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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.
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

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.

References

This article includes 34 references
  1. Woolf AD, Pfleger B. Burden of major musculoskeletal conditions.. Bull World Health Organ 2003;81(9):646-56.
    pmc: PMC2572542pubmed: 14710506
  2. Brown TD, Johnston RC, Saltzman CL, Marsh JL, Buckwalter JA. Posttraumatic osteoarthritis: a first estimate of incidence, prevalence, and burden of disease.. J Orthop Trauma 2006 Nov-Dec;20(10):739-44.
  3. Cushnaghan J, Dieppe P. Study of 500 patients with limb joint osteoarthritis. I. Analysis by age, sex, and distribution of symptomatic joint sites.. Ann Rheum Dis 1991 Jan;50(1):8-13.
    pmc: PMC1004316pubmed: 1994877doi: 10.1136/ard.50.1.8google scholar: lookup
  4. Saltzman CL, Salamon ML, Blanchard GM, Huff T, Hayes A, Buckwalter JA, Amendola A. Epidemiology of ankle arthritis: report of a consecutive series of 639 patients from a tertiary orthopaedic center.. Iowa Orthop J 2005;25:44-6.
    pmc: PMC1888779pubmed: 16089071
  5. Valderrabano V, Horisberger M, Russell I, Dougall H, Hintermann B. Etiology of ankle osteoarthritis.. Clin Orthop Relat Res 2009 Jul;467(7):1800-6.
    pmc: PMC2690733pubmed: 18830791doi: 10.1007/s11999-008-0543-6google scholar: lookup
  6. Haugen IK, Englund M, Aliabadi P, Niu J, Clancy M, Kvien TK, Felson DT. Prevalence, incidence and progression of hand osteoarthritis in the general population: the Framingham Osteoarthritis Study.. Ann Rheum Dis 2011 Sep;70(9):1581-6.
    pmc: PMC3867970pubmed: 21622766doi: 10.1136/ard.2011.150078google scholar: lookup
  7. Duncan R, Peat G, Thomas E, Hay EM, Croft P. Incidence, progression and sequence of development of radiographic knee osteoarthritis in a symptomatic population.. Ann Rheum Dis 2011 Nov;70(11):1944-8.
    pubmed: 21810840doi: 10.1136/ard.2011.151050google scholar: lookup
  8. Eger W, Schumacher BL, Mollenhauer J, Kuettner KE, Cole AA. Human knee and ankle cartilage explants: catabolic differences.. J Orthop Res 2002 May;20(3):526-34.
    pubmed: 12038627doi: 10.1016/s0736-0266(01)00125-5google scholar: lookup
  9. Orazizadeh M, Cartlidge C, Wright MO, Millward-Sadler SJ, Nieman J, Halliday BP, Lee HS, Salter DM. Mechanical responses and integrin associated protein expression by human ankle chondrocytes.. Biorheology 2006;43(3,4):249-58.
    pubmed: 16912398
  10. Treppo S, Koepp H, Quan EC, Cole AA, Kuettner KE, Grodzinsky AJ. Comparison of biomechanical and biochemical properties of cartilage from human knee and ankle pairs.. J Orthop Res 2000 Sep;18(5):739-48.
    pubmed: 11117295doi: 10.1002/jor.1100180510google scholar: lookup
  11. Stockwell RA. The interrelationship of cell density and cartilage thickness in mammalian articular cartilage.. J Anat 1971 Sep;109(Pt 3):411-21.
    pmc: PMC1270984pubmed: 5153801
  12. Korhonen RK, Wong M, Arokoski J, Lindgren R, Helminen HJ, Hunziker EB, Jurvelin JS. Importance of the superficial tissue layer for the indentation stiffness of articular cartilage.. Med Eng Phys 2002 Mar;24(2):99-108.
    pubmed: 11886828doi: 10.1016/s1350-4533(01)00123-0google scholar: lookup
  13. Buckley MR, Gleghorn JP, Bonassar LJ, Cohen I. Mapping the depth dependence of shear properties in articular cartilage.. J Biomech 2008 Aug 7;41(11):2430-7.
