Skip to main content
. Author manuscript; available in PMC: 2015 Mar 26.
Published in final edited form as: Nat Rev Rheumatol. 2014 Sep 30;11(1):35–44. doi: 10.1038/nrrheum.2014.162

Figure 1. Relationships between inflammatory mediator networks in OA.

Figure 1

This schematic illustrates how several of the different classes of inflammatory mediators, including PRRs and their DAMP ligands, conventional inflammatory cytokines, and activated complement proteins C5a and C5b-9 network to augment meniscal fibrocartilage and articular cartilage damage in early and progressive OA. These mediators promote macroscopic inflammation, including synovitis, and can drive cartilage matrix catabolism, but some also promote cartilage remodelling and repair. The number and diversity of inflammatory mediators in OA joints, the paradoxical roles of some of these moieties in tissue damage and repair, and the physiological roles of some mediators in host defense, means targeting individual mediators for OA therapy is difficult. Abbreviations: COMP, cartilage oligomeric matrix protein; DAMP, danger associated molecular pattern; HMGB1, high mobility group box protein 1; LMW-HA, low molecular weight hyaluronan; MAC, membrane attack complex; OA, osteoarthritis; PRR, pattern recognition receptor; RAGE, receptor for advanced glycation endproducts; TGF-β, transforming growth factor β; TLR, Toll-like receptor.