正常,龋齿牙髓免疫活性细胞分布的检测

研究龋病不同阶段牙髓免疫活性细胞的分布变化。方法 应用六种单克隆抗体对龋师不同阶段的牙髓免疫活性的ＡＢＣ法进行免疫组化染色。结果 正常牙髓中存在着数目较多的ＨＬＡ－ＤＲ＾＋细胞，Ｔｈ／Ｔｓ比值随龋病进行展略降低，当牙髓暴露后比值显著升高。     

人类牙髓免疫病理机制的细菌检定

龋病继发牙髓炎是最常见的人类流行病之一。除龋病外,尚有别的起因可引起牙髓炎和病理性免疫反应,因此,牙髓炎是较常见的。在牙的生长和实验性龋中,牙髓的过敏作用已证实,然而发生在牙髓内的病理性免疫反应仍了解不多。在牙髓内虽发现一些免疫病理反应或免疫活性细胞,但它们在免疫病理机制或组织破坏中的作用未能证实。尽管许多作者提及有体液免疫系统的因素存在,但无人类牙髓体液性病理免疫反应的证据。本文的目的是鉴定人类牙髓中补体固定免疫复合物中的细菌,以研究病理免疫机制。     

人龋病牙髓中降钙素基因相关肽阳性神经纤维的研究

目的：研究人牙髓降钙素基因相关肽（calicitonin gene-related peptide CGRP）在龋病发展过程中的变化特点，为探讨牙髓局部免疫系统如何参与牙髓的各种病理改变提供理论基础。方法：用免疫组织化学染色法标记牙髓中CGRP并进行定量研究。结果：正常及龋病牙髓中均存在CGRP，牙髓CGRP阳性神经纤维的数量随龋病进展而增多，各组间比较有显著差异。结论：正常牙髓中存在CGRP并与龋坏深度相关。龋坏早期，神经肽对龋源性刺激做出了反应，随着龋坏的发展，局部反应增强，提示CGRP可能参与了牙髓炎症修复过程。     

MMP-8在龋病发展过程中的表达及意义

目的：观察MMP-8在不同程度龋损牙齿中的表达，探讨MMP-8与龋病发展的关系。方法：标本选自因龋未经治疗的第三磨牙，按临床及X线诊断为浅龋、中龋、深龋各10颗，无龋坏第三磨牙10颗为对照组。采用免疫组织化学方法观察MMP-8在不同龋损中表达。结果：正常组MMP-8在成牙本质细胞、前期牙本质、成纤维细胞略有着色；浅龋组成牙本质细胞和前期牙本质、成纤维细胞中有比较浅的阳性表达；中龋组成牙本质细胞增生活跃，前期牙本质增厚，染色阳性，牙髓细胞染色加深；深龋组成牙本质细胞呈阳性表达，牙本质基质中呈散在条索性表达。牙髓组织中成纤维细胞、血管内皮细胞强阳性表达，在修复性牙本质中MMP-8表达强阳性。结论：MMP-8参与龋病的进展过程。     

牙髓中的免疫活性细胞

免疫活性细胞是指受抗原刺激后能发生免疫反应的一类细胞,主要包括T、B淋巴细胞、Ⅱ类抗原表达细胞和肥大细胞等。本文根据近年有关牙髓中的免疫活性细胞的文献作一综述。 一、牙髓中的淋巴细胞 (一)牙髓的T淋巴细胞及其亚群 早期研究认为牙髓中缺乏细胞介导的免疫反应。Pekovic(1984)用单克隆抗体和双重荧光染色     

牙髓中T,B淋巴细胞的免疫组化研究

为进一步探讨正常和炎产下牙髓中免疫活性细胞的构成及其免疫应答作用，作者进行了正常恒牙和乳、恒牙龋源性炎症牙髓中Ｔ细胞亚群和Ｂ细胞的免疫组化研究及定量分析。结果表明：正常牙髓中Ｔ细胞散在分布于牙髓中央区，ＣＤ４：ＣＤ８＝０．５５，以ＣＤ８阳性细胞居多，无Ｂ细胞；炎症牙髓中Ｔ细胞明显增多，ＣＤ４：ＣＤ８－１．１５，ＣＤ４阳性细胞占优势，Ｔ：Ｂ２．３１。慢性牙髓炎急性发作组的Ｂ细胞我鱼慢性牙髓炎组，恒牙     

