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Home / Equine Research Bank / J Orthop Res / Identification of Antibodies to Chondrocyte and Synoviocyte ...
Journal of orthopaedic research : official publication of the Orthopaedic Research Society2025; 43(12); 2152-2164; doi: 10.1002/jor.70085

Identification of Antibodies to Chondrocyte and Synoviocyte Antigens in Equine Osteoarthritis.

Abstract: Innate immune responses within the joint are now known to play a key role in osteoarthritis (OA) pathogenesis. However, comparatively little is known regarding the role of adaptive immune responses in OA, and whether they may be important for initiating and sustaining progressive low-level joint inflammation. Therefore, we evaluated spontaneous osteoarthritis in horses to investigate whether antibodies recognizing live joint cells (chondrocytes, synoviocytes) were present in blood or synovial fluid, and to identify possible cellular target antigens. We found that horses with advanced OA had antibodies present in synovial fluid (SF) and plasma that recognized antigens expressed by chondrocytes and synoviocytes isolated from healthy joint tissues. Antibody concentrations correlated with clinical and arthroscopic scoring of OA severity. Antigenic targets for antibody recognition were expressed intracellularly and proteomic analysis of a prominent 60 kD protein band identified several proteins, including vimentin, calreticulin, and Hsp60, all of which are known to be antibody targets in patients with rheumatoid arthritis. Histological analysis of synovial biopsy samples from OA horses revealed the presence of numerous tertiary lymphoid structures with well-formed germinal centers, consistent with local antibody production within the joint synovium. Taken together, these studies in equine osteoarthritis revealed the presence of antibodies recognizing antigens expressed by live cells in the joint, which resembled similar immunologic processes recently described in rheumatoid arthritis. Broader questions raised by these findings include identification of triggers for local antibody production and new strategies to target this immune pathway in progressive OA.
© 2025 The Author(s). Journal of Orthopaedic Research ® published by Wiley Periodicals LLC on behalf of Orthopaedic Research Society.
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Publication Date: 2025-10-21 PubMed ID: 41117710PubMed Central: PMC12604456DOI: 10.1002/jor.70085Google Scholar: Lookup
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  • Journal Article

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.

Overview

  • This study investigates whether antibodies against joint cells exist in horses with osteoarthritis (OA) and explores potential targets of these antibodies within the joint.
  • The research focuses on understanding the adaptive immune response in OA and its role in chronic joint inflammation and disease progression.

Background and Objective

  • Osteoarthritis (OA) is a joint disease traditionally thought to be driven primarily by mechanical wear and innate immune activation.
  • Recent evidence highlights the role of innate immunity in OA, but the contribution of adaptive immunity, particularly antibodies, remains unclear.
  • The study aims to determine if horses with spontaneous OA produce antibodies targeting live joint cells (chondrocytes and synoviocytes) and to identify the specific cellular proteins involved.

Methodology

  • Samples of synovial fluid (SF) and plasma were collected from horses with advanced OA and compared to healthy controls.
  • Antibody presence and concentration against live chondrocytes and synoviocytes derived from healthy joint tissues were measured.
  • Proteomic analysis was conducted to identify the antigenic targets of these antibodies, focusing on a dominant 60 kD protein band.
  • Synovial biopsy samples from OA horses were examined histologically for evidence of localized immune responses.

Key Findings

  • Antibodies recognizing antigens on live chondrocytes and synoviocytes were found in both synovial fluid and plasma of horses with advanced OA.
  • The levels of these antibodies correlated with clinical signs and arthroscopic scores, indicating a relationship between antibody presence and OA severity.
  • Proteomic analysis identified intracellular proteins—including vimentin, calreticulin, and Hsp60—as major antibody targets.
  • These proteins are also known to elicit immune responses in rheumatoid arthritis, suggesting shared immunopathogenic mechanisms.
  • Histological analysis showed numerous tertiary lymphoid structures with germinal centers within synovial tissue, indicating local production of antibodies in the joint.

