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Int J Biol Sci：PTH1-34可改善ACH小鼠骨折愈合过程中的骨形成

2017-12-02 MedSci MedSci原创

PTH1-34ACH成骨
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骨折愈合是通过多个阶段完成的，包括软骨形成愈合和向骨痂转变。FGFR3负调节软骨形成，并增强骨骼发育过程中的骨形成。我们以前在小鼠身上发现了FGFR3功能获得性突变，FGFR3主要是通过软骨内骨化愈合延缓了未稳定骨折的愈合。由于骨折固定是临床的常规治疗，稳定骨折主要通过膜内成骨愈合，本研究旨在探究骨形成的关键调节因子FGFR3是否也影响稳定骨折的再生。结果发现FGFR3的功能获得性突变抑制了软骨形

骨折愈合是通过多个阶段完成的，包括软骨形成愈合和向骨痂转变。FGFR3负调节软骨形成，并增强骨骼发育过程中的骨形成。我们以前在小鼠身上发现了FGFR3功能获得性突变，FGFR3主要是通过软骨内骨化愈合延缓了未稳定骨折的愈合。

由于骨折固定是临床的常规治疗，稳定骨折主要通过膜内成骨愈合，本研究旨在探究骨形成的关键调节因子FGFR3是否也影响稳定骨折的再生。结果发现FGFR3的功能获得性突变抑制了软骨形成的开始和随后的骨形成。进一步研究PTH1-34是否能够改善软骨发育不全患者的稳定性胫骨骨折的骨量减少和延迟愈合。通过X线、显微CT、生物力学测试、组织学和实时聚合酶链反应（RT-PCR）分析来评估骨折愈合。

结果发现，PTH 1-34可以减轻ACH小鼠的骨量下降和结构损害。组织学分析显示，使用PTH1-34可在ACH小鼠手术后第14天增加总愈伤组织和软骨愈伤组织的大小。RT-PCR数据表明，全身应用PTH1-34加速了ACH小鼠骨折愈合组织中软骨发生和软骨细胞成熟，并促进骨折愈合组织的成骨分化。

这些结果表明，PTH1-34的使用增强了ACH小鼠骨折愈合过程中的骨形成，这至少部分是由早期软骨愈伤组织的增加和促进骨愈合中骨形成所介导的。

综上所述，本研究发现FGFR3通过抑制软骨形成和骨生成来延缓稳定骨折的再生，而PTH1-34治疗可以改善FGFR3功能获得性突变导致的骨代谢异常和延迟骨损伤愈合。

原始出处：

Chen H, Sun X, et al., PTH 1-34 Ameliorates the Osteopenia and Delayed Healing of Stabilized Tibia Fracture in Mice with Achondroplasia Resulting from Gain-Of-Function Mutation of FGFR3. Int J Biol Sci. 2017 Sep 21;13(10):1254-1265. doi: 10.7150/ijbs.21258. eCollection 2017.

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    2018-02-11 仁者大医

    #Bio#

    0

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    2018-05-27 HinsMax

    #骨折愈合#

    0

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    2018-05-20 12498ebem31暂无昵称

    #Biol#

    0

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    2018-06-25 lujian

    #PTH#

    0

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    2017-12-02 明心见性

    谢谢分享.学习了

    0