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BMC veterinary research2006; 2; 12; doi: 10.1186/1746-6148-2-12

Degenerative suspensory ligament desmitis as a systemic disorder characterized by proteoglycan accumulation.

Abstract: Degenerative suspensory ligament desmitis (DSLD) is a debilitating disorder thought to be limited to suspensory ligaments of Peruvian Pasos, Peruvian Paso crosses, Arabians, American Saddlebreds, American Quarter Horses, Thoroughbreds, and some European breeds. It frequently leads to persistent, incurable lameness and need to euthanize affected horses. The pathogenesis remains unclear, though the disease appears to run in families. Treatment and prevention are empirical and supportive, and not effective in halting the progression of the disease. Presently, the presumptive diagnosis of DSLD is obtained from patient signalment and history, clinical examination, and ultrasonographic examination of clinically affected horses, and is confirmed at post mortem examination. Presently, there are no reliable methods of diagnosing DSLD in asymptomatic horses. The goal of this study was to characterize and define the disorder in terms of tissue involvement at the macroscopic and microscopic levels. Results: We examined tissues and organs from 28 affected horses (22 Peruvian Pasos, 6 horses of other breeds) and from 8 control horses. Histopathological examination revealed the presence of excessive amounts of proteoglycans in the following tissues removed from DSLD-affected horses: suspensory ligaments, superficial and deep digital flexor tendons, patellar and nuchal ligaments, cardiovascular system, and sclerae. Electron microscopy demonstrated changes in diameters of collagen fibrils in the tendon, and in smooth muscle cells of the media of the aorta compatible with increased cell permeability in DSLD-affected cells. Separation of tendon extracts by gel chromatography revealed the presence of additional proteoglycan(s) in extracts from affected, but not control extracts. Conclusions: This study demonstrates for the first time that DSLD, a disease process previously thought to be limited to the suspensory ligaments of the distal limbs of affected horses, is in fact a systemic disorder involving tissues and organs with significant connective tissue component. Abnormal accumulation of proteoglycans between collagen and elastic fibers rather than specific collagen fibril abnormalities is the most prominent histological feature of DSLD. Because of this observation and because of the involvement of many other tendons and ligaments beside the suspensory ligament, and of non-ligamentous tissue we, therefore, propose that equine systemic proteoglycan accumulation or ESPA rather than DSLD is a more appropriate name for this condition.
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Publication Date: 2006-04-12 PubMed ID: 16611357PubMed Central: PMC1459153DOI: 10.1186/1746-6148-2-12Google Scholar: Lookup
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Summary

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The research investigates a systemic disorder in horses known as Degenerative Suspensory Ligament Desmitis (DSLD), which was previously believed to be limited to certain suspensory ligaments, but now found to affect various organs and tissues. The disease causes excessive proteoglycan accumulation, and the researchers propose the name Equine Systemic Proteoglycan Accumulation (ESPA) for it.

Characterization of DSLD

  • The disease primarily affected Peruvian Pasos, Peruvian Paso crosses, Arabians, American Saddlebreds, American Quarter Horses, Thoroughbreds, and some European breeds. It caused incurable lameness, often resulting in euthanasia.
  • The disease is hereditary, but the exact pathogenesis remains unknown. The existing diagnosis is based on patient signalment and history, clinical and ultrasonographic examinations. Confirmation only occurs post mortem.

Goals and Methodology

  • The aim was to define DSLD in terms of tissue involvement at macroscopic and microscopic levels, to diagnose it in asymptomatic horses.
  • To investigate, they examined tissues and organs from 28 affected horses and 8 control horses, observing proteoglycan accumulation in ligaments, cardiovascular system, and sclerae.
  • Using electron microscopy, researchers observed changes in collagen fibrils and increased cell permeability in the tendon and aorta.
  • Tendon extracts were separated by gel chromatography, with additional proteoglycans found in affected extracts.