Interpretation and Implications

  • The presence of antibodies against joint cell antigens highlights a possible adaptive immune component in the pathogenesis of equine OA.
  • Local antibody production within the joint’s synovium suggests an ongoing immune response that may contribute to chronic inflammation and cartilage damage.
  • The similarity of immunologic targets to those in rheumatoid arthritis implies overlapping pathways between these diseases.
  • The findings raise important questions about what triggers this adaptive immune activation in OA, whether it is antigen-driven or a secondary response to joint damage.
  • Understanding these pathways could lead to novel therapeutic strategies aimed at modulating antibody-mediated immune responses to slow or prevent progression of OA.

Conclusions

  • This study provides evidence that adaptive immunity, through antibodies targeting chondrocyte and synoviocyte antigens, may be integral to the development and progression of osteoarthritis in horses.
  • The identification of specific antigenic targets and the demonstration of local antibody generation within the joint opens new avenues for research into immune-based interventions in OA.
  • Future research should focus on elucidating triggers for local antibody production and exploring treatments that could disrupt this pathogenic immune loop.

Cite This Article

APA
Linde P, Kurihara J, Chow L, Williams ZJ, Hendrickson D, Bass L, Dow S, Pezzanite LM. (2025). Identification of Antibodies to Chondrocyte and Synoviocyte Antigens in Equine Osteoarthritis. J Orthop Res, 43(12), 2152-2164. https://doi.org/10.1002/jor.70085

Publication

Journal of orthopaedic research : official publication of the Orthopaedic Research Society
ISSN: 1554-527X
NlmUniqueID: 8404726
Country: United States
Language: English
Volume: 43
Issue: 12
Pages: 2152-2164

Researcher Affiliations

Linde, Peter
  • Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado, USA.
  • Immunotherapy Research Laboratory, Translational Medicine Institute, Colorado State University, Fort Collins, Colorado, USA.
  • Orthopaedic Research Center, Translational Medicine Institute, Colorado State University, Fort Collins, Colorado, USA.
Kurihara, Jade
  • Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado, USA.
  • Immunotherapy Research Laboratory, Translational Medicine Institute, Colorado State University, Fort Collins, Colorado, USA.
Chow, Lyndah
  • Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado, USA.
  • Immunotherapy Research Laboratory, Translational Medicine Institute, Colorado State University, Fort Collins, Colorado, USA.
  • Orthopaedic Research Center, Translational Medicine Institute, Colorado State University, Fort Collins, Colorado, USA.
Williams, Zoë J
  • Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado, USA.
  • Immunotherapy Research Laboratory, Translational Medicine Institute, Colorado State University, Fort Collins, Colorado, USA.
  • Orthopaedic Research Center, Translational Medicine Institute, Colorado State University, Fort Collins, Colorado, USA.
Hendrickson, Dean
  • Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado, USA.
Bass, Luke
  • Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado, USA.
  • Orthopaedic Research Center, Translational Medicine Institute, Colorado State University, Fort Collins, Colorado, USA.
Dow, Steven
  • Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado, USA.
  • Immunotherapy Research Laboratory, Translational Medicine Institute, Colorado State University, Fort Collins, Colorado, USA.
Pezzanite, Lynn M
  • Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado, USA.
  • Immunotherapy Research Laboratory, Translational Medicine Institute, Colorado State University, Fort Collins, Colorado, USA.
  • Orthopaedic Research Center, Translational Medicine Institute, Colorado State University, Fort Collins, Colorado, USA.

MeSH Terms

  • Animals
  • Horses
  • Osteoarthritis / immunology
  • Osteoarthritis / veterinary
  • Osteoarthritis / pathology
  • Chondrocytes / immunology
  • Horse Diseases / immunology
  • Synoviocytes / immunology
  • Synovial Fluid / immunology
  • Male
  • Female

Grant Funding

  • Department of Clinical Sciences, Colorado State University.
  • K01 OD037846 / NIH HHS
  • T32TR004366 / NIH/NCATS Colorado CTSA.
  • T32 TR004366 / NCATS NIH HHS
  • Boettcher Webb-Waring Foundation.
  • K01OD037846-01A1 / NIH.