  14. Simon WH. Scale effects in animal joints. I. Articular cartilage thickness and compressive stress.. Arthritis Rheum 1970 May-Jun;13(3):244-56.
    pubmed: 5423816doi: 10.1002/art.1780130305google scholar: lookup
  15. Waters NP, Stoker AM, Carson WL, Pfeiffer FM, Cook JL. Biomarkers affected by impact velocity and maximum strain of cartilage during injury.. J Biomech 2014 Sep 22;47(12):3185-95.
  16. Natoli RM, Scott CC, Athanasiou KA. Temporal effects of impact on articular cartilage cell death, gene expression, matrix biochemistry, and biomechanics.. Ann Biomed Eng 2008 May;36(5):780-92.
    pubmed: 18299988doi: 10.1007/s10439-008-9472-5google scholar: lookup
  17. Sauter E, Buckwalter JA, McKinley TO, Martin JA. Cytoskeletal dissolution blocks oxidant release and cell death in injured cartilage.. J Orthop Res 2012 Apr;30(4):593-8.
    pmc: PMC3666162pubmed: 21928429doi: 10.1002/jor.21552google scholar: lookup
  18. Palmer JL, Bertone AL, Litsky AS. Contact area and pressure distribution changes of the equine third carpal bone during loading.. Equine Vet J 1994 May;26(3):197-202.
  19. Brommer H, Brama PA, Barneveld A, van Weeren PR. Differences in the topographical distribution of articular cartilage degeneration between equine metacarpo- and metatarsophalangeal joints.. Equine Vet J 2004 Sep;36(6):506-10.
    pubmed: 15460075doi: 10.2746/0425164044877369google scholar: lookup
  20. Brama PA, Tekoppele JM, Bank RA, Karssenberg D, Barneveld A, van Weeren PR. Topographical mapping of biochemical properties of articular cartilage in the equine fetlock joint.. Equine Vet J 2000 Jan;32(1):19-26.
    pubmed: 10661380doi: 10.2746/042516400777612062google scholar: lookup
  21. Garcia-Seco E, Wilson DA, Cook JL, Kuroki K, Kreeger JM, Keegan KG. Measurement of articular cartilage stiffness of the femoropatellar, tarsocrural, and metatarsophalangeal joints in horses and comparison with biochemical data.. Vet Surg 2005 Nov-Dec;34(6):571-8.
  22. Brittberg M, Aglietti P, Gambardella R, Hangody L, Hauselmann H, Jakob R. ICRS clinical cartilage injury evaluation system-2000. 2000.
  23. Brittberg M, Winalski CS. Evaluation of cartilage injuries and repair.. J Bone Joint Surg Am 2003;85-A Suppl 2:58-69.
  24. Milentijevic D, Rubel IF, Liew AS, Helfet DL, Torzilli PA. An in vivo rabbit model for cartilage trauma: a preliminary study of the influence of impact stress magnitude on chondrocyte death and matrix damage.. J Orthop Trauma 2005 Aug;19(7):466-73.
  25. Novakofski KD, Williams RM, Fortier LA, Mohammed HO, Zipfel WR, Bonassar LJ. Identification of cartilage injury using quantitative multiphoton microscopy.. Osteoarthritis Cartilage 2014 Feb;22(2):355-62.
    pmc: PMC4117377pubmed: 24185113doi: 10.1016/j.joca.2013.10.008google scholar: lookup
  26. Sauvola J, Pietikäinen M. Adaptive document image binarization. Pattern Recognit 2000;33:225–36.
  27. Tellmann G, Geulen O. LightCycler® 480 Real-Time PCR system: Innovative solutions for relative quantification. 2006;4:16.
