Journal of Veterinary Clinics (한국임상수의학회지)

The Korean Society of Veterinary Clinics (한국임상수의학회)
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The Changes of Stifle Joint Fluid with Cranial Cruciate Ligament Rupture in Dogs

개에 있어서 전방십자인대 단열시 슬관절액의 변화

  • Nam-soo, Kim (College of Veterianry Medicine, Chonbuk National University, Bio-Safety Research Institute, Chonbuk National University)
  • Published : 2003.12.01
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Abstract

To determine whether localization of tartrate-resistant acid phosphatase (TRAP) and cathepsin K was associated with rupture of the cranial cruciate ligament (CCL) in dogs. Tissue specimens were obtained from 30 dogs with CCL rupture during surgical treatment, 8 aged normal dogs, and 9 young normal dogs that were necropsied for reasons unrelated to this study and unrelated to musculoskeletal disease. The cranial cruciate ligament was examined histologically. $TRAP^+$ cells and cathepsin $K^+$ cells were identified by histochemical staining and immunohistochemical staining respectively. TRAP and cathepsin $K^+$ were co-localized within the same cells principally located within the epiligamentous region and to a lesser extent in the core region of ruptured CCL. Localization of $TRAP^+$ cells (P < 0.05) and cathepsin $K^+$ cells (P =0.05) within CCL tissue was significantly increased in dogs with CCL rupture, compared with aged-normal dogs, and young normal dogs (P < 0.05 - TRAP, P < 0.001 - cathepsin K). Localization of $TRAP^+$ cells and cathepsin $K^+$ cells within the CCL tissue of aged-normal dogs was also increased compared with young normal dogs (P < 0.05). Small numbers of $TRAP^+$ cells and cathepsin $K^+$ cells were seen in the intact ligaments of aged-normal dogs, which were associated with ligament fasicles in which there was chondroid transformation of ligament fibroblasts and disruption of the organized hierarchical structure of the extracellular matrix. $TRAP^+$ cells and cathepsin $K^+$ cells were not seen in CCL tissue from young-normal dogs. Localization of the proteinases $TRAP^+$ and cathepsin $K^+$ in CCL tissue was significantly associated with CCL rupture. Small numbers of proteinase positive cells were also localized in the CCL of agednormal dogs without CCL rupture, but were not detected in CCL from young-normal dogs. Taken together, these findings suggest that the cell signaling pathways that regulate expression of these proteinases in CCL tissue may form part of the mechanism that leads to upregulation of collagenolytic ligament remodeling and progressive structural failure of the CCL over time.

본 연구는 전십자인대가 단열된 개의 슬관절액에서 tartrate-resistant acid phosphatase (TRAP) 와 cathepsin K의 변화를 알아봄으로서 십자인대에 관련된 질병 또는 십자인대 치료 실패에 따른 퇴행성관절염의의 조기 진단 및 치료에 관한 정보를 얻기 위하여 실시하였다. 실험동물로는 전방십자인대가 단열된 30두의 개와 정상 성견 8 두 그리고 어린 정상 개 9두를 사용하였다. 슬관절액 내의 TRAP 과 Cathepsin K의 변화를 확인하기 위하여 조직화학 염색과 면역조직화학염색을 실시하였다. 조직학적인 검사 결과 정상견에서는 TRAP과 Cathepsin K 세포들은 찾아보기 힘들었으나 전방십자인대가 단열된 개에 있어서는 TRAP 과 Cathepsin K 그리고 chondroid metaplasia가 중심부분에서 증가되고 있음을 관찰하였다. 이러한 결과로 보아 TRAP과 Cathepsin K 세포들은 전방십자인대가 단열 또는 단열 후 회복되는 과정에서 상호 보조적으로 관여하며 세포외 방출과 관계가 있는 것으로 생각된다.

