Osteogenesis of Crouzon-Mutated Cells in an Experimental Model.
Osteogenesis of Crouzon-Mutated Cells in an Experimental Model.
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实验模型中克鲁宗突变细胞的成骨作用。
DOI：
10.1097/scs.0000000000004056
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发表时间：
2018
期刊：
影响因子：
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通讯作者：
Steinbacher,DerekM
中科院分区：
文献类型：
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作者：
Alcon,Andre;Metzler,Philipp;Eswarakumar,Jacob;Wilson,AlexanderT;Steinbacher,DerekM
Crouzon综合征是一种常染色体显性先天性疾病，由成纤维细胞生长因子受体2蛋白突变引起。本研究的目的是在小鼠模型中评估Crouzon成骨细胞和脂肪源性干细胞（ADSCs）的伤口愈合潜力。在Crouzon和成熟野生型（WT） CD-1小鼠中建立顶骨缺损。一组WT和Crouzon小鼠不进行治疗。另一组同时移植WT和Crouzon脂肪干细胞。其他组比较使用纤维蛋白胶支架和去除骨膜。每组取颅骨，于8周和/或16周时进行组织学评估。平均缺陷面积量化，并通过方差分析f检验进行比较。治疗8周和16周后，Crouzon小鼠的平均缺损面积分别为15.37±1.08 cm 2和16.69±1.51 cm 2。未处理WT小鼠在8周和16周后的平均缺损面积分别为14.17±1.88 cm 2和14.96±2.26 cm 2。自体ADSCs的WT小鼠在16周后愈合的平均面积为15.35±1.34 cm 2，而WT ADSCs的Crouzon小鼠愈合的平均面积为12.98±1.89 cm 2。移植到WT小鼠体内的Crouzon ADSCs的平均面积为15.47±1.29 cm 2，而自体的Crouzon ADSCs的平均面积为14.22±3.32 cm 2。方差分析f检验得出P=。415. 在成熟的WT和Crouzon小鼠中，成纤维细胞生长因子受体2突变不会促进临界尺寸缺陷的再骨化。此外，与WT型ADSCs相比，Crouzon型ADSCs不具有成骨优势。
Crouzon syndrome is an autosomal-dominant congenital disease due to a mutation in the fibroblast growth factor receptor 2 protein. The purpose of this study is to evaluate wound-healing potential of Crouzon osteoblasts and adipose-derived stem cells (ADSCs) in a murine model. Parietal skull defects were created in Crouzon and mature wild-type (WT) CD-1 mice. One group of WT and Crouzon mice were left untreated. Another group was transplanted with both WT and Crouzon adipose-derived stem cells. Additional groups compared the use of a fibrin glue scaffold and periosteum removal. Skulls were harvested from each group and evaluated histologically at 8-week and/or 16-week periods. Mean areas of defect were quantified and compared via ANOVA F-test. The average area of defect after 8 and 16 weeks in untreated Crouzon mice was 15.37±1.08 cm 2 and 16.69±1.51 cm 2, respectively. The average area of the defect in untreated WT mice after 8 and 16 weeks averaged 14.17±1.88 cm 2 and 14.96±2.26 cm 2, respectively. WT mice with autologous ADSCs yielded an average area of 15.35±1.34 cm 2 after 16 weeks while Crouzon mice with WT ADSCs healed to an average size of 12.98±1.89 cm 2. Crouzon ADSCs transplanted into WT mice yielded an average area of 15.47±1.29 cm 2 while autologous Crouzon ADSCs yielded an area of 14.22±3.32 cm 2. ANOVA F-test yielded P=. 415. The fibroblast growth factor receptor 2 mutation in Crouzon syndrome does not promote reossification of critical-sized defects in mature WT and Crouzon mice. Furthermore, Crouzon ADSCs do not possess osteogenic advantage over WT ADSCs.