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

Author:

Li Dize1,Tan Xi1,Zheng Liwen1,Tang Han1,Hu Shanshan1,Zhai Qiming1,Jing Xuan2,Liang Panpan1,Zhang Yuxin1,He Qingqing1,Jian Guangyu1,Fan Dongqi1,Ji Ping1,Chen Tao1ORCID,Zhang Hongmei13ORCID

Affiliation:

1. Stomatological Hospital of Chongqing Medical University Chongqing Key Laboratory of Oral Diseases and Biomedical Sciences Chongqing Municipal Key Laboratory of Oral Biomedical Engineering of Higher Education Chongqing Medical University Chongqing 401147 P. R. China

2. Shanxi Medical University School and Hospital of Stomatology Taiyuan 030001 P. R. China

3. Molecular Oncology Laboratory Department of Orthopedic Surgery and Rehabilitation Medicine The University of Chicago Medical Center Chicago IL 60637 USA

Abstract

AbstractSince the microgap between implant and surrounding connective tissue creates the pass for pathogen invasion, sustained pathological stimuli can accelerate macrophage‐mediated inflammation, therefore affecting peri‐implant tissue regeneration and aggravate peri‐implantitis. As the transmucosal component of implant, the abutment therefore needs to be biofunctionalized to repair the gingival barrier. Here, a mussel‐bioinspired implant abutment coating containing tannic acid (TA), cerium and minocycline (TA‐Ce‐Mino) is reported. TA provides pyrogallol and catechol groups to promote cell adherence. Besides, Ce3+/Ce4+ conversion exhibits enzyme‐mimetic activity to remove reactive oxygen species while generating O2, therefore promoting anti‐inflammatory M2 macrophage polarization to help create a regenerative environment. Minocycline is involved on the TA surface to create local drug storage for responsive antibiosis. Moreover, the underlying therapeutic mechanism is revealed whereby the coating exhibits exogenous antioxidation from the inherent properties of Ce and TA and endogenous antioxidation through mitochondrial homeostasis maintenance and antioxidases promotion. In addition, it stimulates integrin to activate PI3K/Akt and RhoA/ROCK pathways to enhance VEGF‐mediated angiogenesis and tissue regeneration. Combining the antibiosis and multidimensional orchestration, TA‐Ce‐Mino repairs soft tissue barriers and effector cell differentiation, thereby isolating the immune microenvironment from pathogen invasion. Consequently, this study provides critical insight into the design and biological mechanism of abutment surface modification to prevent peri‐implantitis.

Funder

Chongqing Medical University

Postdoctoral Research Foundation of China

National Natural Science Foundation of China

Publisher

Wiley

Subject

Pharmaceutical Science,Biomedical Engineering,Biomaterials

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