Travascio Francesco, Jackson Alicia R
Biomechanics Research Laboratory, Department of Industrial Engineering, University of Miami, Coral Gables, FL, United States.
Orthopaedic Biomechanics Laboratory, Department of Biomedical Engineering, University of Miami, Coral Gables, FL, United States.
J Biomech. 2017 Aug 16;61:151-159. doi: 10.1016/j.jbiomech.2017.07.019. Epub 2017 Jul 25.
The meniscus is essential to the functioning of the knee, offering load support, congruency, lubrication, and protection to the underlying cartilage. Meniscus degeneration affects ∼35% of the population, and potentially leads to knee osteoarthritis. The etiology of meniscal degeneration remains to be elucidated, although many factors have been considered. However, the role of nutritional supply to meniscus cells in the pathogenesis of meniscus degeneration has been so far overlooked. Nutrients are delivered to meniscal cells through the surrounding synovial fluid and the blood vessels present in the outer region of the meniscus. During maturation, vascularization progressively recedes up to the outer 10% of the tissue, leaving the majority avascular. It has been hypothesized that vascular recession might significantly reduce the nutrient supply to cells, thus contributing to meniscus degeneration. The objective of this study was to evaluate the effect of vascular recession on nutrient levels available to meniscus cells. This was done by developing a novel computational model for meniscus homeostasis based on mixture theory. It was found that transvascular transport of nutrients in the vascularized region of the meniscus contributes to more than 40% of the glucose content in the core of the tissue. However, vascular recession does not significantly alter nutrient levels in the meniscus, reducing at most 5% of the nutrient content in the central portion of the tissue. Therefore, our analysis suggests that reduced vascularity is not likely a primary initiating source in tissue degeneration. However, it does feasibly play a key role in inability for self-repair, as seen clinically.
半月板对于膝关节的功能至关重要,它为下方的软骨提供负载支撑、适配性、润滑和保护。半月板退变影响约35%的人群,并可能导致膝关节骨关节炎。尽管已经考虑了许多因素,但半月板退变的病因仍有待阐明。然而,营养物质供应对半月板细胞在半月板退变发病机制中的作用迄今一直被忽视。营养物质通过周围的滑液和半月板外层区域存在的血管输送到半月板细胞。在成熟过程中,血管化逐渐退缩至组织外层的10%,使大部分组织无血管。据推测,血管退缩可能会显著减少细胞的营养供应,从而导致半月板退变。本研究的目的是评估血管退缩对半月板细胞可利用营养水平的影响。这是通过基于混合理论开发一种新的半月板稳态计算模型来实现的。研究发现,半月板血管化区域的营养物质跨血管运输对组织核心中葡萄糖含量的贡献超过40%。然而,血管退缩并不会显著改变半月板中的营养水平,最多只会使组织中央部分的营养含量减少5%。因此,我们的分析表明,血管减少不太可能是组织退变的主要起始原因。然而,正如临床上所见,它确实可能在无法自我修复中起关键作用。