Details

Autor(en) / Beteiligte

• Ortutay, Zsuzsanna
• Polgár, Anna
• Gömör, Béla
• Géher, Pál
• Lakatos, Tamás
• Glant, Tibor T.
• Gay, Renate E.
• Gay, Steffen
• Pállinger, Éva
• Farkas, Csaba
• Farkas, Éva
• Tóthfalusi, László
• Kocsis, Katalin
• Falus, András
• Buzás, Edit I.

Titel

Synovial fluid exoglycosidases are predictors of rheumatoid arthritis and are effective in cartilage glycosaminoglycan depletion

Ist Teil von

• Arthritis and rheumatism, 2003-08, Vol.48 (8), p.2163-2172

Ort / Verlag

Hoboken: Wiley Subscription Services, Inc., A Wiley Company

Erscheinungsjahr

2003

Quelle

MEDLINE

Beschreibungen/Notizen

• Objective To analyze enzymes involved in joint damage by simultaneous investigation of glycosidases and matrix metalloproteinases (MMPs) in patients with various joint diseases. Methods Activities of glycosidases (β‐D‐glucuronidase, β‐D‐N‐acetyl‐glucosaminidase, β‐D‐N‐acetyl‐galactosaminidase, β‐D‐galactosidase, and α‐D‐mannosidase) were tested at an acidic pH as well as at the original pH of the synovial fluid (SF) samples in parallel with activities of MMP‐1 and MMP‐9. Results Patients with rheumatoid arthritis (RA) were characterized by significantly elevated activities of β‐D‐glucuronidase and β‐D‐N‐acetyl‐glucosaminidase in SF compared with patients with osteoarthritis, seronegative spondylarthritis, or acute sports injury. To select the best predictor for distinguishing among patient groups, a stepwise logistic regression analysis was performed; the strongest association was found to be between RA and β‐D‐glucuronidase/β‐D‐N‐acetyl‐glucosaminidase activities (measured at the pH of the SF). Further, a significant correlation was observed between the activity of SF β‐D‐N‐acetyl‐glucosaminidase and the level of rheumatoid factor. In vitro digestion of human hyaline cartilage samples revealed that the dominant glycosidases, alone or in combination with MMPs, proved to be effective in depleting glycosaminoglycans (GAGs) from cartilage. Conclusion These results suggest that exoglycosidases, which are present in the SF of RA patients, may contribute to the depletion of GAGs from cartilage and thereby facilitate the invasion of synovial cells and their attachment to cartilage in RA.