人前磨牙牙髓牙本质复合体层粘连蛋白受体的免疫组织化学研究

目的：研究层粘连蛋白受体在牙髓牙本质复合体内的表达，探讨其分布与功能的关系。方法：收集新鲜健康人前磨牙60个，固定，脱钙，石蜡包埋，层粘连蛋白受体SABC免疫组织化学染色。结果：层状连蛋白受体免疫反应物（LNR－IR）普遍存在于牙髓牙本质复合体的神经纤维膜、血管内皮细胞、成牙本质 细胞及成纤维细胞上，以牙髓的神经纤维膜、血管内皮细胞最为丰富。结论：层粘连蛋白受体一般见于牙髓复牙本质复合体的各种细胞 膜上，它与层粘连蛋白一起在支持、固定牙髓牙本质复合体各结构的正常位置、形态和功能的发挥上可能起了重要作用。     

人前磨牙牙髓牙本质复合体层粘连蛋白受体的免疫组织化学研究

目的研究层粘连蛋白受体在牙髓牙本质复合体内的表达,探讨其分布与功能的关系.方法收集新鲜健康人前磨牙60个,固定,脱钙,石蜡包埋,层粘连蛋白受体SABC免疫组织化学染色.结果层粘连蛋白受体免疫反应物(LNR-IR)普遍存在于牙髓牙本质复合体的神经纤维膜、血管内皮细胞、成牙本质细胞及成纤维细胞上,以牙髓的神经纤维膜、血管内皮细胞最为丰富.结论层粘连蛋白受体一般见于牙髓牙本质复合体的各种细胞膜上,它与层粘连蛋白一起在支持、固定牙髓牙本质复合体各结构的正常位置、形态和功能的发挥上可能起了重要作用.     

层粘连蛋白在修复性牙本质形成中的免疫定位

目的 研究层粘连蛋白（laminin,LN）在牙髓修复中的免疫定位和分布特征。方法 在大鼠第一磨牙制备单面洞,分别观察3d、15d和30d后修复性牙本质的形成情况。以免疫组化技术检测LN的免疫反应。结果 术后3d,修复性牙本质尚未形成。牙髓内成牙本质细胞呈阳性染色,前期牙本质为弱阳性。术后15d,可见修复性牙本质形成和成牙本质细胞样细胞的出现,成牙本质细胞样细胞和牙髓细胞免疫染色呈阳性。术后30d,已形成的修复性牙本质内LN染色阳性,免疫活性特别集中于修复性牙本质与牙髓交界处,成牙本质细胞样细胞染色呈强阳性。结论 LN的分布特征提示,在修复性牙本质形成过程中,LN可能是牙髓细胞附着的一个有利因素。     

正常和炎症牙髓中纤维粘连蛋白分布的研究

用免疫组化，图像分析和免疫电镜等方面，对正常、炎症牙髓中的纤维粘连蛋白进行研究，表明正常牙髓中的ＦＮ呈网状分布，外层明显高于中央区：炎症牙髓中ＦＮ呈均质状分布，含量明显降低，ＦＮ存在于细胞、胶原纤维，无定形基质和血管神经束之间。     

纤维粘蛋白在牙本质形成中的作用

纤维粘连蛋白是一种多功能高分子量糖蛋白,广泛存在于胞牙基质中,在发育和损伤修复中调节细胞附着,移行和分化。近年来在牙齿发育和牙髓修复过程中,Ｆｎ在诱导成牙本质细胞及成本成本质细胞样细胞分化,促进本质形成过程中发挥重要的调控作用。本文就Ｆｎ在牙本质形成中的作用研究进展作了一综述。     

