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ND: | ME16278282
PMID: | 16278282
CED: | 20060120
DCO: | 20060306
Autoren: | Verbruggen G
Titel: | Chondroprotective drugs in degenerative joint diseases.
Quelle: | Rheumatology (Oxford, England); VOL: 45 (2); p. 129-38 /200602/
PM: | Print-Electronic
EPD: | 20051108
SU: | AIM IM
Sprache: | English
CY: | England
JID: | 100883501
ISSN: | 1462-0324
CO: | RUMAFK
Institution: | Polikliniek Reumatologie, 0K12, Universitair Hospitaal, De Pintelaan 185, B-9000 Ghent, Belgium. gust.verbruggen@ugent.be
DT: | Journal Article; Review
RN: | 145
Schlagwörter
CT: | ANTIRHEUMATIC AGENTS/*therapeutic use; CARTILAGE, ARTICULAR/*drug effects; CARTILAGE, ARTICULAR/physiopathology; CYTOKINES/physiology; GROWTH SUBSTANCES/physiology; HUMANS; OSTEOARTHRITIS/*drug therapy; OSTEOARTHRITIS/physiopathology; TUMOR NECROSIS FACTOR-ALPHA/antagonists & inhibitors
CTG: | ANTIRHEUMATIKA/*therapeutische Anwendung; KNORPEL, GELENK-/*Arzneimittelwirkungen; KNORPEL, GELENK-/Pathophysiologie; CYTOKINE/Physiologie; WUCHSSTOFFE/Physiologie; MENSCH; OSTEOARTHROSE/*Arzneimitteltherapie; OSTEOARTHROSE/Pathophysiologie; TUMORNEKROSEFAKTOR/Antagonisten & Inhibitoren
TE: | Antirheumatic Agents; Cytokines; Growth Substances; Tumor Necrosis Factor-alpha
AB: | Catabolic cytokine and anabolic growth factor pathways control destruction and repair in osteoarthritis (OA). A unidirectional TNF-alpha/IL-1-driven cytokine cascade disturbs the homeostasis of the extracellular matrix of articular cartilage in OA. Although chondrocytes in OA cartilage overexpress anabolic insulin-like growth factor (IGF) and its specific receptor (IGFRI) autocrine TNF-alpha released by apoptotic articular cartilage cells sets off an auto/paracrine IL-1-driven cascade that overrules the growth factor activities that sustain repair in degenerative joint disease. Chondroprotection with reappearance of a joint space that had disappeared has been documented unmistakably in peripheral joints of patients suffering from spondyloarthropathy when treated with TNF-alpha-blocking agents that repressed the unidirectional TNF-alpha/IL-1-driven cytokine cascade. A series of connective tissue structure-modifying agents (CTSMAs) that directly affect IL-1 synthesis and release in vitro and down-modulate downstream IL-1 features, e.g. collagenase, proteoglycanase and matrix metalloproteinase activities, the expression of inducible nitric oxide synthase, the increased release of nitric oxide, and the secretion of prostaglandin E(2), IL-6 and IL-8, have been shown to possess disease-modifying OA drug (DMOAD) activities in experimental models of OA and in human subjects with finger joint and knee OA. Examples are corticosteroids, some sulphated polysaccharides, chemically modified tetracyclines, diacetylrhein/rhein, glucosamine and avocado/soybean unsaponifiables.

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