ABSTRACT
Events leading to initial crystallization of monosodium urate in a joint after many years of asymptomatic hyperuricemia are unknown. Trauma with disruption of microtophi in cartilage may lead to release of urate crystals into synovial fluid. The urate crystals become coated with immunoglobulin and then complement. They are then phagocytosed by leukocytes with subsequent release of chemotactic protein, activation of the kallikrein system, and disruption of the leukocytes, which release lysosomal enzymes into synovial fluid.
