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The host cells at the material-tissue interface represent the complex biological environment where synthetic biomaterials or medical devices interact with living tissue. This interface is characterized by the foreign body response (FBR), a series of events including protein adsorption, leukocyte infiltration, and the formation of foreign body giant cells (Anderson et al., 2008). The primary cell types involved include macrophages, which orchestrate the inflammatory response and can polarize into pro-inflammatory (M1) or pro-healing (M2) phenotypes, and fibroblasts, which contribute to the eventual encapsulation of the material in a fibrous capsule (Sridharan et al., 2015). While not a single molecular target, this interface is a critical focus for therapeutic intervention to improve the biocompatibility and longevity of implants (Franz et al., 2011). Strategies to modulate this environment often involve drug-eluting coatings or surface modifications designed to reduce inflammation and promote integration with the surrounding tissue.
Modulation of the foreign body response through localized delivery of anti-inflammatory or anti-proliferative agents targeting specific cellular pathways at the interface.
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