Keywords

References

  1. Vasseur PB, Berry CR. Progression of stifle osteoarthrosis following reconstruction of the cranial. cruciate ligament in 21 dogs. J Am Anim Hosp Assoc 1992; 28: 129-136
  2. Innes JF, Bacon D, Lynch C, Pollard A. Long-term outcome of surgery for dogs with cranial cruciate ligament deficiency. Vet Rec 2000; 147: 325-328 https://doi.org/10.1136/vr.147.12.325
  3. Bennett D, Tennant B, Lewis DG, et al. A reappraisal of anterior cruciate ligament disease in the dog. J Small Anim Pract 1988; 29: 275-297 https://doi.org/10.1111/j.1748-5827.1988.tb02286.x
  4. Narama I, Masuoka-Nishiyama M, Matsuura T, et al. Mor-phogenesis of degenerative changes predisposing dogs to rupture of the cranial cruciate ligament. J Vet Med Sci 1996; 58: 1091-1097 https://doi.org/10.1292/jvms.58.11_1091
  5. Vasseur PB, Pool RR, Amozky SP, Lau RE. Correlative biomechanical and histologic study of the cranial cruciate ligament in dogs. Am J Vet Res 1985; 46: 1842-1854
  6. Whitehair JG, Vasseur PB, Willits NH. Epidemiology of cranial cruciate ligament rupture in dogs. J Am Vet Med Assoc 1993; 203: 1016-1019
  7. Duval JM, Budsberg SC, Flo GL, Sarnmarco JL. Breed, sex, and body weight as risk factors for rupture of the cranial cruciate ligament in young dogs. J Am Vet Med Assoc 1999; 215: 811-814
  8. Morris E, Lipowitz AJ. Comparison of tibial plateau angles in dogs with and without cranial cruciate ligament injuries. J Am Vet Med Assoc 2001; 218: 363-366 https://doi.org/10.2460/javma.2001.218.363
  9. Amiel D, Ishizue KK, Harwood FL, et al. Injury of the anterior cruciate ligament: The role of collagenase in ligament degeneration. J Orthop Res 1989; 7: 486-493 https://doi.org/10.1002/jor.1100070405
  10. Spindler KP, Clark SW, Nanney LB, Davidson JM. Expression of collagen and matrix metalloproteinases in ruptured human anterior cruciate ligament: An in situ hybridization study. J Orthop Res 1996; 14: 857-861 https://doi.org/10.1002/jor.1100140603
  11. Muir P, Hayashi K, Manley PA, Colopy SA, Hao Z. Evaluation of tartrate-resistant acid phosphatase and cathepsin K in ruptured cranial cruciate ligaments in dogs. Am J Vet Res 2002; 62: 228-235
  12. Petersen W, TiIlmann B. Structure and vascularization of the cruciate ligaments of the human knee. Anat Embryol 1999; 200: 325-334 https://doi.org/10.1007/s004290050283
  13. Amiel D, Frank C, Harwood F, et al. Tendons and ligaments: A morphological and biochemical comparison. J Orthop Res 1984; 1: 257-265
  14. Bossard MJ, Tomaszek TA, Thompson SK, et al. Pro-teolytic activity of human osteoclast cathepsin K. J Biol Chem 1996; 271: 12517-12524 https://doi.org/10.1074/jbc.271.21.12517
  15. Kafienah W, Bromme D, Buttle DJ, et al. Human cathepsin K cleaves native type I and II collagens at the N-tenninal end of the triple helix. Biochem J 1998; 331: 727-732
  16. Halleen JM, Raisanen S, Salo JJ, et al. Intracellular fragmentation of bone resorption products by reactive oxygen species generated by osteoclastic tartrate-resistant acid phosphatase. J Biol Chem 1999; 274: 22907-22910 https://doi.org/10.1074/jbc.274.33.22907
