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The Changes of Stifle Joint Fluid with Cranial Cruciate Ligament Rupture in Dogs  

Nam-soo, Kim (College of Veterianry Medicine, Chonbuk National University, Bio-Safety Research Institute, Chonbuk National University)
Publication Information
Journal of Veterinary Clinics / v.20, no.4, 2003 , pp. 443-448 More about this Journal
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.
Keywords
tartrate-resistant acid phosphatase (TRAP); cathepsin K; cranial cruciate ligament (CCL);
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