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Anulus fibrosus tension inhibits degenerative structural changes in lamellar collagen

机译:纤维环张力抑制片状胶原的变性结构改变

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摘要

Mechanical stress is one of the risk factors believed to influence intervertebral disc degeneration. Animal models have shown that certain regimes of compressive loading can induce a cascade of biological effects that ultimately results in cellular and structural changes in the disc. It has been proposed that both cell-mediated breakdown of collagen and the compromised stability of collagen with loss of anular tension could result in degradation of lamellae in the anulus fibrosus (AF). To determine whether this may be important in the AF, we subjected entire rings of de-cellularized AF tissue to MMP-1 digestion with or without tension. Biomechanical testing found trends of decreasing strength and stiffness when tissues were digested without tension compared with those with tension. To determine the physiologic significance of tissue level tension in the AF, we used an established in vivo murine model to apply a disc compression insult known to cause degeneration. Afterward, that motion segment was placed in fixed-angle bending to impose tissue level tension on part of the AF and compression on the contralateral side. We found that the AF on the convex side of bending retained a healthy lamellar appearance, while the AF on the concave side resembled tissues that had undergone degeneration by loading alone. Varying the time of onset and duration of bending revealed that even a brief duration applied immediately after cessation of compression was beneficial to AF structure on the convex side of bending. Our results suggest that both cell-mediated events and cell-independent mechanisms may contribute to the protective effect of tissue level tension in the AF.
机译:机械应力是据信影响椎间盘退变的危险因素之一。动物模型表明,某些压缩负荷机制会诱发一系列生物效应,最终导致椎间盘的细胞和结构发生变化。已经提出,细胞介导的胶原蛋白分解和胶原蛋白的稳定性受损,同时伴随着肛门张力的丧失,都可能导致纤维环(AF)中片状细胞的降解。为了确定这在房颤中是否重要,我们对去细胞化的房颤组织的整个环进行了MMP-1消化(有或没有张力)。生物力学测试发现,与无张力组织相比,无张力消化组织时强度和刚度下降的趋势。为了确定房颤中组织水平张力的生理学意义,我们使用已建立的体内鼠模型对已知引起变性的椎间盘加压损伤进行了处理。之后,将该运动段以固定角度弯曲放置,以在部分AF上施加组织水平张力,并在对侧施加压力。我们发现弯曲的凸起侧的AF保留了健康的层状外观,而凹入侧的AF类似于仅通过加载而退化的组织。变化的开始时间和弯曲持续时间表明,即使在停止压缩后立即施加短暂的持续时间也有利于弯曲凸侧的AF结构。我们的结果表明,细胞介导的事件和细胞独立的机制都可能有助于房颤中组织水平张力的保护作用。

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