PDF(Pubmed)
Abstract：
BACKGROUND: Tendon-to-bone healing is a critical challenge in sports medicine, with its cellular and molecular mechanisms yet to be explored. An efficient murine model could significantly advance our understanding of this process. However, most existing murine animal models face limitations, including a propensity for bleeding, restricted operational space, and a steep learning curve. Thus, the need for a novel and efficient murine animal model to investigate the cellular and molecular mechanisms of tendon-to-bone healing is becoming increasingly evident.
METHODS: In our study, forty-four 9-week-old male C57/BL6 mice underwent transection and reattachment of the Achilles tendon insertion to investigate tendon-to-bone healing. At 2 and 4 weeks postoperatively, mice were killed for histological, Micro-CT, biomechanical, and real-time polymerase chain reaction tests.
RESULTS: Histological staining revealed that the original tissue structure was disrupted and replaced by a fibrovascular scar. Although glycosaminoglycan deposition was present in the cartilage area, the native structure had been destroyed. Biomechanical tests showed that the failure force constituted approximately 44.2% and 77.5% of that in intact tissues, and the ultimate tensile strength increased from 2 to 4 weeks postoperatively. Micro-CT imaging demonstrated a gradual healing process in the bone tunnel from 2 to 4 weeks postoperatively. The expression levels of ACAN, SOX9, Collagen I, and MMPs were detected, with all genes being overexpressed compared to the control group and maintaining high levels at 2 and 4 weeks postoperatively.
CONCLUSIONS: Our results demonstrate that the healing process in our model is aligned with the natural healing process, suggesting the potential for creating a new, efficient, and reproducible mouse animal model to investigate the cellular and molecular mechanisms of tendon-to-bone healing.
METHODS: In our study, forty-four 9-week-old male C57/BL6 mice underwent transection and reattachment of the Achilles tendon insertion to investigate tendon-to-bone healing. At 2 and 4 weeks postoperatively, mice were killed for histological, Micro-CT, biomechanical, and real-time polymerase chain reaction tests.
RESULTS: Histological staining revealed that the original tissue structure was disrupted and replaced by a fibrovascular scar. Although glycosaminoglycan deposition was present in the cartilage area, the native structure had been destroyed. Biomechanical tests showed that the failure force constituted approximately 44.2% and 77.5% of that in intact tissues, and the ultimate tensile strength increased from 2 to 4 weeks postoperatively. Micro-CT imaging demonstrated a gradual healing process in the bone tunnel from 2 to 4 weeks postoperatively. The expression levels of ACAN, SOX9, Collagen I, and MMPs were detected, with all genes being overexpressed compared to the control group and maintaining high levels at 2 and 4 weeks postoperatively.
CONCLUSIONS: Our results demonstrate that the healing process in our model is aligned with the natural healing process, suggesting the potential for creating a new, efficient, and reproducible mouse animal model to investigate the cellular and molecular mechanisms of tendon-to-bone healing.
摘要：
背景：肌腱到骨的愈合是运动医学的关键挑战，其细胞和分子机制尚待探索。有效的小鼠模型可以显着提高我们对这一过程的理解。然而,大多数现有的鼠动物模型都面临着局限性，包括出血倾向,有限的操作空间，和陡峭的学习曲线。因此，需要一种新型高效的小鼠动物模型来研究腱-骨愈合的细胞和分子机制正变得越来越明显。
方法：在我们的研究中，44只9周龄的雄性C57/BL6小鼠进行了横切和跟腱插入的重新连接，以研究肌腱到骨的愈合。术后2周和4周，小鼠因组织学而被杀死，Micro-CT,生物力学,和实时聚合酶链反应测试。
结果：组织学染色显示原始组织结构被破坏并被纤维血管瘢痕所取代。尽管软骨区域存在糖胺聚糖沉积，原生结构已被摧毁。生物力学测试表明，破坏力约占完整组织的44.2%和77.5%，极限抗拉强度从术后2周增加到4周。Micro-CT成像显示，术后2至4周，骨隧道逐渐愈合。ACAN的表达水平,SOX9,胶原蛋白I,并检测到MMPs，与对照组相比，所有基因都过表达，并在术后2和4周保持高水平。
结论：我们的结果表明，我们模型中的愈合过程与自然愈合过程一致，暗示了创造新的潜力，高效,和可重复的小鼠动物模型，以研究腱-骨愈合的细胞和分子机制。
方法：在我们的研究中，44只9周龄的雄性C57/BL6小鼠进行了横切和跟腱插入的重新连接，以研究肌腱到骨的愈合。术后2周和4周，小鼠因组织学而被杀死，Micro-CT,生物力学,和实时聚合酶链反应测试。
结果：组织学染色显示原始组织结构被破坏并被纤维血管瘢痕所取代。尽管软骨区域存在糖胺聚糖沉积，原生结构已被摧毁。生物力学测试表明，破坏力约占完整组织的44.2%和77.5%，极限抗拉强度从术后2周增加到4周。Micro-CT成像显示，术后2至4周，骨隧道逐渐愈合。ACAN的表达水平,SOX9,胶原蛋白I,并检测到MMPs，与对照组相比，所有基因都过表达，并在术后2和4周保持高水平。
结论：我们的结果表明，我们模型中的愈合过程与自然愈合过程一致，暗示了创造新的潜力，高效,和可重复的小鼠动物模型，以研究腱-骨愈合的细胞和分子机制。
