It was our purpose to study IgA, IgG, and beta-glucuronidase levels in temporomandibular joint fluid lavage samples in order to find a correlation between biochemical markers and joint pathology.
Our patient population included 20 patients (18 female and 2 male) with severe pain and limitation of mandibular movement that failed to improve with at least 3 months of a full course of nonsurgical therapy. After institutional review board approval, 13 control subjects (6 female and 7 male), with no history of temporomandibular joint pain/dysfunction, were obtained. Arthroscopic examination of the patient and control groups involved classification of joints for osteoarthritis and synovitis using a visual grading system. All synovial fluid samples were analyzed for beta-glucuronidase, IgA, and IgG using fluorometric assay and enzyme-linked immunosorbent assay.
beta-Glucuronidase was significantly elevated (P<.05, t test) in the patient group compared with the control group (4.13+/-8.30 versus 0.9+/-0.83 [mean+/-SD]). The difference in the IgG level was also statistically significant (31,638+/-70,714 versus 4,407+/-1,324) (P<.05, t test). IgA level showed a similar trend between the patient and control groups (6,315+/-19,037 versus 425+/-192) (P=.10, t test).
Quantitative synovial fluid analysis of beta-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 beta-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.