Abstract
Regardless of function, location, or biomaterial used, infection is one of the most serious complications arising from the use of implanted medical devices. Every surgical procedure has an inherent risk for bacterial contamination with surgical site contaminants originating from the patient's own skin, the surgical theater, or even the outside environment. The reason some patients become infected and others do not is unfortunately less than clear. In the majority of cases, host defenses and prophylactic antibiotic administration effectively clear any contaminating bacteria. Bacterial adhesion to a biomaterial is often considered to be the event that initiates biomaterial-associated infection. Given that the number of biomaterial-associated infections is expected to rise in response to an increase in implant demand, reducing bacterial adhesion is of critical clinical importance. Small changes in topography or surface chemistry can result in large differences in bacterial adhesion in vitro and in vivo. Changes in the topography of PEEK due to manufacturing methods alter bacterial adhesion by common clinical pathogens. Additionally, altering the surface chemistry of PEEK for increased osseointegration by oxygen plasma treatment leads to no change in bacterial adhesion in the absence of a protein conditioning film. However, the presence of a protein conditioning film led to large differences in bacterial adhesion. The role of the immune response, tissue integration, individual patient variation, and the broad variation of bacteria potentially present all play important roles in the outcome of a bacterium encountering a biomaterial in the human body.
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