Localized Intervertebral Disc Injury Leads to Organ Level Changes in Structure, Cellularity, and Biosynthesis.

Localized Intervertebral Disc Injury Leads to Organ Level Changes in Structure, Cellularity, and Biosynthesis.
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局部椎间盘损伤会导致结构,细胞和生物合成的器官水平变化。

DOI:
10.1007/s12195-009-0072-8
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发表时间:
2009-09-01
影响因子:
2.8
通讯作者:
Korecki, C. L.
Korecki, C. L.
中科院分区:
工程技术4区
文献类型:
--
作者:
Iatridis, James C.;Michalek, A. J.;Purmessur, D.;Korecki, C. L.

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文献综述和新数据旨在评估椎间盘 (IVD) 损伤对生物力学、细胞结构、炎症和生物合成的影响。文献和新的实验证据支持这样的假设:椎间盘局部损伤可导致 IVD 生物力学和生物学的即时和长期器官水平变化。定义运动节段弯曲行为的生物力学特性对影响纤维环 (AF) 完整性和髓核 (NP) 加压的损伤敏感。轴向力学和 IVD 高度测量显示对穿刺和其他减少 NP 加压的损伤的敏感性。扭转生物力学受 AF 病变范围和位置的强烈影响,但对 NP 压力降低不太敏感。穿刺和刺伤等 IVD 损伤也可能导致一系列与退化一致的生物学变化,包括细胞结构的丧失、生物合成的改变和炎症。向牛 IVD 器官培养模型中注射 25G 针盐水效果的新结果表明,细胞结构丧失,基质基因表达下调,为轻微损伤如何影响 IVD 器官反应提供了具体例子。我们得出的结论是,体外诊断中的局部损伤可以通过生物力学和生物机制及其相互作用诱导器官水平的退行性级联反应。 IVD 修复的尝试应针对环带的双重生物力学作用,即维持核加压和跨椎骨传递负载。从生物学角度来看,在损伤后维持 IVD 细胞结构和生物合成率以防止下游退行性变化仍然很重要。
A literature review and new data are presented to evaluate the influence of intervertebral disc (IVD) injury on biomechanics, cellularity, inflammation, and biosynthesis. Literature and new experimental evidence support the hypothesis that localized injury in the disc can lead to immediate and long-term organ level changes in biomechanics and biology of the IVD. Biomechanical properties defining motion segment bending behaviors sensitive to injuries that affect anulus fibrosus (AF) integrity and nucleus pulposus (NP) pressurization. Axial mechanics and IVD height measurements show sensitivity to puncture and other injuries that reduce NP pressurization. Torsional biomechanics are strongly affected by the extent and location of AF lesions but are less sensitive to reduced NP pressurization. IVD injuries such as puncture and stab incisions may also lead to a cascade of biological changes consistent with degeneration, including loss of cellularity, altered biosynthesis and inflammation. New results on effects of 25G needle injection of saline into a bovine IVD organ culture model demonstrated a loss of cellularity and down-regulation of matrix gene expression, providing a specific example of how a minor injury affects the IVD organ response. We conclude that localized injuries in the IVD can induce an organ level degenerative cascade through biomechanical and biological mechanisms, and their interactions. Attempts at IVD repair should target the dual biomechanical roles of the anulus of maintaining nucleus pressurization and transmitting loads across the vertebrae. Biologically, it remains important to maintain IVD cellularity and biosynthesis rates following injury to prevent downstream degenerative changes.
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