牙髓修复过程中Fn表达的实验研究

目的：探讨钙维它（Ｃａｌｖｉｔａｌ）盖髓后纤维粘连蛋白（Ｆｉｂｒｏｎｅｃｔｉｎ，Ｆｎ）在牙髓中的分布和作用。方法：家犬前磨牙Ｃａｌｖｉｔａｌ盖髓术。用免疫组织化学方法观察Ｆｎ的分布和表达。结果：术后２周，Ｆｎ染色见于变性坏死层、修复性牙本质基质表面，牙髓中炎细胞、成纤维细胞、成牙本质细胞样细胞、成牙本质细胞周围。术后６周～１０周，成纤维细胞、成牙本质细胞样细胞与牙本质基质交界处，成纤维细胞细胞浆Ｆｎ阳性，成牙本质细胞样细胞Ｆｎ弱染或阴性。矿化的牙本质Ｆｎ阴性。结论：Ｃａｌｖｉｔａｌ盖髓后的牙髓修复过程中有Ｆｎ表达，其过程可能与Ｆｎ的分布及其作用有关     

纤维粘连蛋白在牙本质形成中的作用

纤维粘连蛋白(fibronectin,Fn),是一种多功能高分子量糖蛋白,广泛存在于胞外基质中,在发育和损伤修复中调节细胞附着、移行和分化。近年来在牙齿发育和牙髓修复过程中,Fn在诱导成牙本质细胞及成牙本质细胞样细胞分化,促进牙本质形成过程中发挥重要的调控作用,本文就Fn在牙本质形成中的作用研究进展作一综述。     

牛血浆纤维粘连蛋白对人牙髓成纤维细胞增殖,DNA合成,细胞…

采用四唑盐比色法（ＭＴＴ）、３Ｈ－ＴｄＲ掺入试验、细胞大小测定的图象分析等方法，观察不同浓度牛血浆纤维粘连蛋白（ＦＮ）和人工合成肽段（ＲＧＤＳ，４０ｕｇ／ｍｌ）对外培养的人牙髓细胞的影响。ＦＮ（２０、４０ｕｇ／ｍｌ）可促进牙髓成纤维细胞增殖、刺激细胞ＤＮＡ合成，ＦＮ（１０、８０ｕｇ／ｍｌ）、ＲＧＤＳ（４０ｕｇ／ｍｌ）和空白组成对牙髓细胞无上述效应。４种浓度ＦＮ和ＲＧＤＳ（４０ｕｇ／ｍｌ）均使牙髓细     

Ⅰ型和Ⅲ型胶原在修复性牙本质形成中的免疫定位

目的：研究Ⅰ型和Ⅲ型胶原在修复性牙本质形成中的免疫定位和分布特征。方法：在大鼠第一磨牙制备单面洞,观察修复性牙本质形成,免疫组化ＳＡＢＣ法检测Ⅰ型胶原和Ⅲ型胶原的免疫反应。结果：在术后３ｄ,修复性牙本质尚未形成。Ⅰ型胶原和Ⅲ型胶原均分布于牙髓内,前期牙本质为弱阳性,术后１５ｄ,Ⅰ型胶原和Ⅲ型胶原在牙髓细胞内呈阳性染色。Ⅰ型胶原在前期牙本质中呈弱阳性,术后３０ｄ,Ⅰ型胶原和Ⅲ型胶原的旨阳性染色集中于     

生长因子在牙髓损伤修复中的作用

生长因子在组织的损伤修复过程中起着十分重要的作用。本文回顾了与牙髓、牙本质损伤修复有关的几种生长因子的生物学效应以及它们在牙髓生物学领域的研究现状。     

Temporospatial Expression of Neuropeptide Substance P in Dental Pulp Stem Cells During Odontoblastic Differentiation in Vitro and Reparative Dentinogenesis in Vivo

