Figure 2.

Modulating implant surface properties is a common strategy to enhance tissue integration while simultaneously reducing the incidence and severity of implant FBR and fibrosis. Protein coverage and cell interactions with the surface both determine the ability of cells to attach and spread on implants. Various physical and chemical modifications to the Implants surface are used to inhibit FBR. (A) Chemical modifications of surface properties include coating with local and slow releasing anti-fibrotic drugs to prevent implant fibrosis. In addition, subcutaneously implanted tissue expanders coated with decellularized ECM into non-human primates display minimal fibrotic. Inhibiting αv-integrin binding, e.g., with the RGD-peptidomimetic inhibitor CWHM-12 attenuate implant encapsulation by preventing mechanical activation of latent TGF-β1 and myofibroblasts. (B) In addition to or combined with altering implant surface chemistry, other treatments include modulation of physical parameters such as surface hydrophilicity or wettability, porosity, stiffness (elastic modulus), anisotropic ‘roughness’, and regular topographies. Perceived stiffness and ‘true’ modulus of the implant surface can be used to control cell responses. Restriction of focal adhesion sizes by micropatterning stiff surfaces with adhesion sized fibronectin islets limits myofibroblast spreading, intracellular stress and α-SMA stress fiber incorporation. Modulating implant geometry (size, thickness, shape, and pore size) or coating with low fouling material such as zwitterions reduces protein adsorption to implant surfaces and reduces implant fibrosis. Scheme was prepared using Biorender.