No abstract

Background: Osteoarthritis (OA) is a leading cause of morbidity affecting 54 million Americans per year at an annual cost of 304 billion dollars to the US healthcare system. OA is characterized as a disease of joint wear and tear, but mounting evidence suggests a role for aberrant activation of immunity to contribute to disease progression. Methods: We hypothesized that OA patients have differential profiles of immunity between peripheral and synovial compartments as an indication that in situ immunity is affected by OA or vice versa. We used FACS analysis to phenotype T cell and myeloid populations between peripheral and synovial compartments from 16 patients undergoing total joint replacement due to advanced OA. Results: Our finding that Foxp3[Formula: see text] T regulatory (Tregs) increasingly comprise SF immunity of OA patients is novel ([Formula: see text]). Though the periphery harbored greater numbers of lymphocyte and myeloid cells compared to synovial fluid ([Formula: see text]), the synovial fluid revealed elevated percentages of myeloid (Cd11b[Formula: see text]) cells that comprised the CD45[Formula: see text] population ([Formula: see text]). Further, characterization elucidated that CD45/CD11b/CD14[Formula: see text]/CD15- cells upregulated HLADR in the affected synovial fluid ([Formula: see text]) and that these cells increase expression of CD68 ([Formula: see text]). Conclusions: Our data indicate that the affected joint space in OA patients harbors phenotypically distinct T-cell and myeloid populations compared to autologous-matched peripheral immunity. The contribution of aberrant immune populations to development and progression of OA is of interest for novel immunotherapies.