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- Author or Editor: Joseph D. Frank x
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Objective—To compare the bending properties of pantarsal arthrodesis constructs involving either a commercially available medial arthrodesis plate (MAP1) or a specially designed second-generation plate (MAP2) implanted in cadaveric canine limbs and evaluate the effect of calcaneotibial screw (CTS) augmentation on the structural properties of both constructs.
Sample Population—5 pairs of canine hind limbs.
Procedures—Within pairs, specimens were stabilized with an MAP1 or MAP2 and loaded to 80% of body weight, with and without CTS augmentation. Compliance, angular deformation (AD), and plate strains were compared.
Results—Construct compliance and AD did not differ between plates. Maximum plate strain was lower in the MAP2 than in the MAP1 (difference of approx 30%). Augmentation with a CTS reduced compliance, AD, and strains in MAP1 constructs but had no effect on those variables in MAP2 constructs.
Conclusions and Clinical Relevance—Because of lower peak strains, the MAP2 may be less susceptible to failure than the MAP1. Furthermore, CTS augmentation was unnecessary with MAP2s, which could minimize intra- and postoperative morbidity. Compared with what is known for dorsal plates, MAP2 constructs were associated with approximately 35% less AD. As a result of improved local stability, one might anticipate earlier fusion of the talocrural joint with an MAP2. In addition, plate peak strain was approximately 3.5 times lower in MAP2s than in dorsal plate constructs, which should result in greater fatigue resistance. The use of MAP2s may be a better alternative to both MAP1s and dorsal plates and could contribute to lower patient morbidity.
Objective—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.
Animals—32 dogs with ruptured CCLs, and 8 aged and 19 young dogs with intact CCLs.
Procedure—Markers of cell viability (lactate dehydrogenase [LDH]), apoptosis (terminal deoxynucleatidyl transferase-mediated deoxyuridine triphosphate-nick end labeling [TUNEL] method), and hypoxia (hypoxiainducible factor-1α [HIF-1α] monoclonal antibody) were applied to CCL specimens; positive cells were assessed objectively (LDH) and subjectively (TUNEL and HIF-1α) in the main axial tissue component (core) and synovial intima and subintima (epiligamentous tissue).
Results—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-1αstaining was only found in the epiligamentous region of ruptured CCLs.
Conclusions and Clinical Relevance—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. (Am J Vet Res 2003;64:1010–1016)