Possible Mechanical and Biological Drivers of Osteoarthritis Following ACL Injury
Date
2013-11-05
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Abstract
Anterior cruciate ligament (ACL) rupture has been reported as one of the most prevalent injuries of the knee joint, leading to cartilage degeneration and increased risk of osteoarthritis (OA) development. The present work was aimed at providing a better understanding of some of the potential mechanobiological drivers of OA following trauma, by assessing joint biomechanics (i.e. relative tibiofemoral motions, and ligament and meniscal loading) and boundary lubrication of the ovine stifle joint (i.e. proteoglycan-4 (PRG4) and hyaluronan (HA) composition and lubrication function of ovine synovial fluid) following ACL injury, serially “in vivo”, and their association with gross joint damage. The general working hypothesis was that early (2-4 weeks) lubrication changes after trauma and later mechanical changes (20 weeks) may both contribute to OA development in any individual with an ACL injury. Signs of damage (mild OA) to the cartilage surfaces and menisci of stifle joints in all subjects were observed after ACL injury. Mechanical results demonstrated a significant increase in both medial and lateral meniscal loads 20 weeks following ACL rupture, with interesting inter-subject variability. MCL loads during gait also indicated a general increase; whereas, PCL and LCL loads showed a significant decrease. In terms of biology, the PRG4 and HA composition of ovine synovial fluid was compromised early after injury, but returned to normal state in the long term. Consequently, the cartilage boundary lubricating ability of ovine synovial fluid was also significantly diminished short term post injury, retuning to within normal ranges at 20 weeks. Collectively, these results indicate early changes in joint lubrication and longer term changes in tissue loads after an ACL injury, which, in turn, appear to be associated with some early OA development in the ovine model. This implies that early synovial fluid changes after ACL injury might initiate joint damage; whereas, longer term mechanical changes may amplify that damage toward OA. Further investigation is required to test these speculations, along with the impacts of potential prevention strategies such as enhancement of joint lubrication.
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Applied Mechanics, Engineering--Biomedical, Engineering--Mechanical
Citation
Atarod Pilambaraei, M. (2013). Possible Mechanical and Biological Drivers of Osteoarthritis Following ACL Injury (Doctoral thesis, University of Calgary, Calgary, Canada). Retrieved from https://prism.ucalgary.ca. doi:10.11575/PRISM/27389