Analysis of Inflammatory Mediators in Temporomandibular Joint Synovial Fluid Lavage Samples of Symptomatic Patients and Asymptomatic Controls

Quantitative synovial fluid analysis of β-glucuronidase, IgA, and IgG demonstrates elevated levels of inflammatory mediators in diseased joints compared with asymptomatic nondiseased joints. We hypothesize that high levels of IgA, IgG, and β-glucuronidase in the TMJ synovial fluids are due to infiltration from the sera and chronic inflammatory cells residing in the synovium. High levels of immunoglobulins in a closed joint space can elicit strong inflammatory reaction and cause destruction to the joint tissues via complement activation and immune complex deposition. Complement activation increases blood vessel permeability to enable recruitment of neutrophilic leukocytes, which then liberate various lysosomal enzymes and damage the articular cartilage.