ABSTRACT
Since vascular proliferation may be important in the pathogenesis of rheumatoid arthritis (RA) and/or osteoarthritis (OA), this study examined the induction of angiogenesis by these synovial fluids (SF). Four of 11 (36%) RA and 2 of 6 (33%) OA SF caused early morphological changes in human endothelial cell cultures. SF from 7 of 11 (63%) RA and 4 of 8 (50%) OA patients resulted in the late formation of tabular networks morphologically resembling capillaries observed in vivo. Early morphological changes in cultures were associated with a significantly (p less than 0.05) longer duration of disease in patients with RA. Factors present in the SF of RA and OA patients may play a role in the excessive vascularization which often occurs in these arthropathies.
Subject(s)
Arthritis, Rheumatoid/physiopathology , Osteoarthritis/physiopathology , Synovial Fluid/physiology , Umbilical Veins/physiology , Angiogenesis Inducing Agents/physiology , Cells, Cultured , Endothelium/cytology , Endothelium/physiology , Humans , Microscopy, Electron , Microscopy, Phase-Contrast , Umbilical Veins/cytology , Umbilical Veins/ultrastructureABSTRACT
Amyloid-containing tissues were sampled from 19 capsules and 10 cartilages from hip, knee and sternoclavicular joints of 16 elderly patients. Heart ventricles from 3 of these patients were also studied. Histochemistry and immunofluorescence were performed and amyloid fibrils extracted from one hip capsule. The results indicate that 9 of 13 hip capsules contained prealbumin-like amyloid fibril protein ASc1, a finding characteristic of senile systemic amyloidosis. The amyloid of 16 out of 17 other joint structures showed no reaction with anti-ASc1 or antisera to 3 other systemic forms of amyloid, indicating that they represent localized forms of amyloid.
Subject(s)
Amyloid/analysis , Hip Joint/analysis , Prealbumin/analysis , Aged , Aged, 80 and over , Cartilage, Articular/analysis , Electrophoresis, Polyacrylamide Gel , Fluorescent Antibody Technique , Histocytochemistry , Humans , Microscopy, ElectronABSTRACT
In vitro assays of human neutrophil phagocytosis, adherence, enzyme release, and response to chemotactic factors were utilized to determine the effects of benoxaprofen on these cells. At concentrations of 30 and 300 micrograms/ml benoxaprofen partially inhibited phagocytosis without affecting adherence. High concentrations (300 micrograms/ml) of benoxaprofen, but not aspirin or gold, enhanced the release of the granular enzymes beta-glucuronidase and lysozyme, but not the release of the cytoplasmic enzyme lactic dehydrogenase from both resting and phagocytosing neutrophils. High concentrations (300 micrograms/ml) of benoxaprofen also inhibited the response of neutrophils to chemotactic factors as determined by both the leading front and leukotactic index methods. These unique in vitro effects of this antiinflammatory agent are compatible with recent clinical reports concerning its efficacy and toxicity.