  17. Heffron LE, Campbell JR. Morphology, histology and functional anatomy of the canine cranial cruciate ligament. Vet Rec 1978; 102: 280-283 https://doi.org/10.1136/vr.102.13.280
  18. Scavelli TD, Schrader SC, Matthiesen DT, Skorup DE. Partial rupture of the cranial cruciate ligament of the stifle in dogs: 25 cases (1982-1988). J Am Vet Med Assoc 1990; 196: 1135-1138
  19. Stefanini M, De Martino C, Zamboni L. Fixation of ejaculated spermatozoa for electron microscopy. Nature 1967; 216: 173-174 https://doi.org/10.1038/216173a0
  20. Lang P, Schultzberg M, Andersson G. Expression and distribution of tartrate-resistant acid purple acid phosphatase in the rat nervous system. J Histochem Cytochem 2001; 49: 379-396 https://doi.org/10.1177/002215540104900312
  21. Konttinen YT, Takagi M, Mandelin J, et al. Acid attack and cathepsin K in bone resorption around total hip replacement prosthesis. J Bone Min Res 2001; 16: 1780-1786 https://doi.org/10.1359/jbmr.2001.16.10.1780
  22. Foged NT, Delaisse JM, Hou P, et al. Quantification of collagenolytic activity of isolated osteoclasts by enzyme-linked
  23. Van de Wijngaert FP, Burger EH. Demonstration of tartrate-resistant acid phosphatase in un-decalcified, glycomethacrylate-embedded mouse bone: A possible marker for (Pre) Osteo-clast identification. J Histochem Cytochem 1986; 34: 1317-1323 https://doi.org/10.1177/34.10.3745910
  24. Gomori G. Microscopic histochemistry: Principles and Practice. Chicago, IL, University of Chicago Press, 1952: 137-221
  25. Hillam RA, Skerry TM. Inhibition of bone resorption and stimulation of formation by mechanical loading of the modeling rat ulna in vivo. J Bone Miner Res 1995; 10: 683-689 https://doi.org/10.1002/jbmr.5650100503
  26. Saftig P, Hunziker E, Wehmeyer O, et al. Impaired osteo-clastic bone resorption leads to osteopetrosis in cathepsin-K-deficient mice. Proc Natl Acad Sci 1998; 95: 13453-13458 https://doi.org/10.1073/pnas.95.23.13453
  27. Hayman AR, Jones SJ, Boyde A, et al. Mice lacking tartrate-resistant acid phosphatase (Acp 5) have disrupted endochondral ossifica
  28. Lamp EC, Drexler HG. Biology of tartrate-resistant acid phosphatase. Leuk Lymphoma 2000; 39: 477-484 https://doi.org/10.3109/10428190009113378
  29. Hayman AR, Bune AJ, Bradley JR, et al. Osteoclastic tartrate-resistant acid phosphatase (Acp 5): Its localization to dendritic cells and diverse murine tissues. J Histochem Cytochem 2000; 48: 219-227 https://doi.org/10.1177/002215540004800207
  30. Ljusberg J, Ek-Rylander B, Andersson G. Tartrate-resistant purple acid phosphatase is synthesized as a latent proenzyme and activated by cysteine proteinases. Biochem J 1999; 343: 63-69 https://doi.org/10.1042/0264-6021:3430063
  31. Oddie GW, Schenk G, Angel NZ, et al. Structure, function, and regulation of tartrate-resistant acid phosphatase. Bone 2000; 27: 575-584 https://doi.org/10.1016/S8756-3282(00)00368-9
  32. Shaffer Brehme C, Roman, S, Shaffer J, Wolfert R. Tartrate-resistant acid phosphatase forms complexes with 2-macroglobulin. J Bone Miner Res 1999; 14: 311-318 https://doi.org/10.1359/jbmr.1999.14.2.311
  33. Murray MM, Martin SD, Martin TL, Spector M. Histologicalchanges in the human anterior cruciate ligament after rupture. J Bone Joint Surg 2000; 82A: 1387-1397