龋病牙髓中树突状细胞群与T细胞的双标染色观察

体外实验证实从鼠切牙牙髓中分离培养的牙髓树突状细胞群 ,能辅助经有丝分裂原刺激的Ｔ细胞增殖 ,牙髓树突状细胞群和Ｔ细胞的相互作用在牙髓局部免疫应答中起着重要作用。我们采用免疫组化双标技术标记不同龋坏深度牙髓组织中这两类免疫活性细胞 ,为进一步证实Ｔ细胞和牙髓树突状细胞群的相互作用提供形态学依据。1 材料和方法 :正常及龋坏的第三磨牙牙髓石蜡标本46例 ,按临床诊断及牙体剖面的龋坏深度分为 5组 :正常组10例 ;釉质龋组 8例 ;浅龋组 11例 ;中龋组 9例 ;深龋组 8例。采用免疫组化ＳＡＢＣ双标法染色 ,鼠抗人ＣＤ45ＲＯ作为第 …     

TLR4,NOD2和NLRP3在牙髓炎中的表达

目的:分析牙髓炎中TLR4、NOD2和NLRP3的表达特征。方法:收集健康、龋病及牙髓炎的患牙共47颗分为3个组,采用免疫组织化学染色和单色免疫荧光染色方法检测每组牙髓组织中TLR4、NOD2、NLRP3的表达。结果:健康组中TLR4、NOD2和NLRP3仅在成牙本质细胞中少量表达。TLR4、NOD2和NLRP3在牙髓炎组及龋病组表达均明显高于正常组,大量表达于排列紊乱的成牙本质细胞和多种炎症细胞中,而在炎性病灶周边的牙髓成纤维细胞中三者也有表达。结论:本研究表明TLR4、NOD2和NLRP3在炎性牙髓组织中表达同时增高,提示三者均与牙髓炎的进展相关。     

变异链球菌脂磷壁酸的生物学效应

脂磷壁酸是变异链球菌的毒力因子,在变异链球菌致龋过程中发挥着重要作用,在龋病进展过程中诱导牙髓免疫应答。本文就变异链球菌脂磷壁酸的结构和功能,脂磷壁酸在牙周病进展、补体激活、细胞因子产生和牙髓细胞程序性死亡等方面的生物学效应的研究进展作一综述。     

成牙本质细胞在牙髓免疫反应中作用的研究进展

深龋时龋病相关细菌侵入牙本质深层接近牙髓,成牙本质细胞层位于牙髓牙本质交界处,作为牙髓组织最先接触外源性刺激的第一道防线,可通过模式识别受体(PRRs,如Toll样受体、天然免疫受体NOD)识别多种病原相关分子模式(PAMPs),产生促炎细胞因子、表达细胞粘附分子,启动免疫应答。多种细胞因子、细胞粘附分子参与牙髓炎的发生。本文就成牙本质细胞通过TLRs、NLRs识别细菌性因素、引起牙髓免疫反应导致牙髓炎过程中的作用及其研究进展作一综述。     

大鼠实验性牙髓炎和根尖周炎的组织病理学观察

目的：观察大鼠牙髓在自然暴露状态下组织病理学动态过程。方法：12只Wistar大鼠磨牙开髓后旷置口腔，分别于术后3d、7d、14d分批处死大鼠，组织经HE染色进行观察和测量分析。结果：术后3d，冠髓和近根管口处根髓坏死，根尖周区出现炎症细胞；术后7d，根髓坏死继续发展，根尖周区炎症明显；术后14d，根髓几乎完全坏死，根尖周区见牙槽骨吸收。组织学测量发现，术后3d，约35．18％的牙髓发生坏死；术后14d牙髓坏死达92．23％。根尖区破坏的水平长度和垂直长度随炎症进展而增加，术后7～14d发展速度最快。结论：大鼠磨牙开髓后口髂蔚群可诱导牙髓后,口腔菌群可诱导牙髓炎．炎症随诱导时间延长而加重，最后形成根尖周炎。     

