The aim of our study was to evaluate the effects of intra-articular methotrexate (MTX) in patients with rheumatoid arthritis (RA) and psoriatic arthritis (PsA). Twenty-three consecutive patients, 10 with RA and 13 with PsA, with prevalent or unique arthritic involvement of one knee, were treated with intra-articular injections of MTX 10 mg every 7 days for 8 weeks. Before the beginning of the treatment and after 9 and 17 weeks, the patients underwent a clinical evaluation measuring maximal knee flexion angle, visual analog scale (VAS) and erythrocyte sedimentation rate (ESR). On the same days, an ultrasonographic examination of the involved knee was performed by two independent experienced operators. Synovial thickness in the suprapatellar bursa and the presence of joint effusion and Baker's cyst were assessed. An increase of the mean value of maximal knee flexion angle and a reduction of the mean values of ESR and VAS between TO, T9 and T17 were demonstrated. Ultrasonographic evaluation showed significant reduction of synovial thickness and joint effusion. No differences were detected for the presence of Baker's cyst. We may conclude that repeated intra-articular injections of MTX resulted in a decrease of local as well as systemic inflammatory signs. As far as we know, this is the first study that explores the effects of intra-articular MTX in RA and PsA both clinically and by ultrasonography.

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Background Studies suggest that interleukin-1 (IL-1) is the key mediator of arthritis and we have investigated the effect of IL-1 on cartilage degradation. We demonstrated that IL-1 inhibited proteoglycan (PG) synthesis via enhanced nitric oxide (NO) synthesis by chondrocytes. We also demonstrated that IL-1 increased intracellular Ca 2+ ion concentration ([Ca 2+ ]i) of chondrocytes. On the other hand, interleukin-4 (IL-4) is a T-cell derived 20 kDa glycoprotein and antagonise the cytokine mediated cartilage degradation.Objectives We examined the effect of IL-4 on IL-1-enhanced NO synthesis in parallel with intracellular Ca levels and PG synthesis. Methods Bovine articular chondrocytes were obtained. PG synthesis was measured with [35S] sulfate incorporation. NO levels were measured by use of an NO chemiluminescence analyzer. Ca 2+ imaging was carried out with Fura2-AM loaded chondrocyte using the digital fluorescence-imaging system. Results In the presence of IL-4, IL-1-enhanced NO release was completely abolished. IL-4 functions mainly as anti-inflammatory, as well as IL-10 and IL-13. To our knowledge, this is the first report demonstrating an inhibitory effect of IL-4 in NO release stimulated by IL-1. Alterations in [Ca 2+ ]i provide a ubiquitous cell signalling system that mediates a variety of cellular process. IL-1 evoked an increase in the levels of [Ca 2+ ]i, a response characterised by a steep onset and followed by a slower decline to preexisting values. IL-4 also abolished the IL-1induced [Ca 2+ ]i increase in the chondrocytes. We examined the effect of IL-4 on PG synthesis. Although IL-4 did not affect PG synthesis, IL-1-inhibited PG synthesis was reversed with the addition of IL-4. It is possible that IL-4 reversed the IL-1-inhibited PG synthesis through the inhibition of NO synthesis and [Ca 2+ ]i increase. Conclusion IL-4 plays a chondroprotecting effect antagonising with IL-1-inhibited PG synthesis.