Joint Remodeling Molecules and Complement Components in Septic Arthritis

Abstract

Septic arthritis (SA) is also known as infectious arthritis and unlike other inflammatory joint diseases, it is caused by viruses, bacteria, and fungi. These microorganisms spread to the joints from an existing focus in the body through the bloodstream or enter through a wound in case of injury or surgical intervention of the joint. Pathogenesis of SA is due to specific interactions of the microorganism and the host, especially its immune system. We analyzed the available data in literature about some infections in which molecular factors are produced that are also known to be involved in remodeling processes of arthritis.  We evaluated the role of complement system components and certain joint remodeling markers, such as transforming growth factor beta (TGF-\(\beta\)), bone morphogenic protein (BMP), osteoprotegerin/receptor activator of nuclear factor _k B/ receptor activator of nuclear factor _k B ligand (OPG/RANK/RANKL) and sclerostin in pathogenesis of septic arthritis. We discuss possible treatment strategies based on targeting of these molecules for reduction of inflammatory destructive response in the joints during infections.