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Suchschritt : FT=glucosamine AND FT=osteoarthritis
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ND: | ME15911209
PMID: | 15911209
LR: | 20051116
CED: | 20050524
DCO: | 20050815
Autoren: | Wu CW; Kalunian KC
Titel: | New developments in osteoarthritis.
Quelle: | Clinics in geriatric medicine; VOL: 21 (3); p. 589-601, vii /200508/
PM: | Print
SU: | IM
Sprache: | English
CY: | United States
JID: | 8603766
ISSN: | 0749-0690
CO: | CGMEE
Institution: | Center of Innovative Therapies at the University of San Diego at California, 9320 Campus Point Drive, Suite 225, La Jolla, CA 92037-0943, USA.
DT: | Journal Article; Review
RN: | 70
Schlagwörter
CT: | ACETAMINOPHEN/therapeutic use; ACUPUNCTURE THERAPY; ANALGESICS, NON-NARCOTIC/therapeutic use; ANIMALS; ANTI-INFLAMMATORY AGENTS, NON-STEROIDAL/therapeutic use; BIOMECHANICS; CHONDROITIN/therapeutic use; COLCHICINE/therapeutic use; DISEASE PROGRESSION; GLUCOSAMINE/therapeutic use; GOUT SUPPRESSANTS/therapeutic use; HUMANS; OSTEOARTHRITIS/*drug therapy; OSTEOARTHRITIS/epidemiology; OSTEOARTHRITIS/*physiopathology; OSTEOARTHRITIS/radiography; OSTEOARTHRITIS/surgery; SYNOVIAL MEMBRANE/physiopathology
CTG: | ACETAMINOPHEN/therapeutische Anwendung; AKUPUNKTURBEHANDLUNG; ANALGETIKA, NICHTNARKOTISCHE/therapeutische Anwendung; TIER; ANTIPHLOGISTIKA, NICHTSTEROIDALE/therapeutische Anwendung; BIOMECHANIK; CHONDROITIN/therapeutische Anwendung; COLCHICIN/therapeutische Anwendung; KRANKHEITSPROGRESSION; GLUCOSAMIN/therapeutische Anwendung; GICHTMITTEL/therapeutische Anwendung; MENSCH; OSTEOARTHROSE/*Arzneimitteltherapie; OSTEOARTHROSE/Epidemiologie; OSTEOARTHROSE/*Pathophysiologie; OSTEOARTHROSE/Röntgenuntersuchung; OSTEOARTHROSE/Chirurgie; SYNOVIALMEMBRAN/Pathophysiologie
TE: | Analgesics, Non-Narcotic; Anti-Inflammatory Agents, Non-Steroidal; Gout Suppressants; Acetaminophen/103-90-2; Glucosamine/3416-24-8; Colchicine/64-86-8; Chondroitin/9007-27-6
CR: | 103-90-2; 3416-24-8; 64-86-8; 9007-27-6
AB: | Osteoarthritis (OA) has been a frustrating disease for both the patient and the physician. Its current impact on society is tremendous, and rivals that of ischemic heart disease in many regards. As the baby boomers reach late adulthood and the obesity epidemic rages on, OA will assume an even greater impact on society. The current OA armamentarium only reduces pain and perhaps improves function, and has no impact on the disease incidence or progression. Thus, the challenge for researchers to develop disease-modifying OA drugs becomes an issue of paramount importance. Several advances in our understanding of OA pathophysiology have provided a glimpse of optimism that disease modification is a real possibility. Appreciation of the local factors involved in OA progression as well as the inflammatory nature in a subset of patients has led to different treatment strategies based on predominant phenotype. Further understanding of the initiating events in cartilage destruction, the relationship between the different pathologic influences, and the role of the chondrocyte in maintaining extracellular matrix homeostasis will be necessary to reveal potential targets of therapy.

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