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The extracellular matrix and serum proteins at the material–tissue interface represent the dynamic layer of biological molecules that coat a synthetic surface upon implantation. This interface is primarily formed through the spontaneous adsorption of proteins from blood or interstitial fluid, a process governed by the Vroman effect where high-abundance proteins are gradually replaced by those with higher surface affinity (Wilson et al., 2005). The specific composition, orientation, and conformation of these adsorbed proteins, such as fibrinogen, fibronectin, and vitronectin, serve as the primary signaling cues for host cells (Anderson et al., 2008). These cues determine the progression of the foreign body response, ranging from successful tissue integration to chronic inflammation and fibrous encapsulation. While not a single therapeutic target in the classical sense, this interface is a focal point for biomaterial engineering, where surface modifications like PEGylation or zwitterionic coatings are employed to control protein interactions and improve device biocompatibility (Castner & Ratner, 2002).
Surface passivation and modulation of host immune recognition to prevent fibrous encapsulation or thrombosis.
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