IN-VITRO RELEASE OF PROSTAGLANDINS AND LEUKOTRIENES FROM SYNOVIAL TISSUE, CARTILAGE, AND BONE IN DEGENERATIVE JOINT DISEASES

Objective. To determine the major source of eicosanoid release in arth ritic joint tissues and to examine the modulation of this release by i ndomethacin and diclofenac. Methods. Release of prostaglandin E2 (PGE2 ), 6-keto-PGF1alpha, leukotriene B4 (LTB4), and LTC4 was measured in s upernatants of synovial tissue, cartilage, and bone incubates from pat ients with osteoarthritis, active rheumatoid arthritis (RA), inactive RA, and pseudogout. Radioimmunoassay (RIA) was used to determine the l evels of the eicosanoids. Results. Addition of the divalent cation ion ophore A23187 resulted in significant release of all eicosanoids measu red from synovial tissue, but not from cartilage, cortical bone, or ca ncellous bone. PG release was significantly inhibited by the addition of indomethacin or diclofenac at either 10(-5) moles/liter or 10(-7) m oles/liter. The amount of LTC4 released from cartilage and bone was on ly slightly above the detection limit of the RIA, whereas large amount s were released from synovial tissue. Neither indomethacin nor diclofe nac had an effect on LTC4 release. LTC4 release from synovial tissue o f patients with inactive RA was significantly decreased in comparison with the levels from synovial tissue of patients with the other joint diseases. There was no significant difference in PG release among pati ents in the various disease groups. Conclusion. Synovial tissue appear s to be the major source of eicosanoids in synovial fluid. Indomethaci n and diclofenac inhibit the release of PG, but not LT, from various j oint tissues.