Foreign body response at tissue–polyacrylamide hydrogel interface (FBR)

The foreign body response (FBR) at the tissue–polyacrylamide hydrogel interface is a complex biological process triggered by the implantation of polyacrylamide-based materials, characterized by an orchestrated immune reaction aimed at isolating the foreign object. Upon implantation, host proteins immediately adsorb to the hydrogel surface, facilitating the recruitment of neutrophils and macrophages which attempt to phagocytose the material (Anderson et al., 2008, PMID: 18162407). Persistent activation of these macrophages leads to their fusion into multinucleated foreign body giant cells and the secretion of pro-fibrotic signals such as Transforming Growth Factor-beta (TGF-β). This signaling cascade culminates in the activation of fibroblasts and the deposition of a dense collagenous capsule around the hydrogel, which can impair the function of sensors or the release kinetics of drug-delivery systems (Major et al., 2015, PMID: 25919251). While polyacrylamide is widely used in research due to its tunable elasticity, its clinical application is often limited by this inflammatory sequela and the potential risks associated with residual monomer toxicity (Onuki et al., 2008, PMID: 19885299).

Other names

Foreign body reaction to polyacrylamidePAM-tissue interface responseBiomaterial-mediated inflammatory responseHydrogel-induced fibrosis

Pharmacological mitigation involves the suppression of the inflammatory cascade through glucocorticoid receptor activation and the inhibition of pro-fibrotic signaling pathways, such as TGF-beta, to reduce fibrous capsule thickness and improve biomaterial integration.