Findings and Conclusion

  • DSLD, previously thought to be localized within certain ligaments, was found to be a more systemic disorder, showing abnormal proteoglycan accumulation in various tissues and organs.
  • This study contradicts the prevailing belief that DSLD centers on specific collagen fibril abnormalities, instead pointing at proteoglycan accumulation as the key concern.
  • Giving the extent of the disease beyond the suspensory ligament, the researchers proposed renaming it to Equine Systemic Proteoglycan Accumulation (ESPA).

Cite This Article

APA
Halper J, Kim B, Khan A, Yoon JH, Mueller PO. (2006). Degenerative suspensory ligament desmitis as a systemic disorder characterized by proteoglycan accumulation. BMC Vet Res, 2, 12. https://doi.org/10.1186/1746-6148-2-12

Publication

BMC veterinary research
ISSN: 1746-6148
NlmUniqueID: 101249759
Country: England
Language: English
Volume: 2
Pages: 12

Researcher Affiliations

Halper, Jaroslava
  • Department of Pathology, College of Veterinary Medicine, The University of Georgia, Athens, GA 30602, USA. jhalper@vet.uga.edu
Kim, Byoungjae
    Khan, Ahrar
      Yoon, Jung Hae
        Mueller, P O Eric

          References

          This article includes 38 references
          1. Dowling BA, Dart AJ, Hodgson DR, Smith RK. Superficial digital flexor tendonitis in the horse.. Equine Vet J 2000 Sep;32(5):369-78.
            pubmed: 11037257doi: 10.2746/042516400777591138google scholar: lookup
          2. Genovese RL. Prognosis of superficial digital flexor tendon and suspensory ligament injuries.. Proc Am Assoc Equine Pract 1993. pp. 17–19.
          3. Goodship AE. The pathophysiology of flexor tendon injury in the horse.. Equine Vet Educ 1993;5:23–29.
          4. Peloso JG, Mundy GD, Cohen ND. Prevalence of, and factors associated with, musculoskeletal racing injuries of thoroughbreds.. J Am Vet Med Assoc 1994 Feb 15;204(4):620-6.
            pubmed: 8163419
          5. Bramlage LR, Hogan PM. Career results of 137 Thoroughbred racehorses that have undergone superior check ligament desmotomy for treatment of tendinitis.. Proc Am Assoc Equine Pract 1996. pp. 162–163.
          6. Madison JB. Acute and chronic tendinitis in horses.. Comp Cont Educ Pract Vet 1995;17:853–856.
          7. Sawdon H, Yovich JV, Booth T. Superficial digital flexor tendinitis in racehorses: Long term follow up in conservatively managed cases.. Aust Equine Vet 1996;14:21–25.
          8. Webbon PM. Equine tendon stress injuries.. Equine Vet J 1973 Apr;5(2):58-64.
            pubmed: 4791732doi: 10.1111/j.2042-3306.1973.tb03195.xgoogle scholar: lookup
          9. Birch HL, Bailey AJ, Goodship AE. Macroscopic 'degeneration' of equine superficial digital flexor tendon is accompanied by a change in extracellular matrix composition.. Equine Vet J 1998 Nov;30(6):534-9.
            pubmed: 9844973doi: 10.1111/j.2042-3306.1998.tb04530.xgoogle scholar: lookup
          10. Birch HL, Bailey JV, Bailey AJ, Goodship AE. Age-related changes to the molecular and cellular components of equine flexor tendons.. Equine Vet J 1999 Sep;31(5):391-6.
            pubmed: 10505954doi: 10.1111/j.2042-3306.1999.tb03838.xgoogle scholar: lookup
          11. Kannus P, Józsa L. Histopathological changes preceding spontaneous rupture of a tendon. A controlled study of 891 patients.. J Bone Joint Surg Am 1991 Dec;73(10):1507-25.
