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Osteoarthritis and cartilage2013; 21(5); 746-755; doi: 10.1016/j.joca.2013.02.653

Non-terminal animal model of post-traumatic osteoarthritis induced by acute joint injury.

Abstract: Develop a non-terminal animal model of acute joint injury that demonstrates clinical and morphological evidence of early post-traumatic osteoarthritis (PTOA). Methods: An osteochondral (OC) fragment was created arthroscopically in one metacarpophalangeal (MCP) joint of 11 horses and the contralateral joint was sham operated. Eleven additional horses served as unoperated controls. Every 2 weeks, force plate analysis, flexion response, joint circumference, and synovial effusion scores were recorded. At weeks 0 and 16, radiographs (all horses) and arthroscopic videos (OC injured and sham joints) were graded. At week 16, synovium and cartilage biopsies were taken arthroscopically from OC injured and sham joints for histologic evaluation and the OC fragment was removed. Results: OC fragments were successfully created and horses were free of clinical lameness after fragment removal. Forelimb gait asymmetry was observed at week 2 (P = 0.0012), while joint circumference (P < 0.0001) and effusion scores (P < 0.0001) were increased in injured limbs compared to baseline from weeks 2 to 16. Positive flexion response of injured limbs was noted at multiple time points. Capsular enthesophytes were seen radiographically in injured limbs. Articular cartilage damage was demonstrated arthroscopically as mild wear-lines and histologically as superficial zone chondrocyte death accompanied by mild proliferation. Synovial hyperemia and fibrosis were present at the site of OC injury. Conclusions: Acute OC injury to the MCP joint resulted in clinical, imaging, and histologic changes in cartilage and synovium characteristic of early PTOA. This model will be useful for defining biomarkers of early osteoarthritis and for monitoring response to therapy and surgery.
Copyright © 2013 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.
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Publication Date: 2013-03-01 PubMed ID: 23467035PubMed Central: PMC3624059DOI: 10.1016/j.joca.2013.02.653Google 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 focused on developing an animal model that can simulate acute joint injury leading to early stages of post-traumatic osteoarthritis (PTOA). They successfully created traumatic osteochondral (OC) lesions in the metacarpophalangeal (MCP) joint of horses and monitored physical and histologic changes over 16 weeks, noting evidences of early osteoarthritic changes, making the model suited for studying PTOA’s onset and various therapeutic responses.

Methodology

  • The researchers developed an osteochondral (OC) fragment in one metacarpophalangeal (MCP) joint of 11 horses through arthroscopy. A sham operation was performed on the contralateral joint as a comparative measure, while 11 other horses were left unoperated as controls.
  • The horses were assessed every two weeks for flexion response, force plate analysis, synovial effusion scores, and joint circumference.
  • Radiographs and arthroscopic videos were taken at week 0 and 16 for grading, while synovium and cartilage biopsies were collected during the 16th week from the sham and OC injured joints.

Findings

  • The researchers were able to successfully create OC fragments and the horses showed no clinical lameness post fragment removal.
  • Forelimb gait asymmetry was observed in week 2. Additionally, increased joint circumference and effusion scores were recorded from weeks 2 to 16 in the injured limbs.
  • Radiographs revealed capsular enthesophytes in the injured limbs, indicating an abnormal increase in bone density at the attachment of ligaments or tendons.
  • The injured limbs displayed a positive flexion response at different points in time, suggesting joint discomfort or lameness.
  • Via arthroscopy, mild wear-lines were visible, indicating articular cartilage damage. Histologically, there was superficial zone chondrocyte death accompanied by mild proliferation.
  • The site of OC injury showed synovial hyperemia and fibrosis, indicating increased blood flow and thickening of the synovial membrane respectively.

Conclusions

  • The study demonstrated that the acute OC injury to the MCP joint brought about observable clinical, imaging, and histologic changes characteristic of early post-traumatic osteoarthritis (PTOA).
  • The researchers concluded that this model can be useful in identifying early osteoarthritis biomarkers as well as in observing and assessing the response to different therapies and surgical interventions.

Cite This Article

APA
Boyce MK, Trumble TN, Carlson CS, Groschen DM, Merritt KA, Brown MP. (2013). Non-terminal animal model of post-traumatic osteoarthritis induced by acute joint injury. Osteoarthritis Cartilage, 21(5), 746-755. https://doi.org/10.1016/j.joca.2013.02.653

Publication

Osteoarthritis and cartilage
ISSN: 1522-9653
NlmUniqueID: 9305697
Country: England
Language: English
Volume: 21
Issue: 5
Pages: 746-755
PII: S1063-4584(13)00703-6

Researcher Affiliations

Boyce, M K
  • Veterinary Population Medicine, College of Veterinary Medicine, University of Minnesota, St. Paul, MN 55108, United States.
Trumble, T N
    Carlson, C S
      Groschen, D M
        Merritt, K A
          Brown, M P

            MeSH Terms

            • Animals
            • Arthritis, Experimental / diagnostic imaging
            • Arthritis, Experimental / etiology
            • Arthritis, Experimental / pathology
            • Arthritis, Experimental / physiopathology
            • Arthroscopy
            • Cartilage, Articular / pathology
            • Exudates and Transudates
            • Female
            • Forelimb / pathology
            • Gait
            • Horses
            • Joints / injuries
            • Male
            • Osteoarthritis / diagnostic imaging
            • Osteoarthritis / etiology
            • Osteoarthritis / pathology
            • Osteoarthritis / physiopathology
            • Radiography
            • Synovial Membrane / pathology

            Grant Funding

            • R15 AR059612 / NIAMS NIH HHS
            • T32 OD010993 / NIH HHS
            • 1R15AR059612-01 / NIAMS NIH HHS
            • 1T32RR018719-01 / NCRR NIH HHS

            Conflict of Interest Statement

            . The authors have no conflict of interest.

            References

            This article includes 53 references

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