Study on the poroelastic behaviors of the defected osteochondral unit.

Bibliographic Details
Title: Study on the poroelastic behaviors of the defected osteochondral unit.
Authors: Zhong, Hao1 (AUTHOR), Lou, Xinqi1 (AUTHOR), Fan, Xuanze1 (AUTHOR), Wang, Songyuan1 (AUTHOR), Wang, Xiyu1 (AUTHOR), Ma, Lei1 (AUTHOR), Li, Pengcui2 (AUTHOR), Wang, Yanqin1 (AUTHOR), Wei, Xiaochun2 (AUTHOR), Chen, Jing1 (AUTHOR), Xue, Yanru1,3 (AUTHOR) xueyanru@tyut.edu.cn, Wu, Xiaogang1,2 (AUTHOR) wuxiaogangtyut@163.com, Chen, Weiyi1 (AUTHOR) chenweiyi211@163.com
Source: Medical & Biological Engineering & Computing. Apr2024, Vol. 62 Issue 4, p1139-1152. 14p.
Subject Terms: *Finite element method, Extracellular fluid, Flow velocity, Fluid pressure, Articular cartilage
Abstract: Osteoarthritis has become a major disease threatening human health. The mechanism of injury under fluid involvement can be studied by finite element method. However, most models only model the articular cartilage to study the subchondral bone structure, which is too simplistic. In this study, a complete osteochondral unit was modeled and provided with a poroelastic material, and as osteoarthritis develops and the size, thickness, and shape of the osteochondral unit defect varies, the fluid flow behavior is altered, which may have functional consequences that feed back into the progression of the injury. The results of the study showed that interstitial fluid pressure and velocity decreased in defective osteochondral units. This trend was exacerbated as the size and thickness of the defect in the osteochondral unit increased. When the defect reached the trabeculae, pressure around the cartilage defect in the osteochondral unit was greatest, flow velocity in the subchondral cortical bone was greatest, and pressure and flow velocity around the trabecular defect were lowest. As osteoarthritis develops, the osteochondral unit becomes more permeable, and the pressure of the interstitial fluid decreases while the flow rate increases, resulting in severe nutrient loss. This may be the fluid flow mechanism behind osteochondral defects and osteoarthritis. [ABSTRACT FROM AUTHOR]
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