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Osteoarthritis and cartilage2015; 23(7); 1130-1137; doi: 10.1016/j.joca.2015.02.023

Joint-dependent response to impact and implications for post-traumatic osteoarthritis.

Abstract: The prevalence of osteoarthritis (OA) varies between joints. Cartilage in eight different joints was evaluated to elucidate the disparate susceptibilities between joints to post-traumatic OA (PTOA) and provide evidence for joint-specific clinical treatments. The hypothesis was that cartilage in different joints would have varying cell death and anabolic gene expression profiles after injury. Methods: Adult equine cartilage explants were harvested from shoulder (SH), elbow (EL), carpal (CA), metacarpophalangeal (MC), patellofemoral (FP), tarsal (TA), metatarsophalangeal (MT), and proximal interphalangeal (PP) joints, and injured by loading with 30 MPa within 1 s. Fractional dissipated energy, cell density, cell death, and gene expression were quantified. Results: PP had the highest fractional dissipated energy (94%, 95% confidence interval [CI] 88 to 101%). Cell density was highest in the superficial zone in all samples, with MC and MT having the highest peak density. Injured samples had significantly increased cell death (13.5%, 95% CI 9.1 to 17.9%) than non-injured samples (6.8%, 95% CI 2.5 to 11.1%, P = 0.016); however, cell death after injury was not significantly different between joints. Gene expression was significantly different between joints. CD-RAP expression in normal cartilage was lowest in FP (Cp = 21, 95% CI -80 to 122). After injury, the change in CD-RAP expression increased and was highest in FP (147% relative increase after injury, 95% CI 64 to 213). Conclusions: Different joints have different baseline characteristics, including cell density and gene expression, and responses to injury, including energy dissipation and gene expression. These unique characteristics may explain differences in OA prevalence and suggest differences in susceptibility to PTOA. Conclusions: Understanding differences in the response to injury and potential susceptibility to OA can lead to the development of preventative or treatment strategies. Background: Gene expression, cartilage injury, chondrocyte, multiphoton microscopy, cartilage biomechanical properties, PTOA. Unassigned: The prevalence of OA is variable among joints; however, most laboratory studies are performed on a single joint - most commonly the knee, and extrapolated to other joints such as the ankle or shoulder. A small number of studies have compared knee and ankle cartilage and reported differences in mechanical properties and gene expression. Conclusions: There are differences in baseline cell density and gene expression, and differences in response to injury, including gene expression and cell death. This suggests that there are inherent differences leading to varying susceptibilities in OA prevalence among joints. Joint-specific treatments may improve OA therapies.
Copyright © 2015 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.
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Publication Date: 2015-02-26 PubMed ID: 25725390PubMed Central: PMC4778978DOI: 10.1016/j.joca.2015.02.023Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • N.I.H.
  • Extramural
  • Research Support
  • Non-U.S. Gov't

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

The research investigates the varying susceptibilities of different joints to post-traumatic osteoarthritis (OA). It shows that each joint has different characteristics which affect how they react to injuries and that these differences may also explain the varying prevalence of the disease in different joints.

Research Methodology

  • The scientists started by gathering cartilage explants from eight different joints in adult horses: shoulder, elbow, carpal, metacarpophalangeal, patellofemoral, tarsal, metatarsophalangeal, and proximal interphalangeal joints.
  • These were then injured by loading with 30 MPa within a second. The variables measured post-injury included energy dissipation, cell density, cell death, and gene expression.

Research Results

  • The proximal interphalangeal joint had the highest energy dissipation of 94%.
  • The cell density was highest in the superficial zone in all samples, with metacarpophalangeal and metatarsophalangeal having the highest peak density.
  • There was a significant increase in cell death in injured samples as compared to those that were not.
  • There was, however, no significant difference in cell death between the different joints post-injury.
  • The expression of genes was significantly different in all joints examined.

Implication of the Results

  • Different joints have different baseline characteristics, including cell density and gene expression, and responses to injury, such as energy dissipation and gene expression.
  • These unique characteristics may explain the differences in OA prevalence across different joints.
  • Understanding these differences can lead to the development of preventative or treatment strategies that are unique to specific joints, improving OA therapies overall.

Conclusion

  • Most studies on osteoarthritis are performed on a single joint, most commonly the knee, and then extrapolated to other joints. However, this study highlights the inherent differences between joints that lead to varying susceptibilities to OA. The outcome suggests that a one-size-fits-all approach to OA management may not be the most effective, and instead, joint-specific treatments may need to be developed.

Cite This Article

APA
Novakofski KD, Berg LC, Bronzini I, Bonnevie ED, Poland SG, Bonassar LJ, Fortier LA. (2015). Joint-dependent response to impact and implications for post-traumatic osteoarthritis. Osteoarthritis Cartilage, 23(7), 1130-1137. https://doi.org/10.1016/j.joca.2015.02.023

Publication

Osteoarthritis and cartilage
ISSN: 1522-9653
NlmUniqueID: 9305697
Country: England
Language: English
Volume: 23
Issue: 7
Pages: 1130-1137
PII: S1063-4584(15)00067-9

Researcher Affiliations

Novakofski, K D
  • Department of Clinical Sciences, Cornell University, Ithaca, NY, USA.
Berg, L C
  • Department of Clinical Veterinary and Animal Science, University of Copenhagen, København, Denmark.
Bronzini, I
  • Department of Comparative Biomedicine and Food Science, University of Padova, Padova, Italy.
Bonnevie, E D
  • Department of Biomedical Engineering, Cornell University, Ithaca, NY, USA.
Poland, S G
  • Department of Clinical Sciences, Cornell University, Ithaca, NY, USA.
Bonassar, L J
  • Department of Biomedical Engineering, Cornell University, Ithaca, NY, USA.
Fortier, L A
  • Department of Clinical Sciences, Cornell University, Ithaca, NY, USA. Electronic address: laf4@cornell.edu.

MeSH Terms

  • Animals
  • Arthritis, Experimental / etiology
  • Arthritis, Experimental / pathology
  • Arthritis, Experimental / physiopathology
  • Cartilage, Articular / injuries
  • Cartilage, Articular / pathology
  • Cartilage, Articular / physiopathology
  • Cell Death
  • Chondrocytes / pathology
  • Gene Expression
  • Gene Expression Profiling / methods
  • Horse Diseases / etiology
  • Horse Diseases / pathology
  • Horse Diseases / physiopathology
  • Horses
  • Osteoarthritis / etiology
  • Osteoarthritis / pathology
  • Osteoarthritis / physiopathology
  • Osteoarthritis / veterinary
  • RNA, Messenger / genetics
  • Stress, Mechanical

Grant Funding

  • KL2 TR000458 / NCATS NIH HHS
  • TL1 TR000459 / NCATS NIH HHS
  • UL1 TR000457 / NCATS NIH HHS
  • TL1RR000459 / NCRR NIH HHS

Conflict of Interest Statement

. The authors have no competing financial interests to disclose.

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