Journal of orthopaedic research : official publication of the Orthopaedic Research Society
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Comparative Study
Orthotopic ossification of the spinal ligaments of Zucker fatty rats: a possible animal model for ossification of the human posterior longitudinal ligament.
Ossification of the posterior longitudinal ligament is a human genetic disease in which pathological ectopic ossification of the spinal ligaments develops. This leads to myelopathy or radiculopathy due to compression of the spinal cord. In this study, we investigated the histological features of orthotopic ossification of the spinal ligaments of senile Zucker fatty rats. ⋯ In the controls, no expression of bone morphogenetic protein receptors or of activin receptors was observed. In conclusion, there is a great degree of similarity between orthotopic ossification of the spinal ligaments of Zucker fatty rats and ossification of the posterior longitudinal ligament of humans. Thus, the rats provide a useful animal model for the study of ossification of the human posterior longitudinal ligament.
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The efficacy of a bone-graft substitute (bovine-derived bone protein in a carrier of natural coral) in the healing of a segmental defect of a weight-bearing long bone was evaluated. Twenty dogs, divided into two groups, underwent bilateral radial osteotomies with creation of a 2.5 cm defect. On one side of each dog, the defect was filled with autogenous cancellous bone graft. ⋯ In this model, bovine-derived bone protein in a natural coral carrier performed consistently better than the gold standard autogenous cancellous bone graft in terms of the amount of bone formation and strength of the healed defect. This may have implications for removal of hardware or resumption of weight-bearing in certain clinical situations. These data also indicate that coralline calcium carbonate alone represents a poor option as a bone-graft substitute in this critical-sized segmental defect model.
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Flexible fixation of fractures with minimally invasive surgical techniques has become increasingly popular. Such techniques can lead to relatively large fracture gaps (larger than 5 mm) and considerable interfragmentary movements (0.2-5 mm). We investigated the influence of the size of the fracture gap, interfragmentary movement, and interfragmentary strain on the quality of fracture healing. ⋯ Larger interfragmentary movements and strains (31 compared with 7%) stimulated larger callus formation for small gaps (1-2 mm) but not for larger gaps (approximately 6 mm). The treatment of simple diaphyseal fractures with flexible fixation can be improved by careful reduction of the fracture; this prevents large interfragmentary gaps. The experimental fracture model for the metatarsus showed that the healing process was inferior when the gap was larger than 2 mm.
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The purpose of our investigation was to determine if the near infrared spectroscopy technique was sensitive to changes in tissue oxygenation at low levels of isometric contraction in the extensor carpi radialis brevis muscle. Nine subjects were seated with the right arm abducted to 45 degrees, elbow flexed to 85 degrees, forearm pronated 45 degrees, and wrist and forearm supported on an armrest throughout the protocol. Altered tissue oxygenation was measured noninvasively with near infrared spectroscopy. ⋯ Tissue oxygenation levels at 10, 15, and 50% of the maximum voluntary contraction were significantly lower (p < 0.05) than the baseline value. Our results indicate that tissue oxygenation significantly decreases during brief, low levels of static muscle contraction and that near infrared spectroscopy is a sensitive technique for detecting deoxygenation noninvasively at low levels of forearm muscle contraction. Our findings have important implications in occupational medicine because oxygen depletion induced by low levels of muscle contraction may be directly linked to muscle fatigue.
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If we are to fully understand mechanisms of cartilage homeostasis, it is essential that we know the full catalogue of receptors present on the surface of a chondrocyte and the pathways regulated by ligands that bind to these receptors. In this study, we describe chondrocyte responses to adenosine 5'-triphosphate and related molecules. Adenosine 5'-triphosphate stimulated a statistically significant, dose-dependent, transient rise in the concentration of calcium ions in Fura 2-loaded, differentiated, primary chondrocytes. ⋯ Matrix degradation, measured by release of glycosaminoglycan from cartilage explants, was also unaltered by adenosine 5'-triphosphate or uridine 5'-triphosphate (1-100 microM). Production of prostaglandin E2 was upregulated by incubation with either adenosine 5'-triphosphate or uridine 5'-triphosphate. These data demonstrate the presence of a functional P2U-like purine receptor on the surface of primary articular chondrocytes and support the hypothesis that altered concentrations of extracellular purines may influence chondrocyte metabolism.