New concepts and new weapons in implant infections

Molecular studies have cast light on new facts about the virulence factors of bacteria responsible for implant infections. Recently, the biofilm matrix has been shown to include a variety of important structural components, including DNA, in addition to polysaccharides and proteins. This finding has stimulated interest in substances able to disrupt biofilms by attacking both the poly-N-acetylglucosamine surface polysaccharide (PNAG) and the extracellular DNA (eDNA), namely, dispersin B, a PNAG-degrading enzyme, and DNase I. The therapeutic potential of these enzymes are reviewed in this issue of IJAO, as well as the ability of the excretions/secretions of the medicinal maggot Lucilia sericata to disrupt Staphylococcus epidermidis biofilms. The activity of bacterial proteases causes the release of eDNA, critical for the early development of biofilms. This complex process, including suicidal and fratricidal mechanisms, is also presented in the current issue of IJAO. The different sensitivities of S. aureus and S. epidermidis to enzymatic anti-biofilm agents and to the host's first line of defense, as well as the importance of knowing the cascade of regulatory genes in bacteria so as to interfere with biofilm production using gene therapy or quorum sensing inhibitors are also discussed in this issue. Other innovative approaches consist in disrupting biofilms by exposing them to photodynamic substances and simultaneously to visible light, and in coating biomaterial surfaces with organic molecules to prevent protein adsorption and biofilm formation. (Int J Artif Organs 2009; 32: 533-6)