Leong Mimi, Basu C Bob, Hicks M John
Dr Leong is a plastic surgeon at Michael E. DeBakey VA Medical Center, and Clinical Assistant Professor of Surgery and Pediatrics, Division of Plastic Surgery, Baylor College of Medicine, Houston, Texas. Dr Basu is a plastic surgeon in private practice in Houston, Texas. Dr Hicks is a professor in the Department of Pathology, Baylor College of Medicine, Houston, Texas.
Aesthet Surg J. 2015 Jan;35(1):40-7. doi: 10.1093/asj/sju014.
Human acellular dermal matrix (HADM; previously termed "acellular cadaveric dermis") may limit inflammatory changes believed to play a role in capsular contracture, a common complication of implant-based breast reconstruction.
Differences between HADM and native breast capsule specimens were evaluated by immunohistochemical analysis of key inflammatory markers involved in capsule formation.
Twenty consecutive patients underwent immediate, 2-stage, implant-based breast reconstruction with dual-plane HADM. During tissue expander-implant exchange, full-thickness biopsies of biointegrated HADM and native breast capsule (internal control) from the tissue-expander envelope were obtained. Immunohistochemical analysis was performed for endothelial cells (CD31), B cells (CD20), T cells (CD3), macrophages (CD68), collagen I and III, and myofibroblasts (α-smooth muscle actin). Observed levels of marker labeling were semiquantitatively scored from 0 (none) to 3 (severe) by a blinded histopathologist and were statistically analyzed with the Wilcoxon rank sum test.
A bilateral sample was obtained from 1 patient; all other samples were unilateral. Compared with capsule samples from native breast tissue, HADM samples had significantly lower levels of all inflammatory markers (P < .001).
These lower levels of inflammatory markers support previous evidence that HADM may inhibit inflammatory and profibrotic signaling characteristics of breast capsule development and