Temporal effects of impact on articular cartilage cell death, gene expression, matrix biochemistry, and biomechanics.
Articular cartilage injury can cause post-traumatic osteoarthritis, but early processes leading to the disease are not well understood. The objective of this study was to characterize two levels of impact loading at 24 h, 1 week, and 4 weeks in terms of cell death, gene expression, extracellular matrix biochemistry, and tissue biomechanical properties. The data show cell death increased and tissue stiffness decreased by 24 h following High impact (2.8 J). These degradative changes persisted at 1 and 4 weeks, and were further accompanied by measurable changes in ECM biochemistry. Moreover, following High impact at 24 h there were specific changes in gene expression that distinguished injured tissue from adjacent tissue that was not loaded. In contrast, Low impact (1.1 J) showed little change from control specimens at 24 h or 1 week. However, at 4 weeks, a significant increase in cell death and significant decrease in tissue stiffness were present. The constellation of findings indicates Low impacted tissue exhibited a delayed biological response. The study characterizes a model system for examining the biology of articular cartilage post-impact, as well as identifies possible time points and success criteria to be used in future studies employing intervention agents.
Natoli
Roman M
RM
Department of Bioengineering, Rice University, 6100 Main Street, Keck Hall Suite 116, Houston, TX 77005, USA.
Scott
C Corey
CC
Athanasiou
Kyriacos A
KA
D000818:Animals; D017209:Apoptosis; D002358:Cartilage, Articular / Q000293:injuries* / Q000473:pathology / Q000503:physiopathology*; D002417:Cattle; D003198:Computer Simulation; D004548:Elasticity; D016326:Extracellular Matrix Proteins / Q000378:metabolism*; D005786:Gene Expression Regulation; D066298:In Vitro Techniques; D040542:Mechanotransduction, Cellular; D008954:Models, Biological; D010812:Physical Stimulation / Q000009:adverse effects*; D013314:Stress, Mechanical; D014949:Wounds, Nonpenetrating / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*
D016326:Extracellular Matrix Proteins