IntroductionSubstance P (SP) is a neuropeptide released from the nervous fibers in response to injury. In addition to its association with pain and reactions to anxiety and stress, SP exerts various physiological functions by binding to the neurokinin-1 receptor (NK1R). However, the expression and role of SP in reparative dentinogenesis remain elusive. Here, we explored whether SP is involved in odontoblastic differentiation during reparative dentinogenesis.MethodsDental pulp stem cells (DPSCs) were isolated from healthy human dental pulp tissues and subjected to odontoblastic differentiation. The expression of SP and NK1R during odontoblastic differentiation was investigated in vitro. The effects of SP on odontoblastic differentiation of DPSCs were evaluated using alizarin red staining, alkaline phosphatase staining, and real-time polymerase chain reaction. After direct pulp capping with mineral trioxide aggregate, the expression of SP and NK1R during reparative dentin formation in rats were identified using histological and immunohistochemical staining.ResultsSP and NK1R expression increased during the odontoblastic differentiation of DPSCs. SP translocated to the nucleus when DPSCs were exposed to differentiation medium. NK1R was always present in the nuclei of DPSCs and odontoblast-like cells. Additionally, we discovered that 10^?8 M SP marginally enhanced the odontoblastic differentiation of DPSCs, and that these effects could be impaired by the NK1R antagonist. Furthermore, SP and NK1R were expressed in odontoblast-like and dental pulp cells during reparative dentin formation in vivo.ConclusionsSP contributes to odontoblastic differentiation during reparative dentin formation by binding to the NK1R.     

Characterization of Odontoblast-like Cell Phenotype and Reparative Dentin Formation In Vivo: A Comprehensive Literature Review

Introduction

The primary aim was to explore the criteria used in characterization of reparative cells and mineralized matrices formed after treatment of pulp exposures, and the sequence of relative events. The secondary aim was to evaluate whether the reparative events depend on the experimental model species, age, and therapeutic intervention.

内毒素对大鼠牙髓组织形成修复性牙本质的影响

目的：探讨局部内毒素刺激对大鼠牙髓形成修复性牙本质的影响。方法：以内毒素注射于火鼠牙阍组织,内f蟮豢试剂盒检测血液中及逆行进入牙髓组织中的内毒素浓度,HE染色观察修复性牙本质形成情况。结果：血液中实验组勺埘照纰间内毒素的含量差别有统计学意义,P〈0．001。牙髓中实验组与阴性对照组,以及与窄白对照组问内毒素的含量麓川仃统计学意义,P〈O．001。HE染色可见注射位点附近修复性牙本质形成明显,髓腔变窄,牙本质小管排列紊乱。结论：内薄素仡一定条件下能刺激夫鼠牙髓组织,使其发生保护性反应,从而促进其矿化作用,加速修复性牙本质形成。     

Enhancing Effects of Immobilized Chondroitin Sulfate on Odontogenic Differentiation of Dental Pulp Stem Cells and Reparative Dentin Formation

IntroductionChondroitin sulfate (CS) is a major proteoglycan involved in the mineralization of the organic matrix of dentin. In this study, the roles of CS immobilized in cross-linked collagen I (Col I) hydrogels on odontogenic differentiation of dental pulp stem cells (DPSCs) and reparative dentin formation were investigated.MethodsDifferent concentrations of CS were incorporated into the genipin–cross-linked Col I hydrogels (CS-0.05, CS-0.1, and CS-0.2, respectively). The influences of CS on the proliferation and odontogenic differentiation of DPSCs were investigated. Finally, the effect of the functionalized hydrogel on the formation of reparative dentin was analyzed in a rat pulp capping model in vivo.ResultsCS improved the proliferation of DPSCs seeded on the hydrogels (P < .05). CS also enhanced the mineralization activities and increased the expression levels of the odontogenic-related proteins of DPSCs on days 7 and 14 (P < .05). In vivo, CS-0.1 hydrogel induced reparative dentin formation with higher quality compared with mineral trioxide aggregate.ConclusionsCS immobilized in Col I hydrogels could induce odontogenic differentiation of DPSCs in vitro and promote homogeneous mineralized barrier formation in vivo. CS–Col I hydrogel has the potential for reparative dentin formation of high quality in direct pulp capping.     

