Clinical Trial andIn VitroStudy for the Role of Cartilage and Synovia in Acute Articular Infection

Author:

Langenmair Elia R.1,Kubosch Eva J.1,Salzmann Gian M.12,Beck Samuel1,Schmal Hagen13

Affiliation:

1. Department of Orthopedics and Trauma Surgery, Albert-Ludwigs University Medical Center Freiburg, Hugstetter Street 55, 79106 Freiburg, Germany

2. Schulthess Clinic, Zurich, Lenghalde 2, 8008 Zurich, Switzerland

3. Department of Orthopaedics and Traumatology, Odense University Hospital and Department of Clinical Research, University of Southern Denmark, Sdr. Boulevard 29, 5000 Odense C, Denmark

Abstract

Objective. Osteoarthritis is a long-term complication of acute articular infections. However, the roles of cartilage and synovia in this process are not yet fully understood.Methods. Patients with acute joint infections were enrolled in a prospective clinical trial and the cytokine composition of effusions compared in patients with arthroplasty (n= 8) or with intact joints (n= 67). Cytokines and cell function were also analyzed using a humanin vitromodel of joint infection.Results. Synovial IL-1βlevels were significantly higher in patients with arthroplasty (p= 0.004). Higher IL-1βconcentrations were also found in thein vitromodel without chondrocytes (p< 0.05). The anti-inflammatory cytokines IL-4 and IL-10 were consistently expressedin vivoandin vitro, showing no association with the presence of cartilage or chondrocytes. In contrast, FasL levels increased steadilyin vitro, reaching higher levels without chondrocytes (p< 0.05). Likewise, the viability of synovial fibroblasts (SFB) during infection was higher in the presence of chondrocytes. The cartilage-metabolism markers aggrecan and bFGF were at higher concentrations in intact joints, but also synthesized by SFB.Conclusions. Our data suggest an anti-inflammatory effect of cartilage associated with the SFBs’ increased resistance to infections, which displayed the ability to effectively synthesize cartilage metabolites.The trial is registered with DRKS00003536, MISSinG.

Funder

Research Commission of the Albert-Ludwigs University Medical Center Freiburg

Publisher

Hindawi Limited

Subject

Cell Biology,Immunology

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