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本文引用的文献

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Biomimetic promotion of dentin remineralization using l-glutamic acid: inspiration from biomineralization proteins.使用L-谷氨酸仿生促进牙本质再矿化:来自生物矿化蛋白的启示
J Mater Chem B. 2014 Jul 28;2(28):4544-4553. doi: 10.1039/c4tb00451e. Epub 2014 Jun 16.
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Mineral density volume gradients in normal and diseased human tissues.正常和患病人体组织中的矿物质密度体积梯度
PLoS One. 2015 Apr 9;10(4):e0121611. doi: 10.1371/journal.pone.0121611. eCollection 2015.
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Immobilization of phosphate monomers on collagen induces biomimetic mineralization.磷酸单体固定在胶原蛋白上可诱导仿生矿化。
Biomed Mater Eng. 2015;25(1):89-99. doi: 10.3233/BME-141243.
4
Ultrastructural organization of dentin in mice lacking dentin sialo-phosphoprotein.缺乏牙本质涎磷蛋白的小鼠牙本质的超微结构组织
Connect Tissue Res. 2014 Aug;55 Suppl 1(0 1):92-6. doi: 10.3109/03008207.2014.923861.
5
Remineralization of Artificial Dentin Lesions via the Polymer-Induced Liquid-Precursor (PILP) Process.通过聚合物诱导液态前驱体(PILP)工艺实现人工牙本质病变的再矿化。
Mater Res Soc Symp Proc. 2011;1355:1114. doi: 10.1557/opl.2011.1114.
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Loss of dentin sialophosphoprotein leads to periodontal diseases in mice.牙本质涎磷蛋白缺失导致小鼠牙周病。
J Periodontal Res. 2013 Apr;48(2):221-7. doi: 10.1111/j.1600-0765.2012.01523.x. Epub 2012 Aug 31.
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Functional remineralization of dentin lesions using polymer-induced liquid-precursor process.采用聚合物诱导液芯技术对牙本质病损进行功能再矿化。
PLoS One. 2012;7(6):e38852. doi: 10.1371/journal.pone.0038852. Epub 2012 Jun 13.
8
Apatite crystal protection against acid-attack beneath resin-dentin interface with four adhesives: TEM and crystallography evidence.四种黏合剂对树脂-牙本质界面下酸蚀攻击的磷灰石晶体保护作用:TEM 和结晶学证据。
Dent Mater. 2012 Jul;28(7):e89-98. doi: 10.1016/j.dental.2012.04.025. Epub 2012 May 8.
9
Primary structure and phosphorylation of dentin matrix protein 1 (DMP1) and dentin phosphophoryn (DPP) uniquely determine their role in biomineralization.牙本质基质蛋白 1(DMP1)和牙本质磷蛋白(DPP)的一级结构和磷酸化独特地决定了它们在生物矿化中的作用。
Biomacromolecules. 2011 Aug 8;12(8):2933-45. doi: 10.1021/bm2005214. Epub 2011 Jul 18.
10
The role of collagen in bone apatite formation in the presence of hydroxyapatite nucleation inhibitors.胶原在存在羟磷灰石成核抑制剂时对骨磷灰石形成的作用。
Nat Mater. 2010 Dec;9(12):1004-9. doi: 10.1038/nmat2875. Epub 2010 Oct 24.

通过PILP矿化修复DSPP基因敲除小鼠的牙本质缺陷。

Repair of dentin defects from DSPP knockout mice by PILP mineralization.

作者信息

Nurrohman H, Saeki K, Carneiro K, Chien Y C, Djomehri S, Ho S P, Qin C, Marshall S J, Gower L B, Marshall G W, Habelitz S

机构信息

Department of Preventive and Restorative Dental Sciences, University of California, San Francisco, San Francisco, California 94143, USA.

Department of Biomedical Sciences and Center for Craniofacial Research and Diagnosis, Texas A&M University Baylor College of Dentistry, Dallas, Texas 75246, USA.

出版信息

J Mater Res. 2016 Feb 15;31(3):321-327. doi: 10.1557/jmr.2015.406. Epub 2016 Jan 26.

DOI:10.1557/jmr.2015.406
PMID:27239097
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4884014/
Abstract

Dentinogenesis imperfecta type II (DGI-II) lacks intrafibrillar mineral with severe compromise of dentin mechanical properties. A knockout () mouse, with a phenotype similar to that of human DGI-II, was used to determine if poly-L-aspartic acid [poly(ASP)] in the "polymer-induced liquid-precursor" (PILP) system can restore its mechanical properties. Dentin from six-week old and wild-type mice was treated with CaP solution containing poly(ASP) for up to 14 days. Elastic modulus and hardness before and after treatment were correlated with mineralization from Micro x-ray computed tomography (Micro-XCT). Transmission electron microscopy (TEM)/Selected area electron diffraction (SAED) were used to compare matrix mineralization and crystallography. Mechanical properties of the dentin were significantly less than wild-type dentin and recovered significantly ( < 0.05) after PILP-treatment, reaching values comparable to wild-type dentin. Micro-XCT showed mineral recovery similar to wild-type dentin after PILP-treatment. TEM/SAED showed repair of patchy mineralization and complete mineralization of defective dentin. This approach may lead to new strategies for hard tissue repair.

摘要

II型牙本质发育不全(DGI-II)缺乏纤维内矿物质,严重损害牙本质的机械性能。利用一种基因敲除()小鼠(其表型与人类DGI-II相似)来确定“聚合物诱导液态前驱体”(PILP)系统中的聚-L-天冬氨酸[聚(ASP)]是否能恢复其机械性能。将六周龄基因敲除小鼠和野生型小鼠的牙本质用含有聚(ASP)的磷酸钙溶液处理长达14天。处理前后的弹性模量和硬度与显微X射线计算机断层扫描(Micro-XCT)的矿化情况相关。采用透射电子显微镜(TEM)/选区电子衍射(SAED)来比较基质矿化和晶体学情况。基因敲除小鼠牙本质的机械性能显著低于野生型牙本质,经PILP处理后显著恢复(<0.05),达到与野生型牙本质相当的值。Micro-XCT显示经PILP处理后矿化恢复情况与野生型牙本质相似。TEM/SAED显示片状矿化得到修复,缺陷牙本质完全矿化。这种方法可能会带来硬组织修复的新策略。