References

This article includes 50 references
  1. Yelin E, Weinstein S, King T. The Burden of Musculoskeletal Diseases in the United States. Seminars in Arthritis and Rheumatism 46 (2016): 259–260.
    doi: 10.1016/j.semarthrit.2016.07.013pubmed: 27519477google scholar: lookup
  2. Cui A, Li H, Wang D, Zhong J, Chen Y, Lu H. Global, Regional Prevalence, Incidence and Risk Factors of Knee Osteoarthritis in Population‐Based Studies. EClinicalMedicine 29–30 (2020): 100587.
    doi: 10.1016/j.eclinm.2020.100587pmc: PMC7704420pubmed: 34505846google scholar: lookup
  3. Zhao X, Shah D, Gandhi K. Clinical, Humanistic, and Economic Burden of Osteoarthritis Among Noninstitutionalized Adults in the United States. Osteoarthritis and Cartilage 27 (2019): 1618–1626.
    doi: 10.1016/j.joca.2019.07.002pubmed: 31299387google scholar: lookup
  4. Kotlarz H, Gunnarsson CL, Fang H, Rizzo JA. Insurer and Out‐of‐Pocket Costs of Osteoarthritis in the US: Evidence From National Survey Data. Arthritis & Rheumatism 60 (2009): 3546–3553.
    doi: 10.1002/art.24984pubmed: 19950287google scholar: lookup
  5. Murphy L, Schwartz TA, Helmick CG. Lifetime Risk of Symptomatic Knee Osteoarthritis. Arthritis Care & Research 59 (2008): 1207–1213.
    doi: 10.1002/art.24021pmc: PMC4516049pubmed: 18759314google scholar: lookup
  6. de Lange-Brokaar BJE, Ioan-Facsinay A, van Osch GJVM. Synovial Inflammation, Immune Cells and Their Cytokines in Osteoarthritis: A Review. Osteoarthritis and Cartilage 20 (2012): 1484–1499.
    doi: 10.1016/j.joca.2021.08.027pubmed: 22960092google scholar: lookup
  7. Orlowsky EW, Kraus VB. The Role of Innate Immunity in Osteoarthritis: When Our First Line of Defense Goes on the Offensive. The Journal of Rheumatology 42 (2015): 363–371.
    doi: 10.3899/jrheum.140382pmc: PMC4465583pubmed: 25593231google scholar: lookup
  8. Kobayashi M, Squires GR, Mousa A. Role of Interleukin‐1 and Tumor Necrosis Factor in Matrix Degradation of Human Osteoarthritic Cartilage. Arthritis & Rheumatism 52 (2005): 128–135.
    doi: 10.1002/ART.20776pubmed: 15641080google scholar: lookup
  9. Wu CL, Harasymowicz NS, Klimak MA, Collins KH, Guilak F. The Role of Macrophages in Osteoarthritis and Cartilage Repair. Osteoarthritis and Cartilage 28 (2020): 544–554.
    doi: 10.1016/J.JOCA.2019.12.007pmc: PMC7214213pubmed: 31926267google scholar: lookup
  10. Fahy N, de Vries-van Melle ML, Lehmann J. Human Osteoarthritic Synovium Impacts Chondrogenic Differentiation of Mesenchymal Stem Cells via Macrophage Polarisation State. Osteoarthritis and Cartilage 22 (2014): 1167–1175.
    doi: 10.1016/J.JOCA.2014.05.021pubmed: 24911520google scholar: lookup
  11. Manferdini C, Paolella F, Gabusi E. From Osteoarthritic Synovium to Synovial‐Derived Cells Characterization: Synovial Macrophages Are Key Effector Cells. Arthritis Research & Therapy 18 (2016): 83.
    doi: 10.1186/S13075-016-0983-4pmc: PMC4820904pubmed: 27044395google scholar: lookup
  12. Cai S, Ming B, Ye C. Similar Transition Processes in Synovial Fibroblasts From Rheumatoid Arthritis and Osteoarthritis: A Single‐Cell Study. Journal of Immunology Research 2019 (2019): 1–11.
    doi: 10.1155/2019/4080735pmc: PMC6681591pubmed: 31428656google scholar: lookup
