Joint instability and cartilage compression in a mouse model of posttraumatic osteoarthritis. Issue 2 (25th October 2013)

• Record Type: Journal Article
• Authors: Onur, Tarik S.; Wu, Ruobin; Chu, Stacey; Chang, Wenhan; Kim, Hubert T.; Dang, Alexis B.C.
• Is Part Of: Journal of orthopaedic research. Volume 32:Issue 2(2014:Feb.)
• Page Start: 318
• Page End: 323
• Publication Date: 2013-10-25
• Subjects: Orthopedics -- Periodicals; Musculoskeletal system -- Periodicals; 616.7
• DOI: 10.1002/jor.22509
• Languages: English
• ISSNs: 0736-0266

Abstract

<abstract abstract-type="main" xml:lang="en"> <title>ABSTRACT</title> <sec id="jor22509-sec-0001" sec-type="section"> <p>Joint instability and cartilage trauma have been previously studied and identified as key mediators in the development of posttraumatic osteoarthritis (PTOA). The purpose of this study was to use an in vivo model to compare the effect of joint instability, caused by the rupture of the anterior cruciate ligament (ACL), versus cartilage compression. In this study, mice were subjected to cyclical axial loads of twelve Newtons (N) for 240 cycles or until the ACL ruptured. One and eight weeks after this procedure, knees were sectioned coronally and evaluated for osteoarthritis by histology. Using a scoring scale established by [Pritzker K, Gay S, Jimenez S, et al. (2006): Osteoarthritis Cartilage 14:13–29], the articular cartilage across each surface was scored and combined to produce a total degeneration score. The ACL‐ruptured group had a significantly greater total degeneration score than either control or compression treated joints at 1 and 8 weeks. Additionally, only sections from ACL‐ruptured knees consistently showed synovitis after 1 week and osteophyte formation after 8 weeks. Thus, it appears using that ACL rupture consistently creates a severe osteoarthritis phenotype, while axial cartilage compression alone does not appear to be an appropriate method of inducing PTOA in vivo. © 2013 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 32:318–323, 2014.</p> </sec> </abstract>