Shear strain and inflammation-induced fixed charge density loss in the knee joint cartilage following ACL injury and reconstruction : A computational study
(2022) In Journal of Orthopaedic Research 40(7). p.1505-1522- Abstract
Excessive tissue deformation near cartilage lesions and acute inflammation within the knee joint after anterior cruciate ligament (ACL) rupture and reconstruction surgery accelerate the loss of fixed charge density (FCD) and subsequent cartilage tissue degeneration. Here, we show how biomechanical and biochemical degradation pathways can predict FCD loss using a patient-specific finite element model of an ACL reconstructed knee joint exhibiting a chondral lesion. Biomechanical degradation was based on the excessive maximum shear strains that may result in cell apoptosis, while biochemical degradation was driven by the diffusion of pro-inflammatory cytokines. We found that the biomechanical model was able to predict substantial localized... (More)
Excessive tissue deformation near cartilage lesions and acute inflammation within the knee joint after anterior cruciate ligament (ACL) rupture and reconstruction surgery accelerate the loss of fixed charge density (FCD) and subsequent cartilage tissue degeneration. Here, we show how biomechanical and biochemical degradation pathways can predict FCD loss using a patient-specific finite element model of an ACL reconstructed knee joint exhibiting a chondral lesion. Biomechanical degradation was based on the excessive maximum shear strains that may result in cell apoptosis, while biochemical degradation was driven by the diffusion of pro-inflammatory cytokines. We found that the biomechanical model was able to predict substantial localized FCD loss near the lesion and on the medial areas of the lateral tibial cartilage. In turn, the biochemical model predicted FCD loss all around the lesion and at intact areas; the highest FCD loss was at the cartilage–synovial fluid-interface and decreased toward the deeper zones. Interestingly, simulating a downturn of an acute inflammatory response by reducing the cytokine concentration exponentially over time in synovial fluid led to a partial recovery of FCD content in the cartilage. Our novel numerical approach suggests that in vivo FCD loss can be estimated in injured cartilage following ACL injury and reconstruction. Our novel modeling platform can benefit the prediction of PTOA progression and the development of treatment interventions such as disease-modifying drug testing and rehabilitation strategies.
(Less)
- author
- organization
- publishing date
- 2022
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- ACL reconstruction, diffusion, finite element model, fixed charge density, inflammation, posttraumatic osteoarthritis
- in
- Journal of Orthopaedic Research
- volume
- 40
- issue
- 7
- pages
- 1505 - 1522
- publisher
- John Wiley & Sons Inc.
- external identifiers
-
- scopus:85116075611
- pmid:34533840
- ISSN
- 0736-0266
- DOI
- 10.1002/jor.25177
- language
- English
- LU publication?
- yes
- additional info
- Publisher Copyright: © 2021 The Authors. Journal of Orthopaedic Research® published by Wiley Periodicals LLC on behalf of Orthopaedic Research Society.
- id
- 1ad84af0-a7f2-446d-87fb-b3983871380a
- date added to LUP
- 2021-10-22 15:22:28
- date last changed
- 2024-06-15 18:49:17
@article{1ad84af0-a7f2-446d-87fb-b3983871380a,
abstract = {{<p>Excessive tissue deformation near cartilage lesions and acute inflammation within the knee joint after anterior cruciate ligament (ACL) rupture and reconstruction surgery accelerate the loss of fixed charge density (FCD) and subsequent cartilage tissue degeneration. Here, we show how biomechanical and biochemical degradation pathways can predict FCD loss using a patient-specific finite element model of an ACL reconstructed knee joint exhibiting a chondral lesion. Biomechanical degradation was based on the excessive maximum shear strains that may result in cell apoptosis, while biochemical degradation was driven by the diffusion of pro-inflammatory cytokines. We found that the biomechanical model was able to predict substantial localized FCD loss near the lesion and on the medial areas of the lateral tibial cartilage. In turn, the biochemical model predicted FCD loss all around the lesion and at intact areas; the highest FCD loss was at the cartilage–synovial fluid-interface and decreased toward the deeper zones. Interestingly, simulating a downturn of an acute inflammatory response by reducing the cytokine concentration exponentially over time in synovial fluid led to a partial recovery of FCD content in the cartilage. Our novel numerical approach suggests that in vivo FCD loss can be estimated in injured cartilage following ACL injury and reconstruction. Our novel modeling platform can benefit the prediction of PTOA progression and the development of treatment interventions such as disease-modifying drug testing and rehabilitation strategies.</p>}},
author = {{Orozco, Gustavo A. and Eskelinen, Atte S.A. and Kosonen, Joonas P. and Tanaka, Matthew S. and Yang, Mingrui and Link, Thomas M. and Ma, Benjamin and Li, Xiaojuan and Grodzinsky, Alan J. and Korhonen, Rami K. and Tanska, Petri}},
issn = {{0736-0266}},
keywords = {{ACL reconstruction; diffusion; finite element model; fixed charge density; inflammation; posttraumatic osteoarthritis}},
language = {{eng}},
number = {{7}},
pages = {{1505--1522}},
publisher = {{John Wiley & Sons Inc.}},
series = {{Journal of Orthopaedic Research}},
title = {{Shear strain and inflammation-induced fixed charge density loss in the knee joint cartilage following ACL injury and reconstruction : A computational study}},
url = {{http://dx.doi.org/10.1002/jor.25177}},
doi = {{10.1002/jor.25177}},
volume = {{40}},
year = {{2022}},
}