Implant-associated infections The presence of an implant within the body, par- ticularly in open fractures is known to increase susceptibility to infection [10, 11], activating the host defenses and stimulating the host’s immune system [12-14]. The fate of a biomaterial surface may be conceptualized as a “race for the surface”, involving extracellular matrix (ECM) proteins, host cells (fibroblasts, osteoblasts, endothelial cells), and bacteria [15]. Once fracture fixation devices have been implanted, they acquire a conditioning film of ECM proteins [16]. The ECM is a biologically active layer composed of a complex mixture of macromolecules, such as fibronectin, fibrinogen, albumin, vitronectin, and collagen. Host cell adhe- sion, migration, proliferation, and differentiation are all influenced by the composition and structural organization of the surrounding ECM [17]. Interac- tion between host cells and the ECM is known to be mediated by specific receptors such as integrins, which are composed of α and β units and link many ECM proteins to the eukaryotic cellular cytoskeleton [17]. However, the ECM not only serves as a substrate for host cells, but also for colonizing bacteria. If host cells such as fibroblasts arrive at the biomaterial surface and secure bonds are established, bacteria are confronted with a living, integrated cellular surface. Such integrated viable cell layers that have functional host defense mechanisms can resist bac- terial attachment and colonization [15]. However, over the years, it has been found that bacteria, eg, Staphylococcus aureus, express many surface ad- hesins that promote attachment to plasma and ECM proteins of host cells or those adsorbed onto metal or polymer surfaces [18, 19]. The rate of infections associated with closed fractures is much lower than for open ones, 1.5% and 3-40%, respectively [3, 20]. Up to 60% of open fractures are contaminated with bacteria at the time of injury [6, 21, 22]. Management of an open fracture requires adequate wound debridement to Staphylococci and implant surfaces: a review Llinos G Harris, R Geoff Richards AO Research Institute, AO Foundation, Davos, Switzerland KEYWORDS: Staphylococci; implants; infection; adhesion; biofilm; surfaces. Summary 1 Surfaces of internal fracture fixation implants are generally designed to encourage soft- and/or hard-tissue adherence, eventually leading to tissue or osseo integration. Unfortunately, this feature may also encourage bacterial adhe- sion. About half of the two million cases of nosocomial infections per year in the US are associated with indwelling devices [1]. In the UK, implant-associated infections are estimated to cost £ 7-11 million per year [2], and with the rise in antibiotic-resistant bacteria, are an important issue [3, 4]. Soft-tissue infections and osteomyelitis are serious complications associated with implants, particular- ly open fractures [5], external fixation devices [6, 7], and intramedullary nailing [8, 9]. Consequences of implant-associated infections include prolonged hospi- talization with systemic antibiotic therapy, several revision procedures, possible amputation, and even death. This review discusses the issue of implant-associ- ated infections and some of the methods used to prevent bacterial adhesion to osteosynthesis implants. 1 Abstracts in German, French, Italian, Spanish, Japanese, and Russian are printed at the end of this supplement. Injury, Int. J. Care Injured (2006) 37, S3—S14 www.elsevier.com/locate/injury 0020–1383/$ — see front matter # 2006 Published by Elsevier Ltd. doi:10.1016/j.injury.2006.04.003