Reparative hard tissue formation following calcium hydroxide application after partial pulpotomy in cariously exposed pulps of permanent teeth

In a prospective study, partial pulpotomy was performed on six permanent molars with deep carious lesions and pulpal involvement. The bleeding pulp was irrigated with normal tap water until bleeding had stopped and the exposed pulp was covered with calcium hydroxide followed by zinc oxide eugenol, and finally covered with a semipermanent restoration. All teeth showed hard tissue barrier formation, both clinically and radiographically, within three months and were free from subjective and objective symptoms through the observation period (average observation period was 26 months). The patients also experienced the therapy positively. These findings and those of others have helped gain more recognition for partial pulpotomy as a strong possible alternative therapy when pulps are exposed by deep carious lesions and a bleeding pulp is exposed during the excavation process. The rationale for this therapy is to remove the infected and/or inflamed pulpal areas beneath the carious lesion and disintegrated tissue. A rapid and simplified procedure would allow the general practitioner to perform this procedure when necessary at dental clinics, without specialist facilities under conditions that avoid unnecessary contamination of the pulp.     

Pulpal reactions in rat incisors to Caridex™

This study examined the in vivo effects of Caridex, a chemomechanical caries removal system, on rat pulpal tissue. Rat incisors were opened and the pulps exposed to Caridex or physiological saline and sealed with calcium hydroxide. After various time periods, teeth were extracted and examined by light microscopy. Histological evaluation revealed an almost identical response in both test and control teeth which consisted of a transient inflammatory reaction and a limited necrosis in adjacent pulp tissue. Within seven days, formation of hard tissue matrix was seen below the necrotic area and on pulpal walls. It was suggested that the high pH of Caridex may have contributed to the necrotizing effect of calcium hydroxide in adjacent pulp tissue and the formation of hard tissue matrix. Additionally, the solution is most probably bactericidal. The results suggest that the system can be used as a caries removal agent on humans without unfavourable side effects on the dental pulp.     

Gene expression analysis in cells of the dentine-pulp complex in healthy and carious teeth

Knowledge of the molecular events that occur in carious disease has so far been constrained due to difficulties in obtaining sufficient quantities of the dental tissues and cells involved. Our histological findings indicate that a pulp-odontoblast cellular complex can be obtained from carious and healthy human teeth when exposed to low-temperatures prior to pulpal extirpation and from rodent teeth processed at room-temperature. In contrast, pulpal tissue extracted from room-temperature processed human teeth and low-temperature processed rodent teeth resulted in the odontoblast layer remaining attached to the pulp chamber. Semi-quantitative RT-PCR (sq-RT-PCR) analysis confirmed that markers previously shown to be preferentially expressed in odontoblasts, namely dentin sialophosphoprotein (DSPP) and Nestin, amplified more readily from the extracted pulp-odontoblast complex, as compared to pulpal tissue alone, in both human and rodent samples. Subsequent gene expression analysis of collagen-1alpha and collagen-3alpha indicated levels were significantly higher in carious pulpal tissue. In addition, analysis characterising the expression of members of the transforming growth factor and bone morphogenic protein families and their receptors indicated in general, that these genes were expressed by healthy odontoblasts and up-regulated in both pulpal cells and odontoblasts in response to carious injury. Use of this temperature-sensitive dental tissue preparation procedure allows detection of differential gene expression in odontoblasts and other pulpal cells in healthy and carious tissue.     

Flow cytometric analysis of human dental pulp tissue.

