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LÃgia R. Rodrigues
Infections resulting from microbial adhesion to biomaterial surfaces have been observed on nearly all medical devices with severe economic and medical consequences [1]. Biofilm infections, mainly due to their antimicrobial resistance, pose a number of clinical challenges, including disease, chronic inflammation, and rapidly acquired antibiotic resistance. Independently of the superiority of the implant, virtually all medical devices are prone to microbial colonization and infection. Examples of such devices include prosthetic heart valves, orthopaedic implants, intravascular catheters, artificial hearts, left ventricular assist devices, cardiac pacemakers, vascular prostheses, cerebrospinal fluid shunts, urinary catheters, voice prostheses, ocular prostheses and contact lenses, and intrauterine contraceptive devices. A large amount of research to eliminate or reduce infections by developing anti-infective and anti-adhesive devices has been encouraged as a result of the significant resistance of biofilms to conventional antibiotic therapies. These improved devices may be produced by either mechanical design alternatives; physicochemical modification of the biomaterial surface (e.g. biosurfactants, plasma, atom transfer radical polymerization, brushes); anti-infective agents bound to the surface of the material (e.g. biosurfactants, silver, quaternary ammonium compounds, synthetic antibiotics); or release of toxic agents into the adjacent surroundings (e.g. chlorhexidine, antibiotics) [2,3]. The success of the mechanical design alternatives has been residual and with limited applicability [2]. Furthermore, the effectiveness of coatings designed to reduce adhesion by modification of the surface properties has also been reduced and greatly dependent on the bacterial species. Surfaces modified with poly(ethylene glycol) [4], poly(ethylene oxide) brushes [5], and hydrophilic polyurethanes [6], among many others, have been reported. Additionally, surface-bounded anti-infective agents are only toxic to the initial wave of incoming bacteria and provide little residual effects once layers of dead cells accumulate, which are also inflammatory.