To determine if joint effusions encountered in the emergency department (ED) requiring arthrocentesis possess normal lubricating ability or evidence cartilage degeneration. Chondroprotection of articulating joint surfaces is provided by lubricin, a mucinous glycoprotein that is a product of megakaryocyte-stimulating factor gene (GenBank U70136) expression. Loss of synovial fluid's (SF) lubricating ability has been implicated in the pathogenesis of degenerative joint disease.
A retrospective ED observational study from May 1, 1999, to October 1, 2000, of adult and pediatric patients presenting with radiographically negative knee joint complaints and clinical evidence of joint effusion. Knee joints were aspirated by the emergency physician and the synovial fluid tested for lubricating ability and collagen type II degeneration. Lubricating ability was assayed in vitro in an arthrotripsometer oscillating latex apposed to polished glass under a load of 0.35 106 N/m2. Results were reported as the coefficient of friction ( micro ) relative to that of a 0.9% NaCl control; negative deltamicro value indicates lubrication. Comparisons of deltamicro were made to normal SF and aspirates from patients with osteoarthritis (OA) and rheumatoid arthritis. Collagen type II fragments were measured by a novel sandwich ELISA.
Synovial fluid aliquots (n = 57) lubricated poorly with deltamicro = -0.045 (95% confidence interval = -0.006, -0.083) compared to normal SF with D micro = -0.095 (95% CI = -0.088, -0.101). Only 20.6% of knee joint aspirates possessed normal lubricating ability. An association exists between nucleated cell count and deltamicro described by a logarithmic function. Collagen type II fragments were present in aspirates at a concentration of 0.636 microg/ml (95% CI 0.495-0.777 microg/ml), significantly higher than 0.173 microg/ml (95% CI 0.154-0.193 microg/ml) in the OA comparison group.
Knee joints with synovitis, commonly encountered in the ED, are frequently nonlubricated bearings and display catabolism of collagen type II. This may play a role in acute cartilage destruction ultimately resulting in posttraumatic OA.