Cases reported "Pseudarthrosis"

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1/5. Use of a reversed-flow vascularized pedicle fibular graft for treatment of nonunion of the tibia.

    Ten patients with nonunion of the lower tibia were treated with a vascularized ipsilateral fibular graft, that was transferred distally and based on retrograde peroneal vessel flow. Eight patients were treated for congenital pseudarthrosis of the tibia; one had a nonunion subsequent to infection, and another patient had bone and skin loss due to infection. A posterior approach was used to expose the tibia and to harvest the fibula. Bone union and full weight-bearing were achieved in all cases by 9 months. The patients were followed-up for a mean of 1.8 years (range: 1.5 to 3 years).
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2/5. A case of pseudarthrosis of the capitate.

    pseudarthrosis of the capitate bone is extremely rare. In this case, the injury and pseudarthrosis was so old, the bone with a nutrient vessel was grafted, and bone union and excellent results are obtained.
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3/5. Vasculopathy in two cases of NF1-related congenital pseudarthrosis.

    Neurofibromatosis type 1 (NF1) is a common dominantly inherited disease. More than half of NF1 patients suffer from skeletal manifestations, of which congenital pseudarthrosis of tibia (CPT) is one of the most incapacitating lesions. Two NF1 patients with CPT were operated, and the resected tissues were analyzed using immunohistochemistry and/or in situ hybridization for NF1 protein and mRNA, p-p44/42 MAPK, and S100 protein. Both patients displayed thick-walled arteries and veins with a small lumen within the fibrotic tissue in the vicinity of pseudarthrosis. endothelial cells were highly positive for p-p44/42 MAPK. A subpopulation of cells surrounding the blood vessels was S100 protein-positive. However, the exact identity of the S100-positive cells remains to be elucidated. Neurofibromin mRNA and protein labeling was detected in both cell types. In conclusion, decreased NF1 function as a RAS-GAP in the endothelium may contribute to vascular thickening in CPT.
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4/5. arteriovenous fistula complicating operative treatment of an ununited tibial fracture.

    We report the case of a traumatic arteriovenous fistula of the peroneal vessels following a bone graft operation for an un-united tibial fracture. The fistula was recognised as a result of a bruit at the site of the fracture. The fistula was repaired and the fracture subsequently united.
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5/5. Experimental study and clinical observations on hypertrophy of vascularized bone grafts.

    In order to understand the mechanisms involved in the hypertrophy of vascularized bone grafts, a series of animal experiments were carried out and 32 clinical cases were studied. A defect in the tibial shaft was created in puppies and the ipsilateral fibula was transferred into the medullary cavity of the tibia with the anterior tibial artery and vein. The same procedure was performed on a control group but without vessel supply. Radiologically, in the vascularized group mild hypertrophy in the fibula was seen at 2 weeks, became marked by 4 weeks, but in no case did the thickening (hypertrophy) of the graft ever exceed the diameter of the recipient tibia. The control group did not show hypertrophy but fracture callus formed in the recipient tibia at both ends of the graft. On histological evaluation no reactive bone formation was evident in the control group but some reactive bone formation was seen in the vascularized group just beneath the periosteum. There was no change in the periosteum itself. In the clinical cases 47% of patients showed hypertrophy. hypertrophy was noted mainly in the fibulae but rarely in other bones such as ilium or rib. The important factors were age and good vascularity of the grafted bone. During the period of study, weight-bearing was eliminated, so that the effects of mechanical force did not explain hypertrophy. We conclude from these studies that true hypertrophy is an essentially different process from reactive callus which forms normally in response to fracture healing. Vascularized bone grafts show remarkable hypertrophy of the grafted bone, but the exact mechanism is ill defined.(ABSTRACT TRUNCATED AT 250 WORDS)
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