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Titolo:
Anticytokine therapy for osteoarthritis
Autore:
Goldring, MB;
Indirizzi:
Harvard Univ, Inst Med, Beth Israel Deaconess Med Ctr, Dept Med,Div Rheumatol, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 Med,Div Rheumatol, Boston, MA 02115 USA Harvard Univ, Inst Med, New England Baptist Bone & Joint Inst, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 Bone & Joint Inst, Boston, MA 02115 USA
Titolo Testata:
EXPERT OPINION ON BIOLOGICAL THERAPY
fascicolo: 5, volume: 1, anno: 2001,
pagine: 817 - 829
SICI:
1471-2598(200109)1:5<817:ATFO>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTERLEUKIN-1 RECEPTOR ANTAGONIST; COLLAGEN-INDUCED ARTHRITIS; NECROSIS-FACTOR-ALPHA; NF-KAPPA-B; RHEUMATOID-ARTHRITIS; GENE-TRANSFER; TNF-ALPHA; ARTICULAR CHONDROCYTES; SYNOVIAL FIBROBLASTS; IN-VIVO;
Keywords:
animal models; cartilage; chondrocyte; cytokine; gene therapy; IL-1; osteoarthritis; TNF-alpha;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
113
Recensione:
Indirizzi per estratti:
Indirizzo: Goldring, MB Harvard Univ, Inst Med, Beth Israel Deaconess Med Ctr, Dept Med,Div Rheumatol, HIM246,4 Blackfan Circle, Boston, MA 02115 USA Harvard Univ HIM246,4 Blackfan Circle Boston MA USA 02115 USA
Citazione:
M.B. Goldring, "Anticytokine therapy for osteoarthritis", EXPERT OP B, 1(5), 2001, pp. 817-829

Abstract

Osteoarthritis (OA) is a joint disease that involves degeneration of articular cartilage, weakening of the subchondral bone and limited intra-articular inflammation manifested by synovitis. Since the pathogenesis of OA involves multiple aetiologies, including mechanical, biochemical and genetic factors, it has been difficult to identify unique targets for therapy. Currentpharmaco logical interventions focus primarily on improving symptoms. The rationale for the use of anticytokine therapy in OA is based on evidence from studies in vitro and in vivo that interleukin-1 (IL-1) and tumour necrosis factor (TNF)-alpha are the predominant pro-inflammatory and catabolic cytokines involved in the initiation and progression of articular cartilage destruction. Since the increased levels of catabolic enzymes, prostaglandins, nitric oxide (NO) and other markers in OA fluids and tissues appear to berelated to elevated levels of IL-1 and TNF-U, therapies that interfere with the expression or actions of these cytokines are most promising. Other cytokines that are anti-inflammatory and are often detected, paradoxically, in OA tissues are also potential therapeutic agents for counteracting the cartilage destruction in OA. Identification of methods for early diagnosis isof key importance, since therapeutic interventions aimed at blocking or reversing structural damage will be more effective when there is the possibility of preserving normal homeostasis. At later stages, cartilage tissue engineering with or without gene therapy will also require anticytokine therapy to block damage to newly repaired cartilage. This review will focus on experimental approaches currently under study that may lead to elucidation ofeffective strategies for therapy in OA, with special emphasis on anticytokine therapy.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/02/20 alle ore 16:39:02