L Zevenbergen1, W Gsell2, D D Chan3, J Vander Sloten4, U Himmelreich5, C P Neu6, I Jonkers7. 1. Department of Movement Sciences, KU Leuven, Leuven, Belgium. Electronic address: lianne.zevenbergen@kuleuven.be. 2. Department of Imaging and Pathology, KU Leuven, Leuven, Belgium. Electronic address: willy.gsell@kuleuven.be. 3. Department of Biomedical Engineering, Rensselaer Polytechnic Institute, Troy, NY, USA. Electronic address: chand5@rpi.edu. 4. Department of Mechanical Engineering, KU Leuven, Leuven, Belgium. Electronic address: jos.vandersloten@kuleuven.be. 5. Department of Imaging and Pathology, KU Leuven, Leuven, Belgium. Electronic address: uwe.himmelreich@kuleuven.be. 6. Department of Mechanical Engineering, University of Colorado Boulder, Boulder, CO, USA. Electronic address: cpneu@colorado.edu. 7. Department of Movement Sciences, KU Leuven, Leuven, Belgium. Electronic address: ilse.jonkers@kuleuven.be.
Abstract
OBJECTIVE: The objective of this study was to evaluate the effect of full-thickness chondral defects on intratissue deformation patterns and matrix constituents in an experimental model mimicking in vivo cartilage-on-cartilage contact conditions. DESIGN: Pairs of bovine osteochondral explants, in a unique cartilage-on-cartilage model system, were compressed uniaxially by 350 N during 2 s loading and 1.4 s unloading cycles (≈1700 repetitions). Tissue deformations under quasi-steady state load deformation response were measured with displacement encoded imaging with stimulated echoes (DENSE) in a 9.4 T magnetic resonance imaging (MRI) scanner. Pre- and post-loading, T1, T2 and T1ρ relaxation time maps were measured. We analyzed differences in strain patterns and relaxation times between intact cartilage (n = 8) and cartilage in which a full-thickness and critical sized defect was created (n = 8). RESULTS: Under compressive loading, strain magnitudes were elevated at the defect rim, with elevated tensile and compressive principal strains (Δϵmax = 4.2%, P = 0.02; Δϵmin = -4.3%, P = 0.02) and maximum shear strain at the defect rim (Δγmax = 4.4%, P = 0.007). The opposing cartilage showed minimal increase in strain patterns at contact with the defect rim but decreased strains opposing the defect. After defect creation, T1, T2 and T1ρ relaxation times were elevated at the defect rim only. Following loading, the overall relaxations times of the defect tissue and especially at the rim, increased compared to intact cartilage. CONCLUSIONS: This study demonstrates that the local biomechanical changes occurring after defect creation may induce tissue damage by increasing shear strains and depletion of cartilage constituents at the defect rim under compressive loading.
OBJECTIVE: The objective of this study was to evaluate the effect of full-thickness chondral defects on intratissue deformation patterns and matrix constituents in an experimental model mimicking in vivo cartilage-on-cartilage contact conditions. DESIGN: Pairs of bovine osteochondral explants, in a unique cartilage-on-cartilage model system, were compressed uniaxially by 350 N during 2 s loading and 1.4 s unloading cycles (≈1700 repetitions). Tissue deformations under quasi-steady state load deformation response were measured with displacement encoded imaging with stimulated echoes (DENSE) in a 9.4 T magnetic resonance imaging (MRI) scanner. Pre- and post-loading, T1, T2 and T1ρ relaxation time maps were measured. We analyzed differences in strain patterns and relaxation times between intact cartilage (n = 8) and cartilage in which a full-thickness and critical sized defect was created (n = 8). RESULTS: Under compressive loading, strain magnitudes were elevated at the defect rim, with elevated tensile and compressive principal strains (Δϵmax = 4.2%, P = 0.02; Δϵmin = -4.3%, P = 0.02) and maximum shear strain at the defect rim (Δγmax = 4.4%, P = 0.007). The opposing cartilage showed minimal increase in strain patterns at contact with the defect rim but decreased strains opposing the defect. After defect creation, T1, T2 and T1ρ relaxation times were elevated at the defect rim only. Following loading, the overall relaxations times of the defect tissue and especially at the rim, increased compared to intact cartilage. CONCLUSIONS: This study demonstrates that the local biomechanical changes occurring after defect creation may induce tissue damage by increasing shear strains and depletion of cartilage constituents at the defect rim under compressive loading.
Authors: Gustavo A Orozco; Paul Bolcos; Ali Mohammadi; Matthew S Tanaka; Mingrui Yang; Thomas M Link; Benjamin Ma; Xiaojuan Li; Petri Tanska; Rami K Korhonen Journal: J Orthop Res Date: 2020-07-20 Impact factor: 3.102
Authors: Lianne Zevenbergen; Colin R Smith; Sam Van Rossom; Darryl G Thelen; Nele Famaey; Jos Vander Sloten; Ilse Jonkers Journal: PLoS One Date: 2018-10-16 Impact factor: 3.240