OBJECTIVES: To determine changes to the cells and collagenous and amorphous extracellular matrix (ECM) structure in ruptured canine cranial cruciate ligaments (CCL). STUDY DESIGN: Prospective clinical study. ANIMALS: CCL specimens obtained from 29 dogs with ruptured CCL and 6 young dogs with intact CCL. METHODS: Ligament fibroblast number density and phenotype were determined in the core and epiligamentous regions. ECM birefringence and crimp structure in the core region were also studied. RESULTS: Loss of fibroblasts from the core region of ruptured CCL was seen (P <.001), whereas, in the epiligamentous region, cell number densities were similar in ruptured and intact CCL (P =.7). In ruptured CCL, numbers of typical ligament fibroblasts (fusiform and ovoid cells) were decreased, and numbers of cells exhibiting chondroid transformation (spheroid cells) were increased in the core region (P <.001). Expansion of the volume of the epiligamentous region was also seen, although bridging scar tissue was not seen between the ends of ruptured CCL. The structure of the ECM collagen in the core region was extensively disrupted in ruptured CCL. This was, in part, because of decreased birefringence and elongation of the crimp in the remaining collagen fibers when compared with intact CCL (P <.01). CONCLUSIONS: Extensive alterations to the cell populations and collagenous ECM structure were seen in ruptured CCL. Although a proliferative epiligamentous repair response was seen in ruptured CCL, there was a lack of any bridging scar between the ruptured ends of the CCL. CLINICAL RELEVANCE: The cellular and ECM changes in ruptured CCL that we have described appear to result from the cumulative effects of remodeling and adaptation to mechanical loading and microinjury. Treatment of early cruciate disease in dogs will need to inhibit or reverse these progressive changes to CCL tissue, which are directly associated with partial or complete structural failure of the CCL under conditions of normal activity. Copyright 2003 by The American College of Veterinary Surgeons
OBJECTIVES: To determine changes to the cells and collagenous and amorphous extracellular matrix (ECM) structure in ruptured canine cranial cruciate ligaments (CCL). STUDY DESIGN: Prospective clinical study. ANIMALS: CCL specimens obtained from 29 dogs with ruptured CCL and 6 young dogs with intact CCL. METHODS: Ligament fibroblast number density and phenotype were determined in the core and epiligamentous regions. ECM birefringence and crimp structure in the core region were also studied. RESULTS: Loss of fibroblasts from the core region of ruptured CCL was seen (P <.001), whereas, in the epiligamentous region, cell number densities were similar in ruptured and intact CCL (P =.7). In ruptured CCL, numbers of typical ligament fibroblasts (fusiform and ovoid cells) were decreased, and numbers of cells exhibiting chondroid transformation (spheroid cells) were increased in the core region (P <.001). Expansion of the volume of the epiligamentous region was also seen, although bridging scar tissue was not seen between the ends of ruptured CCL. The structure of the ECM collagen in the core region was extensively disrupted in ruptured CCL. This was, in part, because of decreased birefringence and elongation of the crimp in the remaining collagen fibers when compared with intact CCL (P <.01). CONCLUSIONS: Extensive alterations to the cell populations and collagenous ECM structure were seen in ruptured CCL. Although a proliferative epiligamentous repair response was seen in ruptured CCL, there was a lack of any bridging scar between the ruptured ends of the CCL. CLINICAL RELEVANCE: The cellular and ECM changes in ruptured CCL that we have described appear to result from the cumulative effects of remodeling and adaptation to mechanical loading and microinjury. Treatment of early cruciate disease in dogs will need to inhibit or reverse these progressive changes to CCL tissue, which are directly associated with partial or complete structural failure of the CCL under conditions of normal activity. Copyright 2003 by The American College of Veterinary Surgeons
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