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Synovial Hyperplasia (synovial + hyperplasia)

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Medical Sciences	100%

Selected Abstracts

Late clinical, plain X-ray and magnetic resonance imaging findings in haemophilic joints treated with radiosynoviorthesis

HAEMOPHILIA, Issue 6 2000
R. Nuss
The clinical, plain X-ray and magnetic resonance imaging (MRI) findings were studied in 13 haemophilic joints previously treated with radiosynoviorthesis. 32P had been injected into the joints at a median of 16 years earlier in an attempt to halt recurrent haemorrhage. Prior to 32P injection, the majority of joints demonstrated bone damage evident on plain X-ray, secondary to recurrent haemorrhage. At the follow-up evaluation we found plain X-rays were adequate to identify cysts, erosions and cartilage loss in these very damaged joints. MRI was superior to clinical examination and plain X-ray in identifying synovial hyperplasia and effusions. [source]

Liposome-bound APO2L/TRAIL is an effective treatment in a rabbit model of rheumatoid arthritis

ARTHRITIS & RHEUMATISM, Issue 8 2010
Luis Martinez-Lostao
Objective We previously observed that T lymphocytes present in synovial fluid (SF) from patients with rheumatoid arthritis (RA) were sensitive to APO2L/TRAIL. In addition, there was a drastic decrease in the amount of bioactive APO2L/TRAIL associated with exosomes in SF from RA patients. This study was undertaken to evaluate the effectiveness of bioactive APO2L/TRAIL conjugated with artificial lipid vesicles resembling natural exosomes as a treatment in a rabbit model of antigen-induced arthritis (AIA). Methods We used a novel Ni2+ -(N -5-amino-1-carboxypentyl)-iminodiacetic acid),containing liposomal system. APO2L/TRAIL bound to liposomes was intraarticularly injected into the knees of animals with AIA. One week after treatment, rabbits were killed, and arthritic synovial tissue was analyzed. Results Tethering APO2L/TRAIL to the liposome membrane increased its bioactivity and resulted in more effective treatment of AIA compared with soluble, unconjugated APO2L/TRAIL, with substantially reduced synovial hyperplasia and inflammation in rabbit knee joints. The results of biophysical studies suggested that the increased bioactivity of APO2L/TRAIL associated with liposomes was due to the increase in the local concentration of the recombinant protein, augmenting its receptor crosslinking potential, and not to conformational changes in the protein. In spite of this increase in bioactivity, the treatment lacked systemic toxicity and was not hepatotoxic. Conclusion Our findings indicate that binding APO2L/TRAIL to the liposome membrane increases its bioactivity and results in effective treatment of AIA. [source]

Inhibition of synovial hyperplasia, rheumatoid T cell activation, and experimental arthritis in mice by sulforaphane, a naturally occurring isothiocyanate

ARTHRITIS & RHEUMATISM, Issue 1 2010
Jin-Sun Kong
Objective To investigate whether sulforaphane (SFN), an isothiocyanate derived from cruciferous vegetables such as broccoli, regulates synoviocyte hyperplasia and T cell activation in rheumatoid arthritis (RA). Methods Synoviocyte survival was assessed by MTT assay. The levels of Bcl-2, Bax, p53, and pAkt were determined by Western blot analysis. Cytokine concentrations in culture supernatants from mononuclear cells were analyzed by enzyme-linked immunosorbent assay. The in vivo effects of SFN were examined in mice with experimentally induced arthritis. Results SFN induced synoviocyte apoptosis by modulating the expression of Bcl-2/Bax, p53, and pAkt. In addition, nonapoptotic doses of SFN inhibited T cell proliferation and the production of interleukin-17 (IL-17) and tumor necrosis factor , (TNF,) by RA CD4+ T cells stimulated with anti-CD3 antibody. Anti-CD3 antibody,induced increases in the expression of retinoic acid,related orphan receptor ,t and T-bet were also repressed by SFN. Moreover, the intraperitoneal administration of SFN to mice suppressed the clinical severity of arthritis induced by injection of type II collagen (CII), the anti-CII antibody levels, and the T cell responses to CII. The production of IL-17, TNF,, IL-6, and interferon-, by lymph node cells and spleen cells from these mice was markedly reduced by treatment with SFN. Anti-CII antibody,induced arthritis in mice was also alleviated by SFN injection. Conclusion SFN was found to inhibit synovial hyperplasia, activated T cell proliferation, and the production of IL-17 and TNF, by rheumatoid T cells in vitro. The antiarthritic and immune regulatory effects of SFN, which were confirmed in vivo, suggest that SFN may offer a possible treatment option for RA. [source]

Hydroxychloroquine potentiates Fas-mediated apoptosis of rheumatoid synoviocytes

CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2006
W.-U. Kim
Summary Inadequate apoptosis may contribute to the synovial hyperplasia associated with rheumatoid arthritis (RA). The Fas-associated death domain protein (FADD)-like interleukin (IL)-1,-converting enzyme (FLICE)-inhibitory protein (FLIP), which is an apoptotic inhibitor, has been implicated in the resistance to Fas-mediated apoptosis of synoviocytes. This study investigated whether hydroxychloroquine (HCQ), an anti-rheumatic drug, induces the apoptosis of rheumatoid synoviocytes, and modulates the expression of FLIP. Fibroblast-like synoviocytes (FLS) were prepared from the synovial tissues of RA patients, and were cultured with various concentrations of HCQ in the presence or absence of the IgM anti-Fas monoclonal antibodies (mAb) (CH11). Treatment with HCQ, ranging from 1 to 100 µM, induced the apoptosis of FLS in a dose- and time-dependent manner. The increase in synoviocytes apoptosis by HCQ was associated with caspase-3 activation. A combined treatment of HCQ and anti-Fas mAb increased FLS apoptosis and caspase-3 activity synergistically, compared with either anti-Fas mAb or HCQ alone. The Fas expression level in the FLS was not increased by the HCQ treatment, while the FLIP mRNA and protein levels were decreased rapidly by the HCQ treatment. Moreover, time kinetics analysis revealed that the decreased expression of FLIP by HCQ preceded the apoptotic event that was triggered by HCQ plus anti-Fas mAb. Taken together, HCQ increases the apoptosis of rheumatoid synoviocytes by activating caspase-3, and also sensitizes rheumatoid synoviocytes to Fas-mediated apoptosis. Our data suggest that HCQ may exert its anti-rheumatic effect in rheumatoid joints through these mechanisms. [source]