Department of Plastic and Reconstructive Surgery, Seoul National University College of Medicine, Seoul, Korea.
Department of Plastic and Reconstructive Surgery, Hanyang University Medical Center, Hanyang University College of Medicine, Seoul, Korea.
Ann Surg Oncol. 2018 Aug;25(8):2279-2287. doi: 10.1245/s10434-018-6549-8. Epub 2018 May 31.
Capsular contracture is one of the most common complications of expander-implant breast reconstruction. Recently, clinical reports have shown that use of an acellular dermal matrix (ADM) to cover breast implants decreases incidence of capsular contracture, but the underlying mechanism is unclear. Here, we examine how ADM reduces capsular formation in expander-implant breast reconstruction and identify cellular and molecular mechanisms of ADM-mediated reduction of capsular contracture in nonirradiated and irradiated patients.
Thirty patients who underwent immediate two-stage implant-based breast reconstruction were included; 15 received radiotherapy. While the tissue expander was changed to permanent silicone implant, biopsies of the subpectoral capsule and ADM capsule were performed. Capsule thickness, immunohistochemistry of α-smooth muscle actin (αSMA), vimentin, CD31, F4/80 expression, αSMA and CD31 coexpression, and relative gene expression levels of transforming growth factor (TGF)-β1 and platelet-derived growth factor (PDGF)-B were investigated.
Irradiated submuscular capsules were thicker than nonirradiated submuscular capsules, but the thickness of ADM capsules did not significantly differ between nonirradiated and irradiated groups. Levels of myofibroblasts, fibroblasts, vascularity, EndoMT, and macrophages were significantly lower in ADM capsules than in submuscular capsules. With the exception of EndoMT, all others were increased in irradiated submuscular capsules compared with nonirradiated submuscular capsule, while none significantly differed between nonirradiated and irradiated ADM capsules.
Use of ADM reduced myofibroblasts, vascularity, fibroblasts, and EndoMT in capsule tissues. Moreover, ADM use decreased macrophages, a key regulator of tissue fibrosis, as well as TGF-β1 and PDGF-B expression. We hope that these results provide basic concepts important for prevention of capsular contracture.
包膜挛缩是扩张器-植入物乳房重建最常见的并发症之一。最近,临床报告显示,使用脱细胞真皮基质 (ADM) 覆盖乳房植入物可降低包膜挛缩的发生率,但潜在机制尚不清楚。在这里,我们研究了 ADM 如何减少扩张器-植入物乳房重建中的包膜形成,并确定 ADM 介导的非照射和照射患者包膜挛缩减少的细胞和分子机制。
纳入 30 例接受即刻两阶段基于植入物的乳房重建的患者;其中 15 例接受放射治疗。当组织扩张器更换为永久性硅胶植入物时,进行胸肌下包膜和 ADM 包膜活检。研究了包膜厚度、α-平滑肌肌动蛋白 (αSMA)、波形蛋白、CD31、F4/80 表达、αSMA 和 CD31 共表达以及转化生长因子 (TGF)-β1 和血小板衍生生长因子 (PDGF)-B 的相对基因表达水平。
照射后的胸肌下包膜比未照射的胸肌下包膜厚,但未照射和照射组的 ADM 包膜厚度无显著差异。ADM 包膜中的肌成纤维细胞、成纤维细胞、血管生成、EndoMT 和巨噬细胞水平明显低于胸肌下包膜。除 EndoMT 外,所有其他指标在照射后的胸肌下包膜中均高于未照射的胸肌下包膜,而未照射和照射的 ADM 包膜之间均无显著差异。
使用 ADM 减少了包膜组织中的肌成纤维细胞、血管生成、成纤维细胞和 EndoMT。此外,ADM 的使用减少了巨噬细胞,这是组织纤维化的关键调节因子,以及 TGF-β1 和 PDGF-B 的表达。我们希望这些结果为预防包膜挛缩提供重要的基础概念。