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首页> 外文期刊>Journal of Dental Research: Official Publication of the International Association for Dental Research >CPNE7 Induces Biological Dentin Sealing in a Dentin Hypersensitivity Model
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CPNE7 Induces Biological Dentin Sealing in a Dentin Hypersensitivity Model

机译:Cpne7在牙本质过敏模型中诱导生物牙本质密封

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Dentin hypersensitivity commonly occurs due to opened dentinal tubules for many reasons. In our previous study, copine 7 (CPNE7) could induce dentin formation for an indirect pulp-capping model in vivo. This study aims to investigate the formation of tertiary dentin when CPNE7 is applied to intentionally exposed dentin with nothing over it in vivo, whether it affects microleakage of the teeth, and the penetration ability of CPNE7 molecules through dentinal tubules in vitro. Cervical dentin areas of 6 maxillary incisors of 5 beagles were exposed to a class V–like lesion, and 1 side of 3 maxillary incisors was adapted with recombinant CPNE7 protein for 5 min as the experimental group. The other side was the control group, and there was no treatment of ethylenediaminetetraacetic acid (EDTA) and CPNE7 after preparation. The defects were exposed without any restorations, and all beagles were sacrificed after 4 wk. The fluid penetration of exposed dentin areas was investigated by a microleakage-testing device and confocal laser scanning microscope. Tertiary dentin formation was confirmed with histological scanning electronic microscopic analysis. Tertiary dentin formation reduces dentinal fluid flow due to occluded tubules or discontinuity with primary or secondary dentin. The in vivo hypersensitivity model with the anterior teeth of beagle dogs showed newly formed tertiary dentin at the dentin-pulp boundary in recombinant CPNE7–treated teeth when compared with the untreated control group in histologic analysis. Scanning electronic microscopic analysis revealed occluded sites with mineral deposition of intratubular dentin. In the permeability test, the mean microleakage value of the CPNE7-treated group was significantly lower than that of the control group ( P < 0.05). The tubular penetration of rhodamine B–combined CPNE7 was confirmed under confocal laser scanning microscope. CPNE7 induces formation of tertiary dentin through shallowly exposed dentinal tubules, which decreases dentin permeability.
机译:由于许多原因,由于打开的牙本质管,常常发生牙本质过敏。在我们以前的研究中,副本7(CPNE7)可以在体内诱导牙本质形成用于间接纸浆封端模型。本研究旨在调查第三牙牙本质的形成,当CPNE7应用于有意暴露的牙本质时,在体内没有任何内容,无论它是否会影响牙齿的微漏,以及CPNE7分子在体外牙本质小管的渗透能力。将5兆头的6个上颌牙本质区域暴露于V类病变等级,并且3张上颌切口的1侧适用于实验组5分钟的重组Cpne7蛋白。另一边是对照组,制备后没有治疗乙二胺四乙酸(EDTA)和CPNE7。缺血在没有任何修复的情况下暴露,并且在4周后牺牲了所有的猎犬。通过微透盖测试装置和共聚焦激光扫描显微镜研究了暴露的牙本质区域的流体渗透。用组织学扫描电子显微镜分析证实了第三型牙本质形成。第三型牙本质肽形成减少了由于咬合小管或初级牙本质或二次牙本质的不连续性而减少了牙本质流量。与未处理对照组在组织学分析中的未处理对照组相比,具有比猎犬犬前齿的体内超敏感模型在重组Cpne7处理的齿中显示出新形成的第三牙本质。扫描电子显微镜分析显示闭塞位点,具有肠道牙本质矿物沉积。在渗透性试验中,CPNE7处理组的平均微额外额度值明显低于对照组(P <0.05)。在共聚焦激光扫描显微镜下确认了罗丹明B组合CPNE7的管状渗透。 CPNE7通过浅暴露的牙本质小管诱导第三节牙本质的形成,这降低了牙本质渗透性。

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