and reversible and irreversible pulpitis tissues through determination of catalase activity by spectrophotometric methods. Thirty-five systemically healthy patients were donors of the pulp tissue, and pulp conditions were assessed using clinical and X-ray evaluations. Catalase activity was 1.61 +/- 0.23 U mg(-1) protein in the healthy tissues, 2.99 +/- 0.45 U mg(-1) protein in the reversible pulpitis tissues, and 2.44 +/- 467 mU mg(-1) protein in the irreversible pulpitis tissues. All differences between the groups were statistically significant. These results point to a role for catalase during dental pulp inflammation in humans, and therefore demonstrate an inherent biological defense system against reactive oxidants in human dental pulp.     

Leptin induces IL-6 and IL-8 expression through leptin receptor Ob-Rb in human dental pulp fibroblasts

Objective: Leptin, through binding to its special receptor (Ob-Rb), has potent effects on immunity and inflammation. This study aimed to investigate the expression of leptin receptor Ob-Rb in human dental pulp fibroblasts (HDPFs) and the effects of leptin on the production of proinflammatory cytokines of IL-6 and IL-8 by HDPFs.

Methods: Ob-Rb expression was determined by quantitative real-time PCR (real-time PCR), Western blot and immunofluorescence analyses in cultured HDPFs. Small interfering RNA (siRNA) was transfected into HDPFs to down-regulate the expression of Ob-Rb. Real-time PCR and enzyme-linked immunosorbent assay (ELISA) were used to determine the proinflammatory cytokines of IL-6 and IL-8 levels in leptin-stimulated HDPFs. The involved signalling pathways that mediate the leptin-stimulated production of proinflammatory cytokines were investigated using Western blot and specific signalling inhibitor analyses.

Results: The expression levels of Ob-Rb mRNA and protein were detected in HDPFs. Leptin could stimulate mRNA and protein expression of IL-6 and IL-8 in HDPFs in a concentration-dependent and time-dependent manner. Transfection with siRNA targeting Ob-Rb resulted in remarkable reduction of IL-6 and IL-8 expressions by HDPFs. In accordance with the enhanced expression of proinflammatory cytokines, leptin stimulation resulted in rapid phosphorylation of STAT3, p38 MAPK, ERK and Akt in HDPFs. Inhibiting JAK2/STAT3, p38 MAPK or PI3K/Akt substantially decreased leptin-induced IL-6 production, whereas blocking ERK and p38 MAPK substantially suppressed IL-8 production from leptin-stimulated HDPFs.

Conclusions: Leptin may up-regulate IL-6 and IL-8 production through binding with Ob-Rb in HDPFs via the activation of different intracellular signalling pathways.     

正常及炎症状态人牙髓中八聚体结合转录因子4B的表达

目的 研究人正常及炎症牙髓组织中八聚体结合转录因子4B(Oct-4B)的表达特点,检测大肠杆菌脂多糖刺激后人牙髓细胞( HDPCs)中Oct-4B的表达水平,以探讨Oct-4B在牙髓炎症中的可能作用.方法 采用免疫组织化学和反转录聚合酶链反应( RT-PCR)方法检测正常及炎症牙髓组织中Oct-4B的表达情况.RT-PCR检测1 mg/L脂多糖刺激HDPC 24、48、72 h后Oct-4B和热休克蛋白70(HSP70)表达水平的变化.结果 正常牙髓组织中未检测到Oct-4B的表达,炎症牙髓组织病灶处牙髓成纤维细胞和炎症细胞胞质中Oct-4B表达强阳性.炎症牙髓组织中Oct-4B mRNA水平显著高于正常牙髓组织(P<0.05).脂多糖刺激48.72 h后,HDPC中Oct-4B和HSP70 mRNA水平同步上调(P<0.05).结论 Oct-4B在炎症牙髓组织中高表达,且脂多糖刺激可上调牙髓细胞内Oct-4B表达,Oct-4B可能参与牙髓炎症修复过程.     

Detection of interleukin-6 in human dental pulp and periapical lesions

Abstract— Pulpal and periapical diseases are characterized by inflammation. The cytokine IL-6 is a major mediator of the host response to tissue injury and infection. This study examined the level of interleukin-6 (IL-6) in six inflamed human pulps and six human periapical lesions of endodontic origin using ELISA. Pulp samples from eight clinically impacted teeth were used as controls. The periapical samples exhibited significant levels of IL-6 (mean= 78.1 ± 9 pg/mg protein) as did inflamed pulpal tissues (mean= 36±3.9 pg/mg protein) compared to healthy pulp (mean= 0.01±0.02 pg/mg protein). These data indicated that IL-6 was produced and released locally in the inflamed pulpal and periapical lesions.     

Up-regulation of nucleotide-binding oligomerization domain 1 in inflamed human dental pulp

Introduction

The innate immune response is activated by recognition of microbial components through specific pattern recognition receptors including nucleotide-binding oligomerization domain (NOD)-like receptors. However, the regulation of NOD-1 in inflamed human dental pulp remains poorly understood. This study aimed to evaluate the expression of NOD-1 in healthy and inflamed human dental pulps. In addition, the secretion of chemokines induced by NOD-1 and the related signaling pathways were studied.

Methods

Samples of human dental pulp tissues were obtained from freshly extracted wisdom teeth. The protein localization of NOD-1 in the pulp tissues was detected by immunohistochemistry. In addition, human dental pulp fibroblasts were stimulated with NOD-1 agonist γ-D-glutamylmeso-diaminopimelic acid. Production of interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) was determined by an enzyme-linked immunosorbent assay. The involvement of mitogen-activated protein kinase (MAPK) signaling pathways was examined by Western blot analysis, and the association of MAPK signaling with chemokine production was determined.

Results

The results demonstrated the expression of NOD-1 in normal dental pulp, and up-regulated NOD-1 expression was observed in inflamed dental pulp. On stimulation with NOD-1 agonist, production of IL-8 and MCP-1 was induced in a dose-dependent manner. Moreover, phosphorylation of p38 MAPK and Jun N-terminal kinase (JNK) was enhanced by stimulation of NOD-1. With the treatment of p38 MAPK and JNK inhibitors, the NOD-1–induced IL-8 production was suppressed.

Conclusions

In response to microbial invasion, the expression of NOD-1 can be regulated in a ligand-inducible manner. NOD-1 might participate in pulp inflammation through chemokine production via MAPK signaling pathways.     

正常与炎症牙髓中降钙素基因相关肽免疫反应神经纤维的研究

目的观察人正常与炎症牙髓中降钙素基因相关肽免疫反应神经纤维（CGRP－IRF）的分布，为深入探讨神经系统如何参与牙髓的各种生理，病理改变的调节作用提供新的资料。方法采用ABC免疫组化法观察人正常牙髓中CGRP－IRF的分布及龋源性炎症牙髓中CGRP－IRF的改变。结果牙髓中CGRP－IRF为许多串珠状棕褐色点状连成的线条，含明显的膨体。正常牙髓中，CGRP－IRF多沿血管走行并分布在血管周围，一些单根CGRP－IRF远离血管，主要分布在造牙本质细胞下神经丛。髓角处，偶尔可见CGRP-IRF突入造牙本质细胞层。炎症牙髓中，在病损下方和血管周围CGRP－IRF明显增多。结论CGRP－IRF广泛分布于人牙髓中，在牙髓炎症中起重要作用。