A Dual-Antioxidative Coating on Transmucosal Component of Implant to Repair Connective Tissue Barrier for Treatment of Peri-Implantitis.

Since the microgap between implant and surrounding connective tissue creates the pass of pathogen invasion, sustained pathological stimuli could accelerate macrophage mediated inflammation, therefore affect peri-implant tissue regeneration and aggravate peri-implantitis. As the transmucosal component of implant, the abutment therefore needs to be biofunctionalized to repair gingival barrier. Here, we provided a mussel-bioinspired implant abutment coating containing tannic acid (TA), cerium and minocycline (TA-Ce-Mino). TA provided pyrogallol and catechol groups to promote cell adherence. Besides, Ce3+ /Ce4+  conversion exhibited enzyme-mimetic activity to remove ROS while generate O2 , therefore promote anti-inflammatory M2 macrophage polarization to help create regenerative environment. Minocycline was involved on TA surface to create local drug storage for responsive antibiosis. Moreover, the underlying therapeutic mechanism was revealed whereby the coating exhibited exogenous antioxidation from inherent properties of Ce and TA and endogens antioxidation through mitochondrial homeostasis maintenance and antioxidases promotion. Besides, it stimulated integrin to activate PI3K/Akt and RhoA/ROCK pathways to enhance VEGF mediated angiogenesis and tissue regeneration. Combining the antibiosis and multi-dimensional orchestration, TA-Ce-Mino repaired soft tissue barrier and effector cell differentiation, thereby isolated immune microenvironment from pathogen invasion. Consequently, our study provided critical insight into the design and biological mechanism of abutment surface modification to prevent peri-implantitis. This article is protected by copyright. All rights reserved.