  28. Ewers BJ, Dvoracek-Driksna D, Orth MW, Haut RC. The extent of matrix damage and chondrocyte death in mechanically traumatized articular cartilage explants depends on rate of loading.. J Orthop Res 2001 Sep;19(5):779-84.
    pubmed: 11562121doi: 10.1016/s0736-0266(01)00006-7google scholar: lookup
  29. Witte TH, Knill K, Wilson AM. Determination of peak vertical ground reaction force from duty factor in the horse (Equus caballus).. J Exp Biol 2004 Oct;207(Pt 21):3639-48.
    pubmed: 15371472doi: 10.1242/jeb.01182google scholar: lookup
  30. Lee H, Kirkland WG, Whitmore RN, Theis KM, Young HE, Richardson AJ, Jackson RL, Hanson RR. Comparison of equine articular cartilage thickness in various joints.. Connect Tissue Res 2014 Oct-Dec;55(5-6):339-47.
    pubmed: 25111191doi: 10.3109/03008207.2014.949698google scholar: lookup
  31. Saito S, Kondo S, Mishima S, Ishiguro N, Hasegawa Y, Sandell LJ, Iwata H. Analysis of cartilage-derived retinoic-acid-sensitive protein (CD-RAP) in synovial fluid from patients with osteoarthritis and rheumatoid arthritis.. J Bone Joint Surg Br 2002 Sep;84(7):1066-9.
    pubmed: 12358374doi: 10.1302/0301-620x.84b7.12177google scholar: lookup
  32. Kondo S, Cha SH, Xie WF, Sandell LJ. Cytokine regulation of cartilage-derived retinoic acid-sensitive protein (CD-RAP) in primary articular chondrocytes: suppression by IL-1, bfGF, TGFbeta and stimulation by IGF-1.. J Orthop Res 2001 Jul;19(4):712-9.
    pubmed: 11518283doi: 10.1016/s0736-0266(00)00068-1google scholar: lookup
  33. Nelson F, Dahlberg L, Laverty S, Reiner A, Pidoux I, Ionescu M, Fraser GL, Brooks E, Tanzer M, Rosenberg LC, Dieppe P, Robin Poole A. Evidence for altered synthesis of type II collagen in patients with osteoarthritis.. J Clin Invest 1998 Dec 15;102(12):2115-25.
    pmc: PMC509166pubmed: 9854047doi: 10.1172/jci4853google scholar: lookup
  34. Trumble TN, Trotter GW, Oxford JR, McIlwraith CW, Cammarata S, Goodnight JL, Billinghurst RC, Frisbie DD. Synovial fluid gelatinase concentrations and matrix metalloproteinase and cytokine expression in naturally occurring joint disease in horses.. Am J Vet Res 2001 Sep;62(9):1467-77.
    pubmed: 11560279doi: 10.2460/ajvr.2001.62.1467google scholar: lookup

Citations

This article has been cited 13 times.
  1. Chang CC, Lin SY, Lu CK, Jupiter JB, Fu YC, Liu WC. Minimum 5-Year Follow-Up Assessment of Volar Plate Interposition Arthroplasty for Post-Traumatic Osteoarthritis in Proximal Interphalangeal Joints.. J Clin Med 2023 Jul 18;12(14).
    doi: 10.3390/jcm12144760pubmed: 37510875google scholar: lookup
  2. Santos S, Neu CP, Grady JJ, Pierce DM. Genipin does not reduce the initiation or propagation of microcracks in collagen networks of cartilage.. Osteoarthr Cartil Open 2022 Mar;4(1):100233.
