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논문 기본 정보

자료유형
학술저널
저자정보
Patrick Hwang (Endomimetics LLC) Chung Min Shin (Department of Plastic and Reconstructive Surgery Chungnam National University College of Medicine) Jennifer A. Sherwood (Endomimetics LLC) 김동호 (충남대학교) Vineeth M. Vijayan (Department of Biomedical Engineering Alabama State University) Krishna C. Josyula (Department of Biomedical Engineering University of Alabama at Birmingham) Reid C. Millican (Endomimetics LLC) Donald Ho (Department of Pediatric Dentistry University of Alabama at Birmingham) Brigitta C. Brott (Endomimetics LLC) Vinoy Thomas (Department of Material Science and Engineering University of Alabama at Birmingham) Chul Hee Choi (Chungnam National University) Sang‑Ha Oh (Department of Plastic and Reconstructive Surgery Chungnam National University College of Medicine) 김동운 (충남대학교) Ho‑Wook Jun (Endomimetics LLC)
저널정보
한국생체재료학회 생체재료학회지 생체재료학회지 제27권
발행연도
2023.3
수록면
967 - 989 (23page)
DOI
https://doi.org/10.1186/s40824-023-00378-7

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Background Capsular contracture is a critical complication of silicone implantation caused by fibrotic tissue formation from excessive foreign body responses. Various approaches have been applied, but targeting the mechanisms of capsule formation has not been completely solved. Myofibroblast differentiation through the transforming growth factor beta (TGF-β)/p-SMADs signaling is one of the key factors for capsular contracture development. In addition, biofilm formation on implants may result chronic inflammation promoting capsular fibrosis formation with subsequent contraction. To date, there have been no approaches targeting multi-facted mechanisms of capsular contracture development. Methods In this study, we developed a multi-targeting nitric oxide (NO) releasing bionanomatrix coating to reduce capsular contracture formation by targeting myofibroblast differentiation, inflammatory responses, and infections. First, we characterized the bionanomatrix coating on silicon implants by conducting rheology test, scanning electron microcsopy analysis, nanoindentation analysis, and NO release kinetics evaluation. In addition, differentiated monocyte adhesion and S. epidermidis biofilm formation on bionanomatrix coated silicone implants were evaluated in vitro. Bionanomatrix coated silicone and uncoated silicone groups were subcutaneously implanted into a mouse model for evaluation of capsular contracture development for a month. Fibrosis formation, capsule thickness, TGF-β/SMAD 2/3 signaling cascade, NO production, and inflammatory cytokine production were evaluated using histology, immunofluorescent imaging analysis, and gene and protein expression assays. Results The bionanomatrix coating maintained a uniform and smooth surface on the silicone even after mechanical stress conditions. In addition, the bionanomatrix coating showed sustained NO release for at least one month and reduction of differentiated monocyte adhesion and S. epidermidis biofilm formation on the silicone implants in vitro. In in vivo implantation studies, the bionanomatrix coated groups demonstrated significant reduction of capsule thickness surrounding the implants. This result was due to a decrease of myofibroblast differentiation and fibrous extracellular matrix production through inhibition of the TGF-β/p-SMADs signaling. Also, the bionanomatrix coated groups reduced gene expression of M1 macrophage markers and promoted M2 macrophage markers which indicated the bionanomatrix could reduce inflammation but promote healing process. Conclusions In conclusion, the bionanomatrix coating significantly reduced capsular contracture formation and promoted healing process on silicone implants by reducing myfibroblast differentiation, fibrotic tissue formation, and inflammation.
#Capsular contracture #Fibrotic tissue formation #Myofibroblast differentiation #Inflammation #Nitric oxide #Bionanomatrix

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