  13. Tetlow LC, Adlam DJ, Woolley DE. Matrix Metalloproteinase and Proinflammatory Cytokine Production by Chondrocytes of Human Osteoarthritic Cartilage Associations With Degenerative Changes. Arthritis & Rheumatism 44 (2001): 585–594.
    doi: 10.1002/1529-0131(200103)44:3pubmed: 11263773google scholar: lookup
  14. Haseeb A, Haqqi TM. Immunopathogenesis of Osteoarthritis. Clinical Immunology 146 (2013): 185–196.
    doi: 10.1016/J.CLIM.2012.12.011pmc: PMC4015466pubmed: 23360836google scholar: lookup
  15. Ishii H, Tanaka H, Katoh K, Nakamura H, Nagashima M, Yoshino S. Characterization of Infiltrating T Cells and Th1/Th2‐type Cytokines in the Synovium of Patients With Osteoarthritis. Osteoarthritis and Cartilage 10 (2002): 277–281.
    doi: 10.1053/JOCA.2001.0509pubmed: 11950250google scholar: lookup
  16. Sakata M, Tsuruha J I, Masuko‐Hongo K. Autoantibodies to Osteopontin in Patients With Osteoarthritis and Rheumatoid Arthritis. The Journal of Rheumatology 28 (2001): 1492–1495.
    pubmed: 11469452
  17. Tsuruha J, Masuko‐Hongo K, Kato T. Autoimmunity Against YKL‐39, a Human Cartilage Derived Protein, in Patients With Osteoarthritis. The Journal of Rheumatology 29 (2002): 1459–1466.
    pubmed: 12136906
  18. Tsuruha J, Masuko‐Hongo K, Kato T, Sakata M, Nakamura H, Nishioka K. Implication of Cartilage Intermediate Layer Protein in Cartilage Destruction in Subsets of Patients With Osteoarthritis and Rheumatoid Arthritis. Arthritis & Rheumatism 44 (2001): 838–845.
    doi: 10.1002/1529-0131(200104)44:4pubmed: 11315923google scholar: lookup
  19. Kato T, Xiang Y, Sekine T. Proteomic Surveillance of Autoimmunity in Osteoarthritis. Arthritis Research & Therapy 5 (2003): 17.
    doi: 10.1186/AR818pubmed: 15146421google scholar: lookup
  20. Du H, Masuko‐Hongo K, Nakamura H. The Prevalence of Autoantibodies Against Cartilage Intermediate Layer Protein, YKL‐39, Osteopontin, and Cyclic Citrullinated Peptide in Patients With Early‐Stage Knee Osteoarthritis: Evidence of a Variety of Autoimmune Processes. Rheumatology International 26 (2005): 35–41.
    doi: 10.1007/S00296-004-0497-2pubmed: 15378262google scholar: lookup
  21. Caspi D, Anouk M, Golan I. Synovial Fluid Levels of Anti‐Cyclic Citrullinated Peptide Antibodies and IgA Rheumatoid Factor in Rheumatoid Arthritis, Psoriatic Arthritis, and Osteoarthritis. Arthritis Care & Research 55 (2006): 53–56.
    doi: 10.1002/ART.21691pubmed: 16463412google scholar: lookup
  22. Trouw L A, Rispens T, Toes R E M. Beyond Citrullination: Other Post‐Translational Protein Modifications in Rheumatoid Arthritis. Nature Reviews Rheumatology 13 (2017): 331–339.
    doi: 10.1038/nrrheum.2017.15pubmed: 28275265google scholar: lookup
  23. Mullazehi M, Mathsson L, Lampa J, Rönnelid J. High Anti‐Collagen Type‐II Antibody Levels and Induction of Proinflammatory Cytokines by Anti‐Collagen Antibody‐Containing Immune Complexes In Vitro Characterise a Distinct Rheumatoid Arthritis Phenotype Associated With Acute Inflammation at the Time of Disease Onset. Annals of the Rheumatic Diseases 66 (2007): 537–541.
    doi: 10.1136/ARD.2006.064782pmc: PMC1856042pubmed: 17040962google scholar: lookup
  24. Corsiero E, Caliste M, Jagemann L. Autoimmunity to Stromal‐Derived Autoantigens in Rheumatoid Ectopic Germinal Centers Exacerbates Arthritis and Affects Clinical Response. Journal of Clinical Investigation 134 (2024): 12.
    doi: 10.1172/JCI169754pmc: PMC11178537pubmed: 38950333google scholar: lookup
