Jackson Alicia R, Huang Chun-Yuh C, Brown Mark D, Gu Wei Yong
Tissue Biomechanics Lab, Department of Biomedical Engineering, University of Miami, Coral Gables, FL 33146, USA.
J Biomech Eng. 2011 Sep;133(9):091006. doi: 10.1115/1.4004944.
The intervertebral disc (IVD) receives important nutrients, such as glucose, from surrounding blood vessels. Poor nutritional supply is believed to play a key role in disc degeneration. Several investigators have presented finite element models of the IVD to investigate disc nutrition; however, none has predicted nutrient levels and cell viability in the disc with a realistic 3D geometry and tissue properties coupled to mechanical deformation. Understanding how degeneration and loading affect nutrition and cell viability is necessary for elucidating the mechanisms of disc degeneration and low back pain. The objective of this study was to analyze the effects of disc degeneration and static deformation on glucose distributions and cell viability in the IVD using finite element analysis. A realistic 3D finite element model of the IVD was developed based on mechano-electrochemical mixture theory. In the model, the cellular metabolic activities and viability were related to nutrient concentrations, and transport properties of nutrients were dependent on tissue deformation. The effects of disc degeneration and mechanical compression on glucose concentrations and cell density distributions in the IVD were investigated. To examine effects of disc degeneration, tissue properties were altered to reflect those of degenerated tissue, including reduced water content, fixed charge density, height, and endplate permeability. Two mechanical loading conditions were also investigated: a reference (undeformed) case and a 10% static deformation case. In general, nutrient levels decreased moving away from the nutritional supply at the disc periphery. Minimum glucose levels were at the interface between the nucleus and annulus regions of the disc. Deformation caused a 6.2% decrease in the minimum glucose concentration in the normal IVD, while degeneration resulted in an 80% decrease. Although cell density was not affected in the undeformed normal disc, there was a decrease in cell viability in the degenerated case, in which averaged cell density fell 11% compared with the normal case. This effect was further exacerbated by deformation of the degenerated IVD. Both deformation and disc degeneration altered the glucose distribution in the IVD. For the degenerated case, glucose levels fell below levels necessary for maintaining cell viability, and cell density decreased. This study provides important insight into nutrition-related mechanisms of disc degeneration. Moreover, our model may serve as a powerful tool in the development of new treatments for low back pain.
椎间盘（IVD）从周围血管接收重要营养物质，如葡萄糖。营养供应不足被认为在椎间盘退变中起关键作用。几位研究者提出了椎间盘的有限元模型来研究椎间盘营养；然而，尚无研究能在结合机械变形的真实三维几何形状和组织特性的情况下预测椎间盘中的营养水平和细胞活力。了解退变和负荷如何影响营养和细胞活力对于阐明椎间盘退变和腰痛的机制是必要的。本研究的目的是使用有限元分析来分析椎间盘退变和静态变形对椎间盘中葡萄糖分布和细胞活力的影响。基于机械 - 电化学混合理论建立了一个真实的椎间盘三维有限元模型。在该模型中，细胞代谢活动和活力与营养物质浓度相关，营养物质的传输特性取决于组织变形。研究了椎间盘退变和机械压缩对椎间盘中葡萄糖浓度和细胞密度分布的影响。为了研究椎间盘退变的影响，改变组织特性以反映退变组织的特性，包括含水量降低、固定电荷密度降低、高度降低和终板通透性降低。还研究了两种机械加载条件：一个参考（未变形）情况和一个10%静态变形情况。一般来说，营养水平从椎间盘周边的营养供应处向外降低。最低葡萄糖水平位于椎间盘髓核和纤维环区域之间的界面处。变形导致正常椎间盘中最低葡萄糖浓度降低6.2%，而退变导致降低80%。虽然在未变形的正常椎间盘中细胞密度未受影响，但在退变情况下细胞活力降低，其中平均细胞密度与正常情况相比下降了11%。退变椎间盘中的变形进一步加剧了这种影响。变形和椎间盘退变都改变了椎间盘中的葡萄糖分布。对于退变情况，葡萄糖水平降至维持细胞活力所需水平以下，细胞密度降低。本研究为椎间盘退变的营养相关机制提供了重要见解。此外，我们的模型可作为开发腰痛新治疗方法的有力工具。