修复性牙本质形成的大鼠模型

目的：建立修复性牙本质形成的动物实验模型,观察修复性牙本质形成的组织开矿学特征。方法：在Ｗｉｓｔａｒ大鼠第一磨牙近中面制备窝洞,分别观察３、１５、３０ｄ,标本切片,ＨＥ染色,显微镜下观察。结果：术后３ｄ未见修复性牙本质形成。１５ｄ后可见修复性牙本工可见骨样牙本质。窝洞下原代成牙本质细胞由新分化的成牙本质细胞样细胞取代。３０ｄ后,修复性牙本质明显增加。新分化的成牙本质细胞样细胞发生极化。结论：大鼠模     

人牙髓细胞诱导牙本质再生的实验观察

目的:观察人成体牙髓细胞体内诱导牙髓组织修复反应的能力.方法:在矿化诱导液作用下,将一定数量级的人牙髓细胞与β-TCP生物陶瓷颗粒进行复合,植入免疫缺陷鼠磨牙穿髓孔处,7 d、14 d后分别取材进行组织学观察.对照组采用氢氧化钙(Oycal)和空白对照组.结果:组织学观察表明,盖髓术后7 d,各组均出现了牙髓细胞向穿髓孔处迁移、聚集.术后14 d,牙髓细胞组炎症反应仅局限于穿髓孔处,有明显的修复性牙本质桥形成;Dycal组炎症反应涉及到少量冠髓,有部分矿化的纤维性屏障形成;空白对照组炎症反应涉及了大部分冠髓,仅有弥散的骨样牙本质形成.结论:在矿化诱导液作用下,牙髓细胞具有向成牙本质细胞样细胞定向分化的能力,将牙髓细胞植入鼠磨牙的穿髓孔处,显示其具有良好的维持牙髓活力和诱导修复性牙本质形成的能力.     

Inability of calcium hydroxide to induce reparative dentinogenesis at non-peripheral sites of dog dental pulp

The ability of 2 calcium hydroxide-containing materials to induce initiation of reparative dentinogenesis was tested at sites remote from the dentinogenically-active regions of the pulp periphery. Pieces of the cements, Dycal and Life, were implanted in central parenchymal sites of dog dental pulps for periods of 6, 14 and 42 days, respectively. Similar pieces were placed in peripheral capping sites as controls. The responses were analyzed by light and transmission electron microscopy. Induction of tubular dentin matrix lined with elongated and polarized odontoblastlike cells was only seen at peripheral capping sites. In response to the centrally implanted cements, only atubular hard tissue with lining fibro–blast–like cells was deposited.     

纤维蛋白粘接剂盖髓的动物实验研究

目的：观察纤维蛋白粘接剂（ＦＳ）对人工暴露的牙髓组织愈合的影响。方法：采用ＦＳ行狗牙直接盖髓术,常规制备牙－颌骨联合切片,光学显微镜观察牙髓创面的愈合及牙本质的修复。结果：ＦＳ盖髓后牙髓无出血,炎性反应轻。氢氧化钙盖髓后牙髓出血多,炎性反应较重。ＦＳ组术后４２ｄ出现骨样牙本质桥修复,氢氧化钙组术后２８ｄ出现骨样牙本质桥修复,术后６３ｄ,ＦＳ组６例中４例有牙本质桥形成,氢氧化钙组６例均有牙本质桥形成。结论：ＦＳ虽无牙本质诱导活性但因其良好的保护及促进牙髓组织创面愈合能力仍不失为一种较为理想的盖髓剂。     

Role of exogenous TGF-β in induction of reparative dentinogenesis in vivo

This study was designed to investigate in vivo i) the role of TGF-β as an active component of the dentin matrix during induction of reparative dentinogenesis; and ii) the ability of TGF-β1 isoform to induce dentinogenic events. Dental pulps of dog molars and canines were mechanically exposed, and the following implants were placed intrapulpally for 42 d: i) Demineralized or native autogenous dentin matrix preincubated with a TGF-β-neutralizing antibody; ii) Millipore filters soaked with solution containing 100 ng/ml of TGF-β1 from human platelets; iii) biomatrices and filters soaked in control solutions. After incubation of biomatrices with the TGF-β-neutralizing antibody, demineralized dentin completely lost its inductive activity, while native dentin was only able to stimulate formation of fibrodentin. Millipore filters soaked with TGF-β1 were consistently surrounded by a thick zone of tubular matrix lined with high columnar polarized cells. The data provide evidence that pulp cells can express their dentinogenic potential in response to an appropriate surface containing exogenous TGF-β1, and that the dentinogenic activity of dentin matrix may at least partly be ascribed to TGF-β molecule(s).