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首页> 外文期刊>Journal of orthopaedics and traumatology: official journal of the Italian Society of Orthopaedics and Traumatology >Structural and biomechanical responses of osseous healing: a novel murine nonunion model
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Structural and biomechanical responses of osseous healing: a novel murine nonunion model

机译：骨愈合的结构和生物力学反应：一种新型的小鼠骨不连合模型

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class="Heading">Background class="Para">Understanding the biological mechanisms of why certain fractures are at risk for delayed healing or nonunion requires translational animal models that take advantage of transgenic and other genetic manipulation technologies. Reliable murine nonunion models can be an important tool to understand the biology of nonunion. In this study, we report the results of a recently established model for creating critical defects that lead to atrophic nonunions based on a unique fracture fixation technique. class="Heading">Materials and methods class="Para">Subcritical (0.6?mm long) and critical (1.6?mm long) defects were created in femurs of 10-week-old double transgenic (Col1/Col2) mice and stabilized using a custom-designed plate and four screws. Four groups were used: normal, sham, subcritical, and critical. Histology (n?=?3 for each group) was analyzed at 2 and 5?weeks, and micro-computed tomography (μCT) and torsional biomechanics (n?=?12 for each group) were analyzed at 5?weeks. class="Heading">Results class="Para">Subcritical defects showed healing at 2?weeks and were completely healed by 5?weeks, with biomechanical properties not significantly different from normal controls. However, critical defects showed no healing by histology or μCT. These nonunion fractures also displayed no torsional stiffness or strength in 10 of 12 cases. class="Heading">Conclusions class="Para">Our murine fracture model creates reproducible and reliable nonunions and can serve as an ideal platform for studying molecular pathways to contrast healing versus nonhealing events and for evaluating innovative therapeutic approaches to promote healing of a challenging osseous injury.
机译：class =“ Heading”>背景 class =“ Para”>要理解为什么某些骨折有延迟愈合或骨不连的危险的生物学机制，需要利用转基因和其他基因操作的转化动物模型技术。可靠的小鼠骨不连贯模型可以成为了解骨不连贯生物学的重要工具。在这项研究中，我们报告了最近建立的基于独特的骨折固定技术来创建导致萎缩性骨不连的严重缺陷的模型的结果。 class =“ Heading”>材料和方法 <在10周大的双转基因（Col1 / Col2）小鼠的股骨中形成亚临界（0.6？mm长）和临界（1.6？mm长）缺陷，并使用定制设计的板将其稳定化，四颗螺丝。使用了四个组：正常，假，次临界和临界。在第2周和第5周对组织学（每组 n ？=？3）进行分析，并进行微计算机断层扫描（μCT）和扭转生物力学（ n ？=？每组12个）在5周时进行了分析。 class =” Heading“>结果 class =” Para“>显示了亚临界缺陷在2周时恢复正常，并在5周时完全愈合，其生物力学特性与正常对照组无明显差异。但是，严重的缺陷通过组织学或μCT均未见愈合。在12例病例中的10例中，这些不愈合的骨折也没有显示出扭转刚度或强度。 class =“ Heading”>结论 class =“ Para”>我们的小鼠骨折模型创建了可再现且可靠的不愈合并可以作为研究分子通路以对比愈合与不愈合事件的分子途径，以及评估创新的治疗方法以促进具有挑战性的骨损伤愈合的理想平台。

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