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首页> 外文期刊>Journal of orthopaedic research >Type III Collagen Modulates Fracture Callus Bone Formation and Early Remodeling
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Type III Collagen Modulates Fracture Callus Bone Formation and Early Remodeling

机译：III型胶原蛋白可调节骨折Call骨的形成和早期重塑

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Type III collagen (Col3) has been proposed to play a key role in tissue repair based upon its temporospatial expression during the healing process of many tissues, including bone. Given our previous finding that Col3 regulates the quality of cutaneous repair, as well as our recent data supporting its role in regulating osteoblast differentiation and trabecular bone quantity, we hypothesized that mice with diminished Col3 expression would exhibit altered long-bone fracture healing. To determine the role of Col3 in bone repair, young adult wild-type (Col3+/+) and haploinsufficent (Col3+/-) mice underwent bilateral tibial fractures. Healing was assessed 7, 14, 21, and 28 days following fracture utilizing microcomputed tomography (microCT), immunohistochemistry, and histomorphometry. MicroCT analysis revealed a small but significant increase in bone volume fraction in Col3+/- mice at day 21. However, histological analysis revealed that Col3+/- mice have less bone within the callus at days 21 and 28, which is consistent with the established role for Col3 in osteogenesis. Finally, a reduction in fracture callus osteoclastic activity in Col3+/- mice suggests Col3 also modulates callus remodeling. Although Col3 haploinsufficiency affected biological aspects of bone repair, it did not affect the regain of mechanical function in the young mice that were evaluated in this study. These findings provide evidence for a modulatory role for Col3 in fracture repair and support further investigations into its role in impaired bone healing. (c) 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 33:675-684, 2015.
机译：III型胶原（Col3）已被提出在组织修复中起关键作用，因为它在包括骨骼在内的许多组织的愈合过程中均表现为颞pat骨表达。鉴于我们先前的发现，Col3调节皮肤修复的质量，以及我们最近的数据支持其在调节成骨细胞分化和小梁骨数量方面的作用，我们假设Col3表达减少的小鼠会表现出长骨骨折愈合的改变。为了确定Col3在骨修复中的作用，对成年野生型（Col3 + / +）和单倍体不足（Col3 +/-）小鼠进行了双侧胫骨骨折。骨折后第7、14、21和28天使用微计算机断层扫描（microCT），免疫组织化学和组织形态学评估愈合情况。 MicroCT分析显示，在第21天，Col3 +/-小鼠的骨体积分数有小幅但显着的增加。但是，组织学分析显示，在第21天和28天，Col3 +/-小鼠的骨call中的骨骼较少，这与既定作用一致Col3在成骨中的作用。最后，Col3 +/-小鼠的骨折愈伤组织破骨细胞活性降低表明，Col3还调节愈伤组织重塑。尽管Col3单倍体不足会影响骨骼修复的生物学方面，但它并未影响本研究中评估的年轻小鼠的机械功能恢复。这些发现为Col3在骨折修复中的调节作用提供了证据，并支持对其在受损骨愈合中的作用的进一步研究。 （c）2015骨科研究学会。由Wiley Periodicals，Inc.出版，J Orthop Res 33：675-684，2015。

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