Existing knowledge regarding the cellular components of the dental pulp has been derived primarily from classical methods of histology and biochemistry. Since observations made from prepared tissue sections are static, it is not clear whether this accurately reflects the cellular dynamics of living pulp tissue. Therefore, we developed a method to analyze vital human pulpal tissue by flow cytometry. To test this method, two analyses of the prepared pulpal tissue were performed. First, the prepared tissue was stained with monoclonal antibodies to detect lymphocyte subpopulations. Second, the tissue was processed for DNA analysis of individual cells. Results demonstrated that lymphocytes bearing CD4 and CD8 antigens were clearly detected in pulpal tissue by this method. No B cells were found in any sample. DNA analysis revealed two distinct cell populations. Approximately 88% were small and 12% were large. According to DNA content, 90% of all cells were noncycling and 10% were cycling. These results demonstrate the feasibility of using flow cytometric analysis to examine, at a quantitative level, the cellular heterogeneity of the human dental pulp.     

Comparison of acetaminophen, ibuprofen, and nabumetone therapy in rats with pulpal pathosis

The purpose of this study was to determine if daily treatment with acetaminophen, ibuprofen, or nabumetone would alter prostaglandin E2 (PGE2)/leukotriene B4 (LTB4) synthesis in exposed, infected dental pulp and periradicular tissue in rats. Dental pulp of the bilateral first and second mandibular molars were exposed for 15 or 24 days. Rats were divided into four groups. A daily pharmacological oral dose of one of the medications or the suspending solution alone was administered to the designated group. Eicosanoids were extracted from pulpal and periradicular tissues and assayed. PGE2 was significantly elevated in pulp-exposed, nontreated rats and was significantly reduced in the ibuprofen- and nabumetone-treated groups. LTB4 was significantly increased in all pulp-exposed groups at 15 days when compared with control nonexposed groups. Results showed that only ibuprofen reduced LTB4 in the exposed dental pulp at 24 days, although it did not do so at 15 days. Repetitive treatment with acetaminophen did not suppress PGE2/LTB4 in pulp-exposed molars.     

Effect of IL-1ra on human dental pulp cells and pulpal inflammation

AIM: This study was conducted to investigate the effect of interleukin-1 receptor antagonist (IL-1ra) on the LPS-induced interleukin-1beta (IL-1beta) synthesis in human dental pulp cells and to assess the role of IL-1ra in pulpal inflammation. METHODS: IL-1beta from human dental pulp cells (HDP) was measured by sandwich ELISA; IL-1ra expression in pulpal tissue was detected by immunohistochemical staining. RESULTS: Stimulation of HDP with increasing concentrations of FnLPS resulted in dose-dependent IL-1beta production. The addition of IL-1ra reduced FnLPS-induced IL-1beta synthesis in human dental pulp cells. Significant inhibition of the FnLPS-induced IL-1beta synthesis was observed when IL-1ra was added before treating with FnLPS for 60 min. Large numbers of IL-1ra positive neutrophils, plasmacytes, endothelial cells and lymphocytes were observed in inflamed pulp tissue. CONCLUSIONS: IL-1ra could reduce LPS-stimulated IL-1beta synthesis, suggesting that IL-1ra may play a role in pulpitis.     

Pulpal Temperature Changes During Desensitisation And Other Low-Power Hard-Tissue CO2 Laser Procedures

Thermal insult to pulpal tissue is recognised as a major limitation to the use of lasers for dental hard tissue procedures. This study examined thermal changes at the level of the dental pulp in human molar teeth irradiated with a CO₂ dental laser using a pulsed mode of operation. Sectioned molar teeth were exposed, in vitro, to CO₂ laser radiation. The laser parameters were those used clinically for laser desensitisation and laser-enhanced fluoride treatment. Fissure regions and root surfaces were irradiated. For settings which might reasonably be used clinically, the temperature rise was not of a magnitude which would be expected to cause pulpal inflammation or necrosis. With regard to thermal properties of tooth structure, times taken to reach the maximum temperature reduced, and times taken to cool to baseline increased with increasing laser exposures.