Studies on the pathogenesis of the venous leg ulcer.
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Biomedical subjects
Publications and source records attributed to C C Arnoldi.
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The opinion is widely held that interruption of the arterial flow through the retinacular arteries to the femoral head is the main cause of avascular necrosis after fracture of the neck. In this study the state of the vascular supply to the femoral head was assessed--prior to osteosynthesis--by means of intramedullary pressure measurements in the femoral head and neck in 72 patients with medial neck fractures. The patients were followed 2 or 3 years or until avascular necrosis became evident. The relative importance of primary avascularity and surgical technique for the development of necrosis suggests that damage to the retinacular arteries may not be the single decisive factor in the pathogenesis of femoral head necrosis. Proper fracture reduction with extensive contact between the cancellous bone surfaces and stable fixation seemed to be more important, probably because they offer the best possibilities for re-establishment of transosseous blood flow across the fracture site.
The ratios of synovial fluid concentration to serum concentration (SF/S) for 4 nonimmunoglobulin proteins were higher in osteoarthritic synovia than in normal. The difference increased with increasing molecular weight and was highly significant for the largest molecules. An almost inverse linear relationship was observed between SF/S ratios of the proteins and their molecular weight. As only slight signs of inflammation were found in the osteoarthritic synovium, no correlation could be demonstrated between ratio and the degree of synovial inflammation as assessed by histologic methods. Two types of synovitis were encountered in patients with osteoarthritis: an early "proliferative" stage, characterized by synovial edema and large numbers of dilated venules and capillaries and a later "fibrous" stage characterized by scarring of the synovium. The highest ratios corresponded to the proliferative type. The abnormal protein pattern in osteoarthritic synovia is a result of increased capillary permeability in the synovial membrane owing to capillary dilation and stasis.