The prevalence of different MRI structural changes in knee osteoarthritis (KOA)

Abstract

s / Osteoarthritis and Cartilage 22 (2014) S57–S489 S288 were analyzed using descriptive and bivariate test, parametric and no-parametric statistical tests were used. Results: We studied 72 patients, mean age 45 years 7.4, 83% female gender, education (years) mean 10.5 3.8, Body Mass Index 30.6 4.9. Score for WOMAC were: pain 1.4, stiffness 1.5, physical function 1.3. EuroQol 0.55 in male population vs. 0.69 in women population. The table 1 show MSUS findings. Conclusions:morpho-structural findings byMSUSwere found in a high prevalence of patients with knee OA classified by radiology in early stages. This shows that although radiology is the most used method for classification of disease, it does not evaluate an early OA, further studies are required to detect early changes of OA. Figure legend. In CIA rats, therapeutic effects of siCx43. Cumulative incidence of paw swelling (A) and kinetic change of paw volume (mean SD) (B) are plotted, *p < 0.05, versus the siNeg, # p < 0.05, versus the control. Representative microscopic images of HE zUniv. of A Coru~ na, A Coru~ na, Spain; xUniversit a della Magna Grecia, Catanzaro, Italy Purpose: Osteoarthritis (OA) is a progressive disease of the joints characterized by degradation of articular cartilage. Although OA is commonly described as non-inflammatory disease, inflammation is recognized as contributing to the symptoms and progression of OA. One of the symptoms of OA is synovitis. Pro-inflammatory cytokines are produced in the inflamed synovium and diffuse into the cartilage, activating chondrocytes that in turn could produce catabolic factors that might contribute to the destruction of extra cellular matrix (ECM). In addition, several studies suggest that adipokines, such as leptin and adiponectin, are involved in the pathophysiology of OA. However, the role of immune component in osteoarthritis is still obscure and poorly investigated. In order to gain further insights into the potential interaction of immune cells in OA and the role of adipokines on these cells, we have performed a series of experiments in CD4þ T cells from OA patients. Namely, we first evaluated the in vitro proliferative effect of several adipokines (adiponectin, lipocalin-2 and leptin) on CD4þ T cells from OA patients. Next, we evaluated whether adipokines were able to induce activation of these cells by inducing CD69 and CD25. Finally, we also investigated the modulation of several inflammatory mediators in these cells. For completeness, the cross talk between activated CD4þ T cells and chondrocytes from OA patients, in presence or not of adipokines, was also explored. Methods: Peripheral blood samples were collected from OA patients. PBMCs were obtained by Ficoll Paque and CD4þ T cells were magnetically purified (Invitrogen). Proliferation was evaluated by CFSE assay and the activation by flow cytometry (CD25, CD69). CD4þ T cells were plated, stimulated with anti-CD3/CD28, in the presence or not of adipokines, during several days. mRNA and protein expression of inflammatory factors was evaluated by qRT-PCR and ELISA assays. To test the cross talk between T lymphocytes and chondrocytes, primary chondrocytes were harvested from human OA articular cartilage samples, and co-cultured with activated CD4þ T cells in two ways: the first way by incubating the cells by direct contact or by transwell system and afterwards treated or not with recombinant adipokines during several days. Results: Adipokines induce the proliferation and activation of CD4þ T cells from OA patients. The exposure of activated CD4þ T cells to adiponectin, lipocalin-2 and leptin, during several days, modulates IL-6, IL8 and CCL-3 production. On the other hand, we observed that the production of macromolecules of ECM, such as aggrecan, in co-cultured chondrocytes with activated CD4þ T cells, in presence or not of adipokines, was altered. Conclusions: This study showed that there is a clear cross talk between T cells and chondrocytes and that this interaction is modulated by adipokines. Our results might contribute to enlighten the understanding of still unclear immune-mediated mechanism/s in OA. 501 THE ROLES OF CONNEXIN 43 IN EXPERIMENTAL ARTHRITIS S. Tsuchida, Y. Arai, S. Nakagawa, R. Terauchi, K. Honjo, H. Inoue, D. Tokunaga, O. Mazda, T. Kubo. Kyoto Prefectural Univ. of Med., Kyoto,