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玻连蛋白衍生肽促进修复性牙本质形成。

Vitronectin-Derived Peptide Promotes Reparative Dentin Formation.

作者信息

Park C, Song M, Kim S Y, Min B M

机构信息

Department of Oral Biochemistry and Program in Cancer and Developmental Biology, Dental Research Institute, School of Dentistry, Seoul National University, Seoul, Korea.

Department of Conservative Dentistry and Dental Research Institute, School of Dentistry, Seoul National University, Seoul, Korea.

出版信息

J Dent Res. 2022 Nov;101(12):1481-1489. doi: 10.1177/00220345221101506. Epub 2022 Jun 16.

Abstract

Exposed dental pulp can maintain its vitality through a pulp-capping procedure with biocompatible materials, followed by reparative dentin formation. Our previous study demonstrated that a vitronectin-derived peptide (VnP-16) promotes osteoblast differentiation and concomitantly restrains osteoclast differentiation and resorptive function. In this study, we aimed to demonstrate that VnP-16 promotes odontoblast differentiation, mineralization, and reparative dentin formation in a pulp exposure model using a rat tooth. VnP-16 showed no cytotoxicity and promoted cellular behavior in human dental pulp cells, enhancing their differentiation into odontoblast-like cells and mineralization, effects that are comparable to those obtained with vitronectin. In a rat pulp exposure model, VnP-16 showed mild inflammatory responses at 2 and 4 wk or none. Mineral trioxide aggregate (MTA) demonstrated a tendency of early formation of reparative dentin at 2 wk when compared with recombinant human bone morphogenetic protein 2 (rhBMP-2) and VnP-16. However, VnP-16 induced reparative dentin formation similar to MTA and rhBMP-2 without inflammation at 4 wk. In addition, VnP-16 showed a thicker and homogeneous reparative dentin formation versus MTA and rhBMP-2. Collectively, these results suggest that VnP-16 can be a useful, direct pulp-capping agent for highly qualified reparative dentin formation by promoting cell behavior and odontoblastic differentiation of human dental pulp cells.

摘要

暴露的牙髓可通过使用生物相容性材料进行盖髓术,随后形成修复性牙本质来维持其活力。我们之前的研究表明,一种玻连蛋白衍生肽(VnP-16)可促进成骨细胞分化,并同时抑制破骨细胞分化和吸收功能。在本研究中,我们旨在证明VnP-16在大鼠牙齿牙髓暴露模型中可促进成牙本质细胞分化、矿化和修复性牙本质形成。VnP-16对人牙髓细胞无细胞毒性,并促进其细胞行为,增强其向成牙本质样细胞的分化和矿化,这些作用与玻连蛋白所获得的作用相当。在大鼠牙髓暴露模型中,VnP-16在2周和4周时显示出轻度炎症反应或无炎症反应。与重组人骨形态发生蛋白2(rhBMP-2)和VnP-16相比,三氧化矿物凝聚体(MTA)在2周时显示出早期形成修复性牙本质的趋势。然而,VnP-16在4周时诱导形成与MTA和rhBMP-2相似的修复性牙本质且无炎症。此外,与MTA和rhBMP-2相比,VnP-16显示出更厚且均匀的修复性牙本质形成。总体而言,这些结果表明,VnP-16通过促进人牙髓细胞的细胞行为和成牙本质细胞分化,可成为一种用于高质量修复性牙本质形成的确有用直接盖髓剂。

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