Gu Weiyong, Zhu Qiaoqiao, Gao Xin, Brown Mark D
Departments of *Biomedical Engineering †Mechanical and Aerospace Engineering, and ‡Orthopaedics, University of Miami, Coral Gables, FL.
Spine (Phila Pa 1976). 2014 Nov 15;39(24):E1411-7. doi: 10.1097/BRS.0000000000000560.
Simulate the progression of human disc degeneration.
The objective of this study was to quantitatively analyze and simulate the changes in cell density, nutritional level, proteoglycan (PG) content, water content, and volume during human disc degeneration using a numerical method.
Understanding the cause and progression of intervertebral disc degeneration is crucial for developing effective treatment strategies for intervertebral disc degeneration-related diseases. During tissue degeneration, the disc undergoes losses of cell viability and activities, changes in extracellular matrix composition and structure, and compromise of the tissue-level integrity and function, which is significantly influenced by the intercoupled biological, chemical, electrical, and mechanical signals in the disc. Characterizing these signals in human discs in vivo is difficult.
A realistic 3-dimensional finite element model of the human intervertebral disc was developed on the basis of biomechanoelectrochemical continuum mixture theory. The theoretical framework and the constitutive relationships were all biophysics based. All the material properties were obtained from experimental results. The cell-mediated disc degeneration process caused by lowered nutritional levels at disc boundaries was simulated and validated by comparing with experimental results.
Cell density reached equilibrium state in 30 days after reduced nutritional supply at the disc boundary, whereas the PG and water contents reached a new equilibrium state in 55 years. The simulated results for the distributions of PG and water contents within the disc were consistent with the results measured in the literature, except for the distribution of PG content in the sagittal direction.
Poor nutritional supply has a long-term effect on disc degeneration.
模拟人类椎间盘退变的进程。
本研究的目的是使用数值方法定量分析和模拟人类椎间盘退变过程中细胞密度、营养水平、蛋白聚糖（PG）含量、含水量和体积的变化。
了解椎间盘退变的原因和进程对于制定有效的椎间盘退变相关疾病治疗策略至关重要。在组织退变过程中，椎间盘会出现细胞活力和活性丧失、细胞外基质组成和结构变化以及组织水平完整性和功能受损，而椎间盘内生物、化学、电和机械信号的相互耦合对其有显著影响。在体内表征人类椎间盘中的这些信号很困难。
基于生物力学电化学连续介质混合理论建立了逼真的人类椎间盘三维有限元模型。理论框架和本构关系均基于生物物理学。所有材料特性均从实验结果中获得。通过与实验结果比较，模拟并验证了椎间盘边界营养水平降低导致的细胞介导的椎间盘退变过程。
在椎间盘边界营养供应减少后30天，细胞密度达到平衡状态，而PG和含水量在55年后达到新的平衡状态。椎间盘内PG和含水量分布的模拟结果与文献中测量的结果一致，但PG含量在矢状方向的分布除外。
营养供应不足对椎间盘退变有长期影响。
