Department of Conservative Dentistry, Dental Research Institute and School of Dentistry, Seoul National University, Jongno-gu, Seoul, South Korea.
Laboratory for the Study of Regenerative Dental Medicine, Department of Oral Histology-Developmental Biology, Dental Research Institute and School of Dentistry, Seoul National University, Jongno-gu, Seoul, South Korea.
J Dent Res. 2019 Oct;98(11):1239-1244. doi: 10.1177/0022034519869577. Epub 2019 Aug 19.
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 ( < 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.
牙本质敏感通常是由于许多原因导致牙本质小管开放引起的。在我们之前的研究中，Copine7（CPNE7）可以在体内诱导间接盖髓模型中的牙本质形成。本研究旨在探讨 CPNE7 应用于体内无覆盖的故意暴露牙本质时形成第三期牙本质的情况，是否会影响牙齿的微渗漏，以及 CPNE7 分子通过牙本质小管的渗透能力。5 只比格犬的 6 颗上颌切牙的颈牙本质区域暴露于 V 类龋损样病变，其中 3 颗上颌切牙的 1 侧用重组 CPNE7 蛋白适应 5 分钟作为实验组。另一侧为对照组，预备后不进行乙二胺四乙酸（EDTA）和 CPNE7 处理。暴露的缺陷不进行任何修复，所有比格犬在 4 周后处死。通过微渗漏测试装置和共聚焦激光扫描显微镜研究暴露牙本质区域的流体渗透。通过组织学扫描电子显微镜分析证实第三期牙本质的形成。第三期牙本质的形成由于小管闭塞或与原发性或继发性牙本质的不连续性而减少牙本质液流。与未处理的对照组相比，在组织学分析中，在重组 CPNE7 处理的牙齿中，在牙本质 - 牙髓边界处发现了形成的新的第三期牙本质，这表明在前牙的体内超敏反应模型中形成了第三期牙本质。扫描电子显微镜分析显示，闭塞部位有管内牙本质的矿物质沉积。在渗透性试验中，CPNE7 处理组的平均微渗漏值明显低于对照组（<0.05）。共聚焦激光扫描显微镜证实了 rhodamine B 结合 CPNE7 的管状渗透。CPNE7 通过浅层暴露的牙本质小管诱导第三期牙本质的形成，从而降低牙本质通透性。
