[Show abstract][Hide abstract] ABSTRACT: The clinical efficacy of oral doxycycline was evaluated in twelve dogs with stifle arthritis and a presumptive diagnosis of early cruciate disease. Doxycycline (2.5-4.5 mg/kg once daily) was administered orally for 3 to 8 weeks. Eight dogs, who presented prior to the treat-ment with clinical signs of 4 weeks or fewer duration (group B), had a good response to doxycycline, whereas four dogs with a longer history of lameness (group A) had a poor response. The follow-up periods ranged from 2 to 12 months after discontinuation of the doxy-cycline treatment (median=6.5 months, 3 months in group A, and 9.5 months in group B). There was a significant correlation between the duration of lameness and the sub-jective grading of clinical improvement. In 68% of these cases of dogs with stifle arthritis (8/12), the oral administration of doxycycline resulted in the improvement of lameness, even after discontinuation of doxycycline. Careful selection of patients based on the duration of their lameness appears to be crucial in order to achieve a positive outcome.
[Show abstract][Hide abstract] ABSTRACT: To report use of combined cisterna chyli ablation (CCA) and thoracic duct ligation (TDL) for treatment of spontaneously occurring chylothorax in dogs.
Eight dogs with chylothorax.
TDL was performed through a right caudal intercostal thoracotomy and CCA through a left flank paracostal approach or ventral median celiotomy. Long-term outcome (range, 2-48 months; median, 11.5 months) was evaluated by telephone communication with owners.
Seven dogs were free of clinical signs related to chylothorax at last follow-up (range, 4-48 months; median, 15.5 months). One dog was euthanatized 2 months after surgery because of lack of improvement. No major complications occurred from CCA.
CCA and TDL resolved chylothorax in most dogs (88%).
CCA combined with TDL may improve the outcome of chylothorax in dogs.
Veterinary Surgery 01/2005; 34(5):519-23. · 1.24 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: To determine fibroblast viability, assess development of apoptosis, and evaluate tissue hypoxia via histochemical, in-situ hybridization, or immunohistochemical staining in ruptured and intact cranial cruciate ligaments (CCLs) of dogs.
32 dogs with ruptured CCLs, and 8 aged and 19 young dogs with intact CCLs.
Markers of cell viability (lactate dehydrogenase [LDH]), apoptosis (terminal deoxynucleatidyl transferase-mediated deoxyuridine triphosphate-nick end labeling [TUNEL] method), and hypoxia (hypoxia-inducible factor-1alpha [HIF-1alpha] monoclonal antibody) were applied to CCL specimens; positive cells were assessed objectively (LDH) and subjectively (TUNEL and HIF-1alpha) in the main axial tissue component (core) and synovial intima and subintima (epiligamentous tissue).
Viable fibroblasts were seen in all intact and ruptured CCLs. More nonviable cells were found in the core regions of ruptured CCLs and intact CCLs of young dogs than in the epiligamentous regions. Number of nonviable cells in the core region of ruptured CCLs was greater than that in intact CCLs of young and aged dogs, whereas the number in the epiligamentous region was similar in all specimens. The TUNEL and HIF-1alpha staining was only found in the epiligamentous region of ruptured CCLs.
Ruptured CCLs contained a high number of nonviable cells but not a great number of apoptotic cells. Repair processes in the epiligamentous region of the CCL include a metabolic response to hypoxia, suggesting that necrosis of ligament fibroblasts and transformation of surviving cells to a spheroid phenotype may be a response to hypoxia cause by microinjury or inadequate blood flow.
American Journal of Veterinary Research 09/2003; 64(8):1010-6. · 1.35 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: To determine changes to the cells and collagenous and amorphous extracellular matrix (ECM) structure in ruptured canine cranial cruciate ligaments (CCL).
Prospective clinical study.
CCL specimens obtained from 29 dogs with ruptured CCL and 6 young dogs with intact CCL.
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.
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).
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.
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.
Veterinary Surgery 01/2003; 32(3):269-77. · 1.24 Impact Factor