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Titolo:
The role of cytokines as inflammatory mediators in osteoarthritis: Lessonsfrom animal models
Autore:
Goldring, MB;
Indirizzi:
Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Boston, MA 02115 USAHarvard Univ Boston MA USA 02115 Deaconess Med Ctr, Boston, MA 02115 USA
Titolo Testata:
CONNECTIVE TISSUE RESEARCH
fascicolo: 1, volume: 40, anno: 1999,
pagine: 1 - 11
SICI:
0300-8207(1999)40:1<1:TROCAI>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; INTERLEUKIN-1 RECEPTOR-ANTAGONIST; COLLAGEN-INDUCED ARTHRITIS; CANINE ARTICULAR-CARTILAGE; VIVO GENE-TRANSFER; ALPHA TNF-ALPHA; FIBRONECTIN FRAGMENTS; RABBIT KNEES; INTRAARTICULAR INJECTION; RHEUMATOID-ARTHRITIS;
Keywords:
inflammation; cytokines; osteoarthritis; interleukins; growth factors;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
98
Recensione:
Indirizzi per estratti:
Indirizzo: Goldring, MB HarvardlackfanInst Med, New England Baptist Bone & Joint Inst, Room 246,4 B Harvard Univ Room 246,4 Blackfan Circle Boston MA USA 02115 B
Citazione:
M.B. Goldring, "The role of cytokines as inflammatory mediators in osteoarthritis: Lessonsfrom animal models", CONNECT TIS, 40(1), 1999, pp. 1-11

Abstract

Studies in animal models of osteoarthritis (OA) have been used extensivelyto gain insight into the pathogenesis of OA, but early studies largely ignored inflammation except as a secondary phenomenon. Synovitis has often been noted as a feature in experimental OA, and more recent work has established a central role for inflammatory cytokines as biochemical signals which stimulate chondrocytes to release cartilage-degrading proteinases. Thus, proteinase inhibitors, cytokine antagonists and receptor blocking antibodies, and growth/differentiation factors have been considered as potential therapeutic agents and targets for gene therapy. Although there is some disagreement, it is generally accepted that IL-1 is the pivotal cytokine at early and late stages, while TNF-alpha is involved primarily in the onset of arthritis. Other cytokines released during the inflammatory process in the OA joint may be regulatory (IL-6, IL-8) or inhibitory (IL-4, IL-10, IL-13, IFN-gamma). Furthermore, studies in animal models have illustrated the potentially beneficial effects of anticytokine therapy with monoclonal antibodies or receptor antagonists, although local rather than systemic delivery would benecessary for the largely localized OA in humans. Transgenic or knockout mice have also provided insights into general mechanisms of cytokine-inducedcartilage degradation but have not directly addressed OA pathogenesis. Similarly, animals with spontaneous or transgenic modifications in cartilage matrix components, growth/differentiation factors, or developmentally regulated transcription factors have provided information about potential gene defects that predispose to OA without addressing the role of inflammatory mediators in cartilage destruction. Although the multiple etiologies of human OA indicate that it is more complex than any animal model, the use of appropriate, well-defined animal models will establish the feasibility of novel forms of therapy.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/09/20 alle ore 06:24:14