4.5 Article

Prediction of local fixed charge density loss in cartilage following ACL injury and reconstruction: A computational proof-of-concept study with MRI follow-up

期刊

JOURNAL OF ORTHOPAEDIC RESEARCH
卷 39, 期 5, 页码 1064-1081

出版社

WILEY
DOI: 10.1002/jor.24797

关键词

ACL reconstruction; cartilage adaptation; computational model; finite element model; posttraumatic osteoarthritis

资金

  1. European Union's Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie [713645]
  2. Sigrid Juselius Foundation
  3. Paivikki ja Sakari Sohlbergin Foundation
  4. NIH Clinical Center [P50 AR065645]
  5. Academy of Finland [286526, 324529]
  6. American Orthopaedic Society of Sports Medicine

向作者/读者索取更多资源

This proof-of-concept study developed three-dimensional patient-specific mechanobiological knee joint models to simulate alterations in fixed charged density (FCD) near cartilage lesions during the walking gait. The study suggests mechanisms through which a local FCD loss might occur near cartilage lesions, potentially due to excessive fluid velocity and strain.
The purpose of this proof-of-concept study was to develop three-dimensional patient-specific mechanobiological knee joint models to simulate alterations in the fixed charged density (FCD) around cartilage lesions during the stance phase of the walking gait. Two patients with anterior cruciate ligament (ACL) reconstructed knees were imaged at 1 and 3 years after surgery. The magnetic resonance imaging (MRI) data were used for segmenting the knee geometries, including the cartilage lesions. Based on these geometries, finite element (FE) models were developed. The gait of the patients was obtained using a motion capture system. Musculoskeletal modeling was utilized to calculate knee joint contact and lower extremity muscle forces for the FE models. Finally, a cartilage adaptation algorithm was implemented in both FE models. In the algorithm, it was assumed that excessive maximum shear and deviatoric strains (calculated as the combination of principal strains), and fluid velocity, are responsible for the FCD loss. Changes in the longitudinal T(1 rho)and T(2)relaxation times were postulated to be related to changes in the cartilage composition and were compared with the numerical predictions. In patient 1 model, both the excessive fluid velocity and strain caused the FCD loss primarily near the cartilage lesion. T(1 rho)and T(2)relaxation times increased during the follow-up in the same location. In contrast, in patient 2 model, only the excessive fluid velocity led to a slight FCD loss near the lesion, where MRI parameters did not show evidence of alterations.Significance: This novel proof-of-concept study suggests mechanisms through which a local FCD loss might occur near cartilage lesions. In order to obtain statistical evidence for these findings, the method should be investigated with a larger cohort of subjects.

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