            pubmed: 1748700
          12. Young JH. Degenerative Suspensory Ligament Desmitis.. Hoofcare and Lameness 1993. pp. 6–19.
          13. Mero JL, Pool R. Twenty cases of degenerative suspensory ligamnet desmitis in Peruvian Paso horses.. Abstract for AAEP, Orlando 2002;48:329–334.
          14. Dyson S. Diagnosis and prognosis of suspensory desmitis.. Proceedings of the 1st Dubai International Symposium 1996. pp. 207–225.
          15. Dyson SJ, Arthur RM, Palmer SE, Richardson D. Suspensory ligament desmitis.. Vet Clin North Am Equine Pract 1995 Aug;11(2):177-215.
            pubmed: 7584734doi: 10.1016/s0749-0739(17)30319-xgoogle scholar: lookup
          16. Gibson KT, Steel CM. Conditions of the suspensory ligament causing lameness in horses.. Equine Vet Ed 2002;4:50–64.
          17. Yoon JH, Halper J. Tendon proteoglycans: biochemistry and function.. J Musculoskelet Neuronal Interact 2005 Mar;5(1):22-34.
            pubmed: 15788868
          18. Iozzo RV. Matrix proteoglycans: from molecular design to cellular function.. Annu Rev Biochem 1998;67:609-52.
            doi: 10.1146/annurev.biochem.67.1.609pubmed: 9759499google scholar: lookup
          19. Danielson KG, Baribault H, Holmes DF, Graham H, Kadler KE, Iozzo RV. Targeted disruption of decorin leads to abnormal collagen fibril morphology and skin fragility.. J Cell Biol 1997 Feb 10;136(3):729-43.
            doi: 10.1083/jcb.136.3.729pmc: PMC2134287pubmed: 9024701google scholar: lookup
          20. Ameye L, Aria D, Jepsen K, Oldberg A, Xu T, Young MF. Abnormal collagen fibrils in tendons of biglycan/fibromodulin-deficient mice lead to gait impairment, ectopic ossification, and osteoarthritis.. FASEB J 2002 May;16(7):673-80.
            doi: 10.1096/fj.01-0848compubmed: 11978731google scholar: lookup
          21. Williams RB, Harkins LS, Hammond CJ, Wood JL. Racehorse injuries, clinical problems and fatalities recorded on British racecourses from flat racing and National Hunt racing during 1996, 1997 and 1998.. Equine Vet J 2001 Sep;33(5):478-86.
            pubmed: 11558743doi: 10.2746/042516401776254808google scholar: lookup
          22. Schultz LB. Howell equine handbook.. Wiley Publishing, Inc., Hoboken, NJ 2004.
          23. Robinson PN, Godfrey M. The molecular genetics of Marfan syndrome and related microfibrillopathies.. J Med Genet 2000 Jan;37(1):9-25.
            doi: 10.1136/jmg.37.1.9pmc: PMC1734449pubmed: 10633129google scholar: lookup
          24. Ng CM, Cheng A, Myers LA, Martinez-Murillo F, Jie C, Bedja D, Gabrielson KL, Hausladen JM, Mecham RP, Judge DP, Dietz HC. TGF-beta-dependent pathogenesis of mitral valve prolapse in a mouse model of Marfan syndrome.. J Clin Invest 2004 Dec;114(11):1586-92.
            doi: 10.1172/JCI200422715pmc: PMC529498pubmed: 15546004google scholar: lookup
          25. Trotter SE, Olsen EG. Marfan's disease and Erdheim's cystic medionecrosis. A study of their pathology.. Eur Heart J 1991 Jan;12(1):83-7.
            pubmed: 2009899doi: 10.1093/oxfordjournals.eurheartj.a059830google scholar: lookup
          26. Sheremet'eva GF, Ivanova AG, Belov IuV, Gens AP, Kocharian EZ. A comparative study of the aortic wall in patients with Marfan's syndrome and Erdheim's disease.. Angiol Sosud Khir 2004;10(4):22-9.
