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Severe Arthritis (severe + arthritis)
Selected AbstractsArthritis induced in rats with non-immunogenic adjuvants as models for rheumatoid arthritisIMMUNOLOGICAL REVIEWS, Issue 1 2001Rikard Holmdahl Summary: Rat models are useful for studies of the pathogenesis of rheumatoid arthritis (RA) since rats are extraordinarily sensitive to induction of arthritis with adjuvants. Injection of not only the classical complete Freund's adjuvant but also mineral oil without mycobacteria and pure adjuvants such as pristane and squalene, induce severe arthritis in many rat strains. Models like pristane-induced arthritis in rats are optimal models for RA since they fulfill the RA criteria including a chronic relapsing disease course. Arthritogenic adjuvants like pristane, avridine, squalene and mineral oil are not immunogenic since they do not contain major histocompatibility complex (MHC) binding peptides. Nevertheless, the diseases are MHC-associated and dependent on the activation of ,,TCR (T-cell receptor)-expressing T cells. However, it has not been possible to link the immune response to joint antigens or other endogenous components although immunization with various cartilage proteins induce arthritis but with different pathogeneses. To unravel the mechanisms behind adjuvant-induced arthritis, a disease-oriented genetic approach is optimal. Several loci that control onset of arthritis, severity and chronicity of the disease have been identified in genetic crosses and most of these have been confirmed in congenic strains. In addition, many of these loci are found in other autoimmune models in the rat as well as associated with arthritis in mice and humans. [source] MicroCT evaluation of normal and osteoarthritic bone structure in human knee specimensJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 1 2003Vikas Patel Abstract Although trabecular bone structure has been evaluated, variation with knee compartment and depth from joint surface is not completely understood. Cadaver knees were evaluated with microcomputed tomography analysis for these variations. Objective differences were compared between: medial vs. lateral compartments; femoral vs. tibial bone; and normal vs. arthritic knees. Depth dependent changes in the parameters were observed for the first 6 mm of the cores in normal knees: BV/TV, Tb.N and Conn.D gradually decrease, while Tb.Sp and SMI increase. In the first 6 mm of the normal tibia BV/TV, Tb.N, and Tb.Th are greater than in the femur on both the medial and lateral compartments while Tb.Sp, SMI, and Conn.D are lower. The medial compartment values for BV/TV, Tb.N, Tb.Th and Conn.D are generally greater than for the lateral in both the femur and tibia while Tb.Sp and SMI are lower. In comparison of normal vs. arthritic knees significant differences are observed in the first 6 mm of the medial tibia. With arthritis BV/TV and Tb.Th are lower, while SMI and Tb.Sp are higher. Tb.N and Conn.D show no statistically significant difference. The bone structure variations are, thus, most prominent in the first 6 mm of depth and medial compartment bone is generally more structurally sound than lateral. Severely arthritic bone changes are most prominent in the medial compartment of the tibia and bone structure is less sound in severe arthritis. © 2002 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved. [source] Novel recombinant congenic mouse strain developing arthritis with enthesopathyPATHOLOGY INTERNATIONAL, Issue 7 2008Shiro Mori Based on the hypothesis that the complex pathological and immunological manifestations of rheumatoid arthritis (RA) and the related diseases are under the control of multiple gene loci with allelic polymorphism, a recombinant congenic mouse strain was prepared between an MRL/Mp- lpr/lpr (MRL/lpr) strain, which develops arthritis resembling RA, and a non-arthritic strain C3H/HeJ- lpr/lpr (C3H/lpr). In MRL/lpr × (MRL/lpr × C3H/lpr) F1 mice, the mice developing severe arthritis were selected based on joint swelling to further continue intercrosses, and then an McH- lpr/lpr -RA1 (McH/lpr-RA1) strain was established and its histopathological phenotypes of joints and autoimmune traits were analyzed. Arthritis in McH/lpr-RA1 mice developed at a higher incidence by 20 weeks of age, compared with that in the MRL/lpr mice, who had severe synovitis (ankle, 60.3%; knee, 65.1%), and also fibrous and fibrocartilaginous lesions of articular ligamenta resembling enthesopathy (ankle, 79.4%; knee, 38.1%), resulting in ankylosis. The lymphoproliferative disorder was less, and serum levels of IgG and IgG autoantibodies including anti-dsDNA and rheumatoid factor were lower than those of both MRL/lpr and C3H/lpr strains. McH/lpr-RA1 mice may provide a new insight into the study of RA regarding the common genomic spectrum of seronegative RA and enthesopathy. [source] A comparative genetic analysis between collagen-induced arthritis and pristane-induced arthritisARTHRITIS & RHEUMATISM, Issue 8 2003Peter Olofsson Objective To compare the genetic regulation of collagen-induced arthritis (CIA) with that of pristane-induced arthritis (PIA) in rats. Methods A genome-wide linkage analysis of an (E3 × DA)DA backcross of rats with CIA (n = 364 male rats; the same strain combinations as previously used to determine the genetic control of PIA) was performed. The strongest loci in both CIA and PIA (i.e., Cia12/Pia4 and Cia13/Pia7) were isolated in congenic strains. Susceptibility in both congenic strains was tested in rats with CIA and in rats with PIA. Results We found a striking, although not complete, similarity of the arthritis-controlling loci in CIA and in PIA, as well as the previously defined loci associated with cartilage destruction, antibody production, and the acute-phase response. All major PIA quantitative trait loci (QTLs) identified in early severe arthritis were also strong regulators of CIA. The 2 strongest QTLs, Cia12/Pia4 on chromosome 12 and Cia13/Pia7 on chromosome 4, were also analyzed in congenic strains with DA or E3 as the background genome. Consistent with the results of linkage analysis, the congenic strain experiments showed that the chromosome 4 locus was more penetrant in CIA than in PIA, while the chromosome 12 locus almost completely dominated the control of PIA severity. Conclusion The underlying genetic control of CIA was found to have many, but not all, pathogenic mechanisms in common with PIA, despite the use of a cartilage-specific antigen (type II collagen) to induce CIA but not PIA. [source] | ||||||||||