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Inflammatory Joint Disease (inflammatory + joint_disease)
Selected AbstractsState of the art: Juvenile idiopathic arthritisINTERNATIONAL JOURNAL OF RHEUMATIC DISEASES, Issue 1 2002Prudence J. Manners Abstract Juvenile idiopathic arthritis (JIA) is the most common of the autoimmune musculoskeletal conditions in children. As awareness of this condition increases, so too does the apparent prevalence reported from countries around the world, suggesting that significant numbers of children with JIA have previously gone undiagnosed. Prevalence varies with race and possibly geography. However, JIA should no longer be considered as a rare condition. In the past decade, there have been definite advances in understanding the pathogenesis of JIA, and there have been parallel advances in therapies. There have been fairly modest advances in the classification of JIA, but there is at least heightened international debate on the issue, which will lead to progress. It is estimated that nearly one-third of children with this condition continue into adult life with inflammatory joint disease, and therefore the burden of disease remains significant. [source] Quantitative cartilage imaging of the human hind foot: Precision and inter-subject variabilityJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 2 2002Dina Al-Ali Alterations of ankle cartilage are observed in degenerative and inflammatory joint disease, but cartilage cannot be directly visualized by radiography. The purpose of this study was therefore to analyze the feasibility and precision of quantitative cartilage imaging in the human hind foot (talocrural, talotarsal, and intertarsal joints), and to report the inter-subject variability for cartilage volume, thickness and surface areas. The feet of 16 healthy volunteers were imaged using a 3D gradient-echo magnetic resonance imaging sequence with water-excitation. After interpolation to a resolution of 1 ± 0.125 ± 0.125 mm3 the cartilage plates were segmented, and the cartilage volume, thickness, and surface areas determined. The precision (four repeated measurements) was examined in eight volunteers, the RMS average CV% being 2.1% to 10.9% in single joint surfaces, and , 3% for the cumulative values of all joints. The mean cartilage thickness ranged from 0.57 ± 0.08 (navicular surface) to 0.89 ± 0.19 mm (trochlear surface for tibia). In conclusion this study shows that it is feasible to quantify thin cartilage layers in the hind foot under in vivo imaging conditions, and that the precision errors are substantially smaller than the inter-subject variability in healthy subjects. © 2002 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved. [source] Trefoil factor 3 is induced during degenerative and inflammatory joint disease, activates matrix metalloproteinases, and enhances apoptosis of articular cartilage chondrocytesARTHRITIS & RHEUMATISM, Issue 3 2010Sophie Rösler Objective Trefoil factor 3 (TFF3, also known as intestinal trefoil factor) is a member of a family of protease-resistant peptides containing a highly conserved motif with 6 cysteine residues. Recent studies have shown that TFF3 is expressed in injured cornea, where it plays a role in corneal wound healing, but not in healthy cornea. Since cartilage and cornea have similar matrix properties, we undertook the present study to investigate whether TFF3 could induce anabolic functions in diseased articular cartilage. Methods We used reverse transcriptase,polymerase chain reaction, Western blot analysis, and immunohistochemistry to measure the expression of TFF3 in healthy articular cartilage, osteoarthritis (OA),affected articular cartilage, and septic arthritis,affected articular cartilage and to assess the effects of cytokines, bacterial products, and bacterial supernatants on TFF3 production. The effects of TFF3 on matrix metalloproteinase (MMP) production were measured by enzyme-linked immunosorbent assay, and effects on chondrocyte apoptosis were studied by caspase assay and annexin V assay. Results Trefoil factors were not expressed in healthy human articular cartilage, but expression of TFF3 was highly up-regulated in the cartilage of patients with OA. These findings were confirmed in animal models of OA and septic arthritis, as well as in tumor necrosis factor ,, and interleukin-1,,treated primary human articular chondrocytes, revealing induction of Tff3/TFF3 under inflammatory conditions. Application of the recombinant TFF3 protein to cultured chondrocytes resulted in increased production of cartilage-degrading MMPs and increased chondrocyte apoptosis. Conclusion In this study using articular cartilage as a model, we demonstrated that TFF3 supports catabolic functions in diseased articular cartilage. These findings widen our knowledge of the functional spectrum of TFF peptides and demonstrate that TFF3 is a multifunctional trefoil factor with the ability to link inflammation with tissue remodeling processes in articular cartilage. Moreover, our data suggest that TFF3 is a factor in the pathogenesis of OA and septic arthritis. [source] Angiogenesis and the persistence of inflammation in a rat model of proliferative synovitisARTHRITIS & RHEUMATISM, Issue 7 2010Sadaf Ashraf Objective To determine whether blood vessel growth at the onset of resolving synovitis leads to its subsequent persistence and whether inhibiting this angiogenesis at the onset of persistent inflammation leads to its subsequent resolution. Methods Inflammation and angiogenesis were induced by injection of 0.03% carrageenan and/or 6 pmoles of fibroblast growth factor 2 (FGF-2) into rat knees. A brief treatment with the angiogenesis inhibitor PPI-2458 (5 mg/kg orally on alternate days) was administered 1 day before and up to 3 days after synovitis induction. Controls comprised naive and vehicle-treated rats. Synovial angiogenesis was measured using the endothelial cell proliferation index, and inflammation was determined by measuring joint swelling and macrophage percentage area. Data are presented as the geometric mean (95% confidence interval). Results Intraarticular injection of 0.03% carrageenan into rat knees produced acute synovitis, which was not associated with synovial angiogenesis and which resolved within 29 days. Injection of FGF-2 (6 pmoles) induced synovial angiogenesis without significant synovitis. Stimulation of angiogenesis with FGF-2 at the time of carrageenan injection was followed by synovitis that persisted for 29 days. Persistence of carrageenan/FGF-2,induced synovitis was prevented by systemic administration of 3 doses of the angiogenesis inhibitor PPI-2458 during the acute phase. Conclusion Our findings indicate that conversion of acute inflammation to chronic inflammation may be due to the stimulation of angiogenesis, and brief antiangiogenic treatment during the acute phase of synovitis may prevent its subsequent progression. Clinical studies will be needed to determine whether brief antiangiogenic treatment may reduce the burden of inflammatory joint diseases such as rheumatoid arthritis by facilitating the resolution of early synovitis. [source] 1266: Main anterior entities 1: non-granulomatousACTA OPHTHALMOLOGICA, Issue 2010P NERI Purpose To describe the clinical course, the laboratory work-up and the treatment of different types of anterior non-granulomatous uveitis. Methods The current literature is reviewed and the experience of a tertiary referral centre is reported. Results The lecture describes the most typical subsets of non-granulomatous uveitis. Most part of the talk is dedicated to the most common form of non-granulomatous anterior uveitis: the acute anterior uveitis (AAU), which is very often associated with the HLA-B27 allele. This antigen is also typically associated with the spondyloarthropathies, which are inflammatory joint diseases of the vertebral column. The correct interpretation of the clinical pattern can drive the decision towards the right therapeutic strategy. Other uveitis entities are described also. Conclusion Non-granulomatous uveitis is one of the most important ocular inflammations. It is mandatory to pay attention to the clinical findings and to the laboratory work-up, in order to achieve a good therapeutic approach. [source] | ||||||||||