首页> 外文期刊>Journal of oral biosciences >Overexpressing the NH2-terminal fragment of dentin sialophosphoprotein (DSPP) aggravates the periodontal defects in Dspp knockout mice
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Overexpressing the NH2-terminal fragment of dentin sialophosphoprotein (DSPP) aggravates the periodontal defects in Dspp knockout mice

机译:患有NH 2 牙本质唾液酸磷蛋白(DSPP)的碎片片段加剧了DSPP敲除小鼠中的牙周缺陷

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摘要

Objective: Previous studies have shown that dentin sialophosphoprotein (DSPP) is not only essential to the formation and mineralization of dentin but also plays an important role in forming and maintaining a healthy periodontium. Under physiological conditions, DSPP is proteolytically processed into the NH2-terminal and COOH-terminal fragments, and these fragments are believed to perform different functions in the mineralized tissues. Previous studies in our group have demonstrated that the NH2-terminal fragment of DSPP inhibits the formation and mineralization of dentin, while the role of this fragment in periodontium is unclear. Methods: We analyzed the periodontal tissues of the transgenic mice overexpressing the NH2-terminal fragment of DSPP in the Dspp knockout background (referred to as "Dspp KO/DSP Tg" mice), in comparison with wild type mice and Dspp knockout mice. The approaches used in this study included histology, micro-computed tomography, back scattered scanning electron microscopy and resin-casted scanning electron microscopy. Results: Dspp KO/DSP Tg mice exhibited a greater reduction of the alveolar bone, more remarkably altered canalicular systems around the osteocytes, less cementum, more radical migration of the epithelial attachment towards the apical direction, and more severe inflammation in molar furcation region, than in the Dspp knockout mice. Conclusion: Overexpressing the NH2-terminal fragment of DSPP worsened the periodontal defects in Dspp knockout mice, indicating that the NH2-terminal fragment of DSPP may exert an inhibitory role in the formation and mineralization of hard tissues in the periodontium.
机译:目的:以前的研究表明,牙本质唾液酸磷蛋白(DSPP)不仅适用于牙本质的形成和矿化,而且在形成和维持健康的课程中起着重要作用。在生理条件下,DSPP被蛋白水解地加工成NH 2末端和COOH-末端片段,并且这些片段被认为在矿化组织中进行不同的功能。我们组的先前研究表明,DSPP的NH2末端片段抑制了牙本质的形成和矿化,而这种片段在牙周炎中的作用尚不清楚。方法:在DSPP敲除背景(称为“DSPP KO / DSP TG”小鼠中,分析了过表达的转基因小鼠的牙周组织,其DSPP中的NH 2 DSPP的终端片段。型小鼠和DSPP敲除小鼠。本研究中使用的方法包括组织学,微计算断层摄影,背部散射扫描电子显微镜和树脂浇铸扫描电子显微镜。结果:DSPP KO / DSP TG小鼠表现出肺泡骨的减少,更显地改变骨细胞周围的穴位系统,豆切除较小,上皮附着朝向顶端方向的更自然迁移,以及摩尔海盗区中的更严重的炎症,比在DSPP敲除小鼠中。结论:过表达DSPP的NH 2末端片段在DSPP敲除小鼠中造成牙周缺陷,表明DSPP的NH 2 - 末端片段可能在牙周结节中硬组织的形成和矿化中发挥抑制作用。

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