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Sökning: id:"swepub:oai:lup.lub.lu.se:1ad84af0-a7f2-446d-87fb-b3983871380a" > Shear strain and in...

Shear strain and inflammation-induced fixed charge density loss in the knee joint cartilage following ACL injury and reconstruction : A computational study

Orozco, Gustavo A. (författare)
Lund University,Lunds universitet,Avdelningen för Biomedicinsk teknik,Institutionen för biomedicinsk teknik,Institutioner vid LTH,Lunds Tekniska Högskola,Department of Biomedical Engineering,Departments at LTH,Faculty of Engineering, LTH,University of Eastern Finland
Eskelinen, Atte S.A. (författare)
University of Eastern Finland
Kosonen, Joonas P. (författare)
University of Eastern Finland
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Tanaka, Matthew S. (författare)
University of California, San Francisco
Yang, Mingrui (författare)
Cleveland Clinic: Lerner Research Institute
Link, Thomas M. (författare)
University of California, San Francisco
Ma, Benjamin (författare)
University of California, San Francisco
Li, Xiaojuan (författare)
Grodzinsky, Alan J. (författare)
Massachusetts Institute of Technology
Korhonen, Rami K. (författare)
University of Eastern Finland
Tanska, Petri (författare)
University of Eastern Finland
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 (creator_code:org_t)
2021-10
2022
Engelska.
Ingår i: Journal of Orthopaedic Research. - : Wiley. - 0736-0266 .- 1554-527X. ; 40:7, s. 1505-1522
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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  • 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.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Ortopedi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Orthopaedics (hsv//eng)

Nyckelord

ACL reconstruction
diffusion
finite element model
fixed charge density
inflammation
posttraumatic osteoarthritis

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