Implant Texture and Capsular Contracture: A Review of Cellular and Molecular Pathways

植入 包膜挛缩 肌成纤维细胞 成纤维细胞 医学 炎症 细胞外基质 肿瘤坏死因子α 化学 病理 生物信息学 细胞生物学 生物 外科 纤维化 内科学 生物化学 癌症 体外 乳腺癌 乳房再造术
作者
Hannah J. Wells,Jenny C.C. Yang,Leah Edelstein‐Keshet,Kathryn V. Isaac
出处
期刊:Plastic and reconstructive surgery. Global open [Ovid Technologies (Wolters Kluwer)]
卷期号:12 (5): e5802-e5802
标识
DOI:10.1097/gox.0000000000005802
摘要

Background: Capsular contracture (CC) is a leading cause of morbidity in implant-based breast surgery. Implant surface texture has been implicated in CC development, yet its etiopathogenesis remains unclear. We conducted a systematic review to determine the influence of implant surface texture on cellular and molecular mechanisms involved in the etiopathogenesis of CC. Methods: A systematic review of the MEDLINE, Embase, Web of Science, and Scopus databases was completed to examine the influence of implant texture on cellular and molecular pathways leading to CC. Excluded articles were reviews and those examining solely the clinical presentation of CC. Results: Development of CC includes prolonged inflammation, increased myofibroblast density, parallel arrangement of collagen fibers, and biofilm formation. When compared with textured implants, smooth implants are associated with reduction in parallel collagen, capsule thickness, and sheer frictional force. Microtextured implants trigger a reduced macrophage response and decreased fibroblast activation as compared with smooth and macrotextured surfaces. Bacterial counts on microtextured and smooth surfaces are significantly lower than that of macrotextured surfaces. Both micro- and macrotextured implants have increased matrix metalloproteinases and activation of tumor necrosis factor α pathway, with increased activation of the transforming growth factor β1 pathway relative to smooth implants. Conclusions: Implant surface texture alters the cellular and molecular mechanisms in the chronic inflammatory process leading to CC. Given the complex biological system of cellular and molecular events in CC, a mathematical model integrating these influences may be optimal to deduce the etiopathogenesis.
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