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骨关节炎膝关节内侧半月板的生物力学

Biomechanics of the medial meniscus in the osteoarthritic knee joint.

作者信息

Daszkiewicz Karol, Łuczkiewicz Piotr

机构信息

Department of Mechanics of Materials and Structures, Faculty of Civil and Environmental Engineering, Gdańsk University of Technology, Gdańsk, Poland.

II Department of Orthopaedics and Kinetic Organ Traumatology, Medical University of Gdańsk, Gdańsk, Poland.

出版信息

PeerJ. 2021 Nov 24;9:e12509. doi: 10.7717/peerj.12509. eCollection 2021.

DOI:10.7717/peerj.12509
PMID:34900428
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8627128/
Abstract

BACKGROUND

Increased mechanical loading and pathological response of joint tissue to the abnormal mechanical stress can cause degradation of cartilage characteristic of knee osteoarthritis (OA). Despite osteoarthritis is risk factor for the development of meniscal lesions the mechanism of degenerative meniscal lesions is still unclear. Therefore, the aim of the study is to investigate the influence of medial compartment knee OA on the stress state and deformation of the medial meniscus.

METHODS

The finite element method was used to simulate the stance phase of the gait cycle. An intact knee model was prepared based on magnetic resonance scans of the left knee joint of a healthy volunteer. Degenerative changes in the medial knee OA model were simulated by nonuniform reduction in articular cartilage thickness in specific areas and by a decrease in the material parameters of cartilage and menisci. Two additional models were created to separately evaluate the effect of alterations in articular cartilage geometry and material parameters of the soft tissues on the results. A nonlinear dynamic analysis was performed for standardized knee loads applied to the tibia bone.

RESULTS

The maximum von Mises stress of 26.8 MPa was observed in the posterior part of the medial meniscus body in the OA model. The maximal hoop stress for the first peak of total force was 83% greater in the posterior horn and only 11% greater in the anterior horn of the medial meniscus in the OA model than in the intact model. The reduction in cartilage thickness caused an increase of 57% in medial translation of the medial meniscus body. A decrease in the compressive modulus of menisci resulted in a 2.5-fold greater reduction in the meniscal body width compared to the intact model.

CONCLUSIONS

Higher hoop stress levels on the inner edge of the posterior part of the medial meniscus in the OA model than in the intact model are associated with a greater medial translation of the meniscus body and a greater reduction in its width. The considerable increase in hoop stresses shows that medial knee OA may contribute to the initiation of meniscal radial tears.

摘要

背景

机械负荷增加以及关节组织对异常机械应力的病理反应可导致膝关节骨关节炎(OA)特征性的软骨退变。尽管骨关节炎是半月板损伤发生的危险因素,但退变半月板损伤的机制仍不清楚。因此,本研究的目的是探讨内侧间室膝关节OA对内侧半月板应力状态和变形的影响。

方法

采用有限元方法模拟步态周期的站立期。基于一名健康志愿者左膝关节的磁共振扫描制备完整膝关节模型。通过特定区域关节软骨厚度的不均匀减少以及软骨和半月板材料参数的降低来模拟内侧膝关节OA模型中的退变变化。创建另外两个模型以分别评估关节软骨几何形状改变和软组织材料参数对结果的影响。对施加于胫骨的标准化膝关节负荷进行非线性动力学分析。

结果

在OA模型中,内侧半月板体后部观察到最大von Mises应力为26.8 MPa。与完整模型相比,OA模型中内侧半月板后角在总力第一个峰值时的最大环向应力高83%,前角仅高11%。软骨厚度的减少导致内侧半月板体向内侧平移增加57%。半月板压缩模量的降低导致半月板体宽度比完整模型减少2.5倍。

结论

与完整模型相比,OA模型中内侧半月板后部内边缘的环向应力水平更高,这与半月板体更大的向内侧平移及其宽度更大的减少有关。环向应力的显著增加表明内侧膝关节OA可能促成半月板放射状撕裂的起始。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b07/8627128/363ab5a3e176/peerj-09-12509-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b07/8627128/b68c6d1b8875/peerj-09-12509-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b07/8627128/f282e0bbf1e7/peerj-09-12509-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b07/8627128/60dc4e4d665a/peerj-09-12509-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b07/8627128/03ae7ef3308f/peerj-09-12509-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b07/8627128/edc5038b939e/peerj-09-12509-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b07/8627128/2d35eba7787a/peerj-09-12509-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b07/8627128/dbb3c5514edd/peerj-09-12509-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b07/8627128/b71d1e8550c7/peerj-09-12509-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b07/8627128/363ab5a3e176/peerj-09-12509-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b07/8627128/b68c6d1b8875/peerj-09-12509-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b07/8627128/f282e0bbf1e7/peerj-09-12509-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b07/8627128/60dc4e4d665a/peerj-09-12509-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b07/8627128/03ae7ef3308f/peerj-09-12509-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b07/8627128/edc5038b939e/peerj-09-12509-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b07/8627128/2d35eba7787a/peerj-09-12509-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b07/8627128/dbb3c5514edd/peerj-09-12509-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b07/8627128/b71d1e8550c7/peerj-09-12509-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b07/8627128/363ab5a3e176/peerj-09-12509-g009.jpg

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