Abstract
Surgical mesh materials are the most frequently used medical devices designed to reinforce fascial structures and thereby treat hernia disease [1, 2]. The implantation of non-absorbable polymeric biomaterials excites perpetual activation of cytokine cascades and proteases that are a chronic inflammatory reaction and postoperative complications like seroma, mesh shrinkage and migration, adhesion, infection and pain may ensue [2]. To circumvent such an on-going foreign body reaction, gold standard meshes have been designed to improve biocompatibility. Such meshes meet the demand for a reduced amount of implanted material, have optimized pore size and adjustment to physiological requirements [3]. Besides this approach to optimize mesh integration and concurrently replace fascial structures in hernia patients, an open question is whether there are alternate means of beneficially influencing the foreign-body reaction. To address this, an in-depth understanding of the molecular mechanisms that guide the extent of foreign-body reactions is required.
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Lynen-Jansen, P., Klinge, U., Lovett, D.H., Mertens, P.R. (2007). Biomaterials: Disturbing Factors in Cell Cross-Talk and Gene Regulation. In: Schumpelick, V., Fitzgibbons, R.J. (eds) Recurrent Hernia. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-68988-1_7
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DOI: https://doi.org/10.1007/978-3-540-68988-1_7
Publisher Name: Springer, Berlin, Heidelberg
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