Bacterial infections can destroy cartilage integrity, resulting in
osteoarthritis. Goal was to develop an in vitro model with in vivo validation of acute joint
inflammation.
Inflammation in cocultivated human synovial fibroblasts (SFB), chondrocytes (CHDR), and mononuclear cells (MNC) was successively relieved for 10 days. Articular effusions from patients with (n = 7) and without (n = 5) postoperative joint
infection in healthy patients (ASA 1-2) were used as model validation.
Inflammation in vitro resulted in an enormous increase in
IL-1 and a successive reduction in SFB numbers. CHDR however, maintained metabolic activity and
proteoglycan synthesis. While concentrations of bFGF in vivo and in vitro rose consistently, the
mRNA increase was only moderate. Concurring with our in vivo data, cartilage-specific
IGF-1 steadily increased, while
IGF-1 mRNA in the CHDR and SFB did not correlate with
protein levels. Similarly,
aggrecan (ACAN)
protein concentrations increased in vivo and failed to correlate in vitro with gene expression in either the CHDR or the SFB, indicating extracellular matrix breakdown. Anabolic cartilage-specific
BMP-7 with highly significant intra-articular levels was significantly elevated in vitro on day 10 following maximum
inflammation. Our in vitro model enables us to validate early
inflammation of in vivo cell- and
cytokine-specific regulatory patterns. This trial is registered with MISSinG, DRKS 00003536.