  25. McIlwraith C W, Frisbie D D, Kawcak C E, Fuller C J, Hurtig M, Cruz A. The OARSI Histopathology Initiative – Recommendations for Histological Assessments of Osteoarthritis in the Horse. Osteoarthritis and Cartilage 18 (2010): S93–S105.
    pubmed: 20864027
  26. Pezzanite L, Chow L, Piquini G. Use of In Vitro Assays to Identify Antibiotics That Are Cytotoxic to Normal Equine Chondrocytes and Synovial Cells. Equine Veterinary Journal 53 (2021): 579–589.
    doi: 10.1111/EVJ.13314pmc: PMC7738387pubmed: 32544273google scholar: lookup
  27. Musaelyan A, Lapin S, Nazarov V. Vimentin as Antigenic Target in Autoimmunity: A Comprehensive Review. Autoimmunity Reviews 17 (2018): 926–934.
    doi: 10.1016/J.AUTREV.2018.04.004pubmed: 30009963google scholar: lookup
  28. Holoshitz J, De Almeida D E, Ling S. A Role for Calreticulin in the Pathogenesis of Rheumatoid Arthritis. Annals of the New York Academy of Sciences 1209 (2010): 91–98.
    doi: 10.1111/J.1749-6632.2010.05745.Xpmc: PMC2959188pubmed: 20958321google scholar: lookup
  29. Bery A I, Shepherd H M, Li W, Krupnick A S, Gelman A E, Kreisel D. Role of Tertiary Lymphoid Organs in the Regulation of Immune Responses in the Periphery. Cellular and Molecular Life Sciences 79, no. 7 (2022): 359.
    doi: 10.1007/s00018-022-04388-xpmc: PMC9188279pubmed: 35689679google scholar: lookup
  30. Shipman W D, Dasoveanu D C, Lu T T. Tertiary Lymphoid Organs in Systemic Autoimmune Diseases: Pathogenic or Protective?. F1000Research 6 (2017): 196.
    doi: 10.12688/f1000research.10595.1pmc: PMC5333609pubmed: 28344775google scholar: lookup
  31. Schumacher TN, Thommen DS. Tertiary Lymphoid Structures in Cancer. Science 375 (2022): eabf9419.
    doi: 10.1126/science.abf9419pubmed: 34990248google scholar: lookup
  32. Di Cicco M, Humby F, Kelly S. O44. Presence of Synovial Lymphocyte Aggregates Correlates With a More Severe Clinical Phenotype in Patients With Early Inflammatory Arthritis. Rheumatology 53, no. Issue suppl_1 (2014): i48.
    doi: 10.1093/rheumatology/keu093.002google scholar: lookup
  33. Holoshitz J, De Almeida DE, Ling S. A Role for Calreticulin in the Pathogenesis of Rheumatoid Arthritis. Annals of the New York Academy of Sciences 1209 (2010): 91–98.
    doi: 10.1111/J.1749-6632.2010.05745.Xpmc: PMC2959188pubmed: 20958321google scholar: lookup
  34. Damasceno LEA, Prado DS, Veras FP. PKM2 Promotes Th17 Cell Differentiation and Autoimmune Inflammation by Fine‐Tuning STAT3 Activation. Journal of Experimental Medicine 217 (2020): 217.
    doi: 10.1084/JEM.20190613pmc: PMC7537396pubmed: 32697823google scholar: lookup
  35. Nandi A, Yan LJ, Jana CK, Das N. Role of Catalase in Oxidative Stress‐ and Age‐Associated Degenerative Diseases. Oxidative Medicine and Cellular Longevity 2019 (2019): 1–19.
    doi: 10.1155/2019/9613090pmc: PMC6885225pubmed: 31827713google scholar: lookup
  36. Dubey D, Beecher G, Hammami MB. Identification of Caveolae‐Associated Protein 4 Autoantibodies as a Biomarker of Immune‐Mediated Rippling Muscle Disease in Adults. JAMA Neurology 79 (2022): 808–816.
    doi: 10.1001/JAMANEUROL.2022.1357pmc: PMC9361081pubmed: 35696196google scholar: lookup
  37. Liu Y, Xie S, Zhu K, Guan X, Guo L, Lu R. CALD1 is a Prognostic Biomarker and Correlated With Immune Infiltrates in Gastric Cancers. Heliyon 7 (2021): e07257.
