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Cell Biology And Molecular Mechanisms In Artificial Device Infections

A. Gristina, G. Giridhar, B. L. Gabriel, P. T. Naylor, Q. Myrvik
Published 1993 · Chemistry, Medicine

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Biomaterials are being used with increasing frequency for tissue substitution. Complex devices such as total joint replacement and the total artificial heart represent combinations of polymers and metal alloys for system and organ replacement. The major barrier to the extended use of these devices is bacterial adhesion to biomaterials, which causes biomaterial-centered infection, and the lack of successful tissue integration or compatibility with biomaterial surfaces. Adhesion-mediated infections are extremely resistant to antibiotics and host defenses and frequently persist until the biomaterial or foreign body is removed. The pathogenesis of adhesive infections is related, in part, to preferential colonization of “inert” substrata whose surfaces are not integrated with healthy tissues composed of living cells and intact extracellular polymers. Tissue integration is an interesting parallel to microbial adhesion and is a desired phenomenon for the biocompatibility of certain implants and biomaterials. Tissue integration requires a form of eukaryocytic adhesion or compatibility with possible chemical integration to an implant surface. Many of the fundamental principles of interfacial science apply to both microbial adhesion and to tissue integration and are general to and independent of the substratum materials involved. Interactions of biomaterials with bacteria and tissue cells are directed not only by specific receptors and outer membrane molecules on the cell surface, but also by the atomic geometry and electronic state of the biomaterial surface. An understanding of these mechanisms is important to all fields of medicine and is derived from and relevant to studies in microbiology, biochemistry, and physics. Modifications of biomaterial surfaces at an atomic level will allow the programming of cell-to-substratum events, thereby diminishing infection by enhancing tissue compatibility or integration, or by directly inhibiting bacterial adhesion.
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