ReviewSpringer seminars in immunopathology1998
Joint inflammation and cartilage destruction may occur uncoupled.
Review in Springer seminars in immunopathology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 105 citations in OpenAlex.
- IL-27 attenuates IL-23 mediated inflammatory arthritis.Clinical immunology (Orlando, Fla.) · 2023Article
- Comparative Expression Analyses of Pro- versus Anti-Inflammatory Mediators within Synovium of Patients with Joint Trauma, Osteoarthritis, and Rheumatoid Arthritis.Mediators of inflammation · 2017Article
- Anti-TNFα alters the natural history of experimental Crohn's disease in rats when begun early, but not late, in disease.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Rodent preclinical models for developing novel antiarthritic molecules: comparative biology and preferred methods for evaluating efficacy.Journal of biomedicine & biotechnology · 2011Review
- Local interleukin-1-driven joint pathology is dependent on toll-like receptor 4 activation.The American journal of pathology · 2009Article
- The evolving systemic and local biomarker milieu at different stages of disease progression in rat adjuvant-induced arthritis.Journal of clinical immunology · 2009Article
- The chrondoprotective actions of a natural product are associated with the activation of IGF-1 production by human chondrocytes despite the presence of IL-1beta.BMC complementary and alternative medicine · 2006Article
- Transcription factor T-bet regulates inflammatory arthritis through its function in dendritic cells.The Journal of clinical investigation · 2006Article
- Decrease in expression of bone morphogenetic proteins 4 and 5 in synovial tissue of patients with osteoarthritis and rheumatoid arthritis.Arthritis research & therapy · 2006Article
- Punica granatum L. extract inhibits IL-1beta-induced expression of matrix metalloproteinases by inhibiting the activation of MAP kinases and NF-kappaB in human chondrocytes in vitro.The Journal of nutrition · 2005Article
- Analysis of the cell infiltrate and expression of proinflammatory cytokines and matrix metalloproteinases in arthroscopic synovial biopsies: comparison with synovial samples from patients with end stage, destructive rheumatoid arthritis.Annals of the rheumatic diseases · 2003Article
- Lifelong voluntary joint loading increases osteoarthritis in mice housing a deletion mutation in type II procollagen gene, and slightly also in non-transgenic mice.Annals of the rheumatic diseases · 2002Article
- Autoantibodies against interleukin 1alpha in rheumatoid arthritis: association with long term radiographic outcome.Annals of the rheumatic diseases · 2002Article
- Cytokines in rheumatoid arthritis.Current rheumatology reports · 2002Review
- Macrophage- and neutrophil-dominant arthritis in human IL-1 alpha transgenic mice.The Journal of clinical investigation · 2001Article
- Update on synovitis.Current rheumatology reports · 2001Review
- Anti-cytokine therapy in chronic destructive arthritis.Arthritis research · 2001Review
- Decline after immobilisation and recovery after remobilisation of synovial fluid IL1, TIMP, and chondroitin sulphate levels in young beagle dogs.Annals of the rheumatic diseases · 2001Article
- Arguments for interleukin 1 as a target in chronic arthritis.Annals of the rheumatic diseases · 2000Review
- Role of interleukin 1 and interleukin 1 receptor antagonist in the mediation of rheumatoid arthritis.Annals of the rheumatic diseases · 2000Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic arthritis is characterized by a persistent joint inflammation and concomitant joint destruction. Although the joint swelling is a major clinical problem, destruction of bone and cartilage may occur uncoupled to inflammation and it is of utmost importance to fully understand the elements of the destructive process. TNF and IL-1 are considered master cytokines in the process of human RA, with a claimed cascade of TNF inducing most of the IL-1 production. Studies in experimental models revealed that TNF is indeed a pivotal cytokine in joint swelling, yet IL-1 is the dominant cartilage destructive cytokine and its production may occur independent of TNF. This was found with anti-TNF/IL-1 neutralizing antibodies and the observations were recently backed up with similar data in arthritis models in TNF and IL-1 knockout mice. Apart from the absolute level of IL-1, the destructive potential of an arthritis is determined by the balance with regulatory cytokines and anabolic growth factors. IL-4, IL-6, and IL-10 can promote inflammation and tissue fibrosis, yet cartilage destruction is found to be greatly reduced by these cytokines, linked to a range of pathways which can reduce the IL-1 impact on the articular cartilage. Finally, the presence of anabolic growth factors in the inflamed synovium may have a major impact on net destruction. Endogenous transforming growth factor-beta (TGF-beta) is found in inflamed synovia, but local coadministration of TGF-beta further enhanced the degree of synovitis, yet almost fully prevented cartilage damage, providing another example of a major lack of correlation between inflammatory mass and destructive potential. It is suggested that novel therapy in RA patients should not only focus on reduction of outer signs of joint inflammation, but should also include attempts at reduction of cartilage destruction.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.