    doi: 10.1016/J.HELIYON.2021.E07257pmc: PMC8219766pubmed: 34189308google scholar: lookup
  38. Burbelo PD, Iadarola MJ, Keller JM, Warner BM. Autoantibodies Targeting Intracellular and Extracellular Proteins in Autoimmunity. Frontiers in Immunology 12 (2021): 12.
    doi: 10.3389/FIMMU.2021.548469pmc: PMC7982651pubmed: 33763057google scholar: lookup
  39. Li YS, Luo W, Zhu SA, Lei GH. T Cells in Osteoarthritis: Alterations and Beyond. Frontiers in Immunology 8 (2017): 356.
    doi: 10.3389/fimmu.2017.00356pmc: PMC5371609pubmed: 28424692google scholar: lookup
  40. Barnas JL, Looney RJ, Anolik JH. B Cell Targeted Therapies in Autoimmune Disease. Current Opinion in Immunology 61 (2019): 92–99.
    doi: 10.1016/j.coi.2019.09.004pmc: PMC6982404pubmed: 31733607google scholar: lookup
  41. Chen Y, Xu Y, Li H. A Novel Anti‐CD38 Monoclonal Antibody for Treating Immune Thrombocytopenia. New England Journal of Medicine 390, no. 23 (2024): 2178–2190.
    doi: 10.1056/NEJMoa2400409pubmed: 38899695google scholar: lookup
  42. Sanchez-Lopez E, Coras R, Torres A, Lane NE, Guma M. Synovial Inflammation in Osteoarthritis Progression. Nature Reviews Rheumatology 18 (2022): 258–275.
    doi: 10.1038/S41584-022-00749-9pmc: PMC9050956pubmed: 35165404google scholar: lookup
  43. Zou Z, Li H, Yu K. The Potential Role of Synovial Cells in the Progression and Treatment of Osteoarthritis. Exploration 3 (2023): 20220132.
    doi: 10.1002/EXP.20220132pmc: PMC10582617pubmed: 37933282google scholar: lookup
  44. Adam MS, Zhuang H, Ren X, Zhang Y, Zhou P. The Metabolic Characteristics and Changes of Chondrocytes In Vivo and In Vitro in Osteoarthritis. Frontiers in Endocrinology 15 (2024): 1393550.
    doi: 10.3389/FENDO.2024.1393550pmc: PMC11162117pubmed: 38854686google scholar: lookup
  45. Guan M, Yu Q, Zhou G. Mechanisms of Chondrocyte Cell Death in Osteoarthritis: Implications for Disease Progression and Treatment. Journal of Orthopaedic Surgery and Research 19 (2024): 550.
    doi: 10.1186/S13018-024-05055-6pmc: PMC11382417pubmed: 39252111google scholar: lookup
  46. Burbelo PD, Iadarola MJ, Alevizos I, Sapio MR. Transcriptomic Segregation of Human Autoantigens Useful for the Diagnosis of Autoimmune Diseases. Molecular Diagnosis & Therapy 20 (2016): 415–427.
    doi: 10.1007/S40291-016-0211-6pmc: PMC5023465pubmed: 27259330google scholar: lookup
  47. Elkon K, Casali P. Nature and Functions of Autoantibodies. Nature Clinical Practice. Rheumatology 4 (2008): 491–498.
    doi: 10.1038/NCPRHEUM0895pmc: PMC2703183pubmed: 18756274google scholar: lookup
  48. McIlwraith CW, Frisbie DD, Kawcak CE. The Horse as a Model of Naturally Occurring Osteoarthritis. Bone & Joint Research 1 (2012): 297–309.
    doi: 10.1302/2046-3758.111.20000132pmc: PMC3626203pubmed: 23610661google scholar: lookup
  49. McIlwraith CW, Fortier LA, Frisbie DD, Nixon AJ. Equine Models of Articular Cartilage Repair. Cartilage 2 (2011): 317–326.
    doi: 10.1177/1947603511406531pmc: PMC4297134pubmed: 26069590google scholar: lookup
  50. Chu CR, Szczodry M, Bruno S. Animal Models for Cartilage Regeneration and Repair. Tissue Engineering Part B: Reviews 16 (2010): 105–115.
    doi: 10.1089/ten.TEB.2009.0452pmc: PMC3121784pubmed: 19831641google scholar: lookup

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