Characterization of a Novel Calcific Achilles Tendinopathy Model in Mice: Contralateral Tendinopathy Induced by Unilateral Tenotomy
Characterization of a Novel Calcific Achilles Tendinopathy Model in Mice: Contralateral Tendinopathy Induced by Unilateral Tenotomy
复制标题
小鼠新型钙化跟腱病模型的表征：单侧跟腱切断术诱发的对侧肌腱病
DOI：
10.1007/s00223-018-0465-6
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发表时间：
2018-12-01
影响因子：
4.2
通讯作者：
Wang, Liang
中科院分区：
文献类型：
--
作者：
Lin, Xuemei;Huang, Minjun;Wang, Liang
跟腱病是一种重要的临床疾病，其特征为与活动相关的疼痛、局部活动受限以及腱内影像学改变。然而，由于其潜在的发病原理和机制尚不明确，跟腱病的治疗主要基于理论依据和临床经验。本研究旨在建立一种简单且可重复的过度使用诱导的小鼠跟腱病动物模型，以便更好地理解其潜在机制并预防钙化性跟腱病。研究共选用80只C57/B6小鼠（8或9周龄），并将其随机分为对照组和实验组。实验组小鼠的右后肢进行单侧跟腱切断术。单侧跟腱切断术后12周，通过影像学评估、组织学分析、电子显微镜观察及生物力学测试来判定对侧跟腱是否发生跟腱病。单侧跟腱切断术后12周，证实对侧跟腱出现钙化性跟腱病。与对照组相比，实验组对侧跟腱表现为细胞增多、新生血管形成以及融合的胶原纤维排列紊乱。重要的是，对侧跟腱呈现腱内软骨内骨化和跟骨畸形。此外，对侧跟腱生物力学性能不佳表明发生了跟腱病。我们在此介绍一种新颖、简单但可重复的小鼠自发性对侧钙化性跟腱病模型，该模型模拟了人类跟腱病发展过程中的过度使用情况。它应是进一步研究钙化性跟腱病潜在发病机制的有用工具。
Achilles tendinopathy is a significant clinical disease characterized by activity-related pain, focal movement limitation, and intratendinous imaging changes. However, treatment of Achilles tendinopathy has been based mainly on theoretical rationale and clinical experience because of its unclear underlying pathogenesis and mechanism. The purpose of the study was to develop a simple but reproducible overuse-induced animal model of Achilles tendinopathy in mice to better understand the underlying mechanism and prevent calcific Achilles tendinopathy. A total of 80 C57/B6 mice (8 or 9 weeks old) were employed and randomly divided into control and experimental groups. Unilateral Achilles tenotomy was performed on the right hind limbs in the experiment group. 12 weeks after unilateral Achilles tenotomy, the onset of Achilles tendinopathy in the contralateral Achilles tendon was determined by radiological assessment, histologic analysis, electron microscopy observation, and biomechanical test. The onset of calcific Achilles tendinopathy in contralateral Achilles tendon was confirmed after 12 weeks of unilateral tenotomy. The contralateral Achilles tendon in the experimental group was characterized as hypercellularity, neovascularization, and fused collagen fiber disarrangement, compared with the control group. Importantly, intra-tendon endochondral ossification and calcaneus deformity were featured in contralateral Achilles tendon. In addition, poor biomechanical properties in the contralateral Achilles tendon revealed the incidence of Achilles tendinopathy. We hereby introduce a novel, simple, but reproducible spontaneous contralateral calcific Achilles tendinopathy model in mice, which represents overuse conditions during tendinopathy development in humans. It should be a useful tool to further study the underlying pathogenesis of calcific Achilles tendinopathy.