    doi: 10.1016/j.ocarto.2022.100233pubmed: 36474465google scholar: lookup
  3. David MA, Chamberlain AM, Lake SP. Preclinical Models of Elbow Injury and Pathology.. Ann Jt 2021 Jan;6.
    doi: 10.21037/aoj.2020.02.09pubmed: 35990575google scholar: lookup
  4. Garcia FL, Williams BT, Polce EM, Heller DB, Aman ZS, Nwachukwu BU, Nho SJ, Chahla J. Preparation Methods and Clinical Outcomes of Platelet-Rich Plasma for Intra-articular Hip Disorders: A Systematic Review and Meta-analysis of Randomized Clinical Trials.. Orthop J Sports Med 2020 Oct;8(10):2325967120960414.
    doi: 10.1177/2325967120960414pubmed: 33195721google scholar: lookup
  5. Peal BT, Gagliardi R, Su J, Fortier LA, Delco ML, Nixon AJ, Reesink HL. Synovial fluid lubricin and hyaluronan are altered in equine osteochondral fragmentation, cartilage impact injury, and full-thickness cartilage defect models.. J Orthop Res 2020 Aug;38(8):1826-1835.
    doi: 10.1002/jor.24597pubmed: 31965593google scholar: lookup
  6. Ghasemi S, Sardari K, Mirshokraei P, Hassanpour H. In vitro study of matrix metalloproteinases 1, 2, 9, 13 and serum amyloid A mRNAs expression in equine fibroblast-like synoviocytes treated with doxycycline.. Can J Vet Res 2018 Apr;82(2):82-88.
    pubmed: 29755186
  7. Duramaz A, Baca E. Microfracture provides better clinical results than debridement in the treatment of acute talar osteochondral lesions using arthroscopic assisted fixation of acute ankle fractures.. Knee Surg Sports Traumatol Arthrosc 2018 Oct;26(10):3089-3095.
    doi: 10.1007/s00167-018-4963-xpubmed: 29696318google scholar: lookup
  8. Coleman MC, Goetz JE, Brouillette MJ, Seol D, Willey MC, Petersen EB, Anderson HD, Hendrickson NR, Compton J, Khorsand B, Morris AS, Salem AK, Fredericks DC, McKinley TO, Martin JA. Targeting mitochondrial responses to intra-articular fracture to prevent posttraumatic osteoarthritis.. Sci Transl Med 2018 Feb 7;10(427).
    doi: 10.1126/scitranslmed.aan5372pubmed: 29437147google scholar: lookup
  9. Labens R, Daniel C, Hall S, Xia XR, Schwarz T. Effect of intra-articular administration of superparamagnetic iron oxide nanoparticles (SPIONs) for MRI assessment of the cartilage barrier in a large animal model.. PLoS One 2017;12(12):e0190216.
    doi: 10.1371/journal.pone.0190216pubmed: 29287105google scholar: lookup
  10. Lv D, Su C, Li Z, Chai X, Xu Z, Pang T. Expression of long non‑coding RNAs in chondrocytes from proximal interphalangeal joints.. Mol Med Rep 2017 Oct;16(4):5175-5180.
    doi: 10.3892/mmr.2017.7274pubmed: 28849021google scholar: lookup
  11. Delco ML, Bonnevie ED, Bonassar LJ, Fortier LA. Mitochondrial dysfunction is an acute response of articular chondrocytes to mechanical injury.. J Orthop Res 2018 Feb;36(2):739-750.
    doi: 10.1002/jor.23651pubmed: 28696002google scholar: lookup
  12. Delco ML, Kennedy JG, Bonassar LJ, Fortier LA. Post-traumatic osteoarthritis of the ankle: A distinct clinical entity requiring new research approaches.. J Orthop Res 2017 Mar;35(3):440-453.
    doi: 10.1002/jor.23462pubmed: 27764893google scholar: lookup
  13. Punzi L, Galozzi P, Luisetto R, Favero M, Ramonda R, Oliviero F, Scanu A. Post-traumatic arthritis: overview on pathogenic mechanisms and role of inflammation.. RMD Open 2016;2(2):e000279.
    doi: 10.1136/rmdopen-2016-000279pubmed: 27651925google scholar: lookup