            pubmed: 15627131
          27. Zweers MC, Hakim AJ, Grahame R, Schalkwijk J. Joint hypermobility syndromes: the pathophysiologic role of tenascin-X gene defects.. Arthritis Rheum 2004 Sep;50(9):2742-9.
            doi: 10.1002/art.20488pubmed: 15457441google scholar: lookup
          28. Pope FM, Martin GR, Lichtenstein JR, Penttinen R, Gerson B, Rowe DW, McKusick VA. Patients with Ehlers-Danlos syndrome type IV lack type III collagen.. Proc Natl Acad Sci U S A 1975 Apr;72(4):1314-6.
            pmc: PMC432523pubmed: 1055406doi: 10.1073/pnas.72.4.1314google scholar: lookup
          29. Germain DP, Herrera-Guzman Y. Vascular Ehlers-Danlos syndrome.. Ann Genet 2004 Jan-Mar;47(1):1-9.
            pubmed: 15127738doi: 10.1016/j.anngen.2003.07.002google scholar: lookup
          30. Oderich GS, Panneton JM, Bower TC, Lindor NM, Cherry KJ, Noel AA, Kalra M, Sullivan T, Gloviczki P. The spectrum, management and clinical outcome of Ehlers-Danlos syndrome type IV: a 30-year experience.. J Vasc Surg 2005 Jul;42(1):98-106.
            doi: 10.1016/j.jvs.2005.03.053pubmed: 16012458google scholar: lookup
          31. Wessel A, Gravenhorst V, Buchhorn R, Gosch A, Partsch CJ, Pankau R. Risk of sudden death in the Williams-Beuren syndrome.. Am J Med Genet A 2004 Jun 15;127A(3):234-7.
            doi: 10.1002/ajmg.a.30012pubmed: 15150772google scholar: lookup
          32. English RF, Colan SD, Kanani PM, Ettedgui JA. Growth of the aorta in children with Williams syndrome: does surgery make a difference?. Pediatr Cardiol 2003 Nov-Dec;24(6):566-8.
            doi: 10.1007/s00246-003-0302-0pubmed: 14758447google scholar: lookup
          33. Morris CA, Mervis CB. Williams syndrome and related disorders.. Annu Rev Genomics Hum Genet 2000;1:461-84.
            doi: 10.1146/annurev.genom.1.1.461pubmed: 11701637google scholar: lookup
          34. Gensure RC, Mäkitie O, Barclay C, Chan C, Depalma SR, Bastepe M, Abuzahra H, Couper R, Mundlos S, Sillence D, Ala Kokko L, Seidman JG, Cole WG, Jüppner H. A novel COL1A1 mutation in infantile cortical hyperostosis (Caffey disease) expands the spectrum of collagen-related disorders.. J Clin Invest 2005 May;115(5):1250-7.
            doi: 10.1172/JCI200522760pmc: PMC1087158pubmed: 15864348google scholar: lookup
          35. Fisher LW, Stubbs JT 3rd, Young MF. Antisera and cDNA probes to human and certain animal model bone matrix noncollagenous proteins.. Acta Orthop Scand Suppl 1995 Oct;266:61-5.
            pubmed: 8553864
          36. Sztrolovics R, Alini M, Roughley PJ, Mort JS. Aggrecan degradation in human intervertebral disc and articular cartilage.. Biochem J 1997 Aug 15;326 ( Pt 1)(Pt 1):235-41.
            pmc: PMC1218660pubmed: 9337874doi: 10.1042/bj3260235google scholar: lookup
          37. Halper J, Leshin LS, Lewis SJ, Li WI. Wound healing and angiogenic properties of supernatants from Lactobacillus cultures.. Exp Biol Med (Maywood) 2003 Dec;228(11):1329-37.
            pubmed: 14681548doi: 10.1177/153537020322801111google scholar: lookup
          38. Hae Yoon J, Brooks R, Hwan Kim Y, Terada M, Halper J. Proteoglycans in chicken gastrocnemius tendons change with exercise.. Arch Biochem Biophys 2003 Apr 15;412(2):279-86.
            doi: 10.1016/S0003-9861(03)00064-Xpubmed: 12667493google scholar: lookup

          Citations

          This article has been cited 12 times.
          1. Momen M, Brauer K, Patterson MM, Sample SJ, Binversie EE, Davis BW, Cothran EG, Rosa GJM, Brounts SH, Muir P. Genetic architecture and polygenic risk score prediction of degenerative suspensory ligament desmitis (DSLD) in the Peruvian Horse. Front Genet 2023;14:1201628.
            doi: 10.3389/fgene.2023.1201628pubmed: 37645058google scholar: lookup
          2. Roberts JH, Zhang J, David F, McLean A, Blumenshine K, Müller-Alander E, Halper J. Expression of genes with biomarker potential identified in skin from DSLD-affected horses increases with age. PLoS One 2023;18(7):e0287740.
            doi: 10.1371/journal.pone.0287740pubmed: 37450486google scholar: lookup
          3. Momen M, Brounts SH, Binversie EE, Sample SJ, Rosa GJM, Davis BW, Muir P. Selection signature analyses and genome-wide association reveal genomic hotspot regions that reflect differences between breeds of horse with contrasting risk of degenerative suspensory ligament desmitis. G3 (Bethesda) 2022 Sep 30;12(10).
            doi: 10.1093/g3journal/jkac179pubmed: 35866615google scholar: lookup
          4. Roberts JH, Halper J. Connective Tissue Disorders in Domestic Animals. Adv Exp Med Biol 2021;1348:325-335.
            doi: 10.1007/978-3-030-80614-9_15pubmed: 34807427google scholar: lookup
          5. Haythorn A, Young M, Stanton J, Zhang J, Mueller POE, Halper J. Differential gene expression in skin RNA of horses affected with degenerative suspensory ligament desmitis. J Orthop Surg Res 2020 Oct 7;15(1):460.
            doi: 10.1186/s13018-020-01994-ypubmed: 33028365google scholar: lookup
          6. Kram V, Shainer R, Jani P, Meester JAN, Loeys B, Young MF. Biglycan in the Skeleton. J Histochem Cytochem 2020 Nov;68(11):747-762.
            doi: 10.1369/0022155420937371pubmed: 32623936google scholar: lookup
          7. Barrachina L, Cequier A, Romero A, Vitoria A, Zaragoza P, Vázquez FJ, Rodellar C. Allo-antibody production after intraarticular administration of mesenchymal stem cells (MSCs) in an equine osteoarthritis model: effect of repeated administration, MSC inflammatory stimulation, and equine leukocyte antigen (ELA) compatibility. Stem Cell Res Ther 2020 Feb 7;11(1):52.
            doi: 10.1186/s13287-020-1571-8pubmed: 32028995google scholar: lookup
          8. Zappia J, Joiret M, Sanchez C, Lambert C, Geris L, Muller M, Henrotin Y. From Translation to Protein Degradation as Mechanisms for Regulating Biological Functions: A Review on the SLRP Family in Skeletal Tissues. Biomolecules 2020 Jan 3;10(1).
            doi: 10.3390/biom10010080pubmed: 31947880google scholar: lookup
          9. Young M, Moshood O, Zhang J, Sarbacher CA, Mueller POE, Halper J. Does BMP2 play a role in the pathogenesis of equine degenerative suspensory ligament desmitis?. BMC Res Notes 2018 Sep 18;11(1):672.
            doi: 10.1186/s13104-018-3776-9pubmed: 30227887google scholar: lookup
          10. Luo W, Sandy J, Trella K, Gorski D, Gao S, Li J, Brounts S, Galante J, Plaas A. Degenerative Suspensory Ligament Desmitis (DSLD) in Peruvian Paso Horses Is Characterized by Altered Expression of TGFβ Signaling Components in Adipose-Derived Stromal Fibroblasts. PLoS One 2016;11(11):e0167069.
            doi: 10.1371/journal.pone.0167069pubmed: 27902739google scholar: lookup
          11. Brosnahan MM, Brooks SA, Antczak DF. Equine clinical genomics: A clinician's primer. Equine Vet J 2010 Oct;42(7):658-70.
            doi: 10.1111/j.2042-3306.2010.00166.xpubmed: 20840582google scholar: lookup
          12. Guest DJ, Birch HL, Thorpe CT. A review of the equine suspensory ligament: Injury prone yet understudied. Equine Vet J 2025 Sep;57(5):1167-1182.
            doi: 10.1111/evj.14447pubmed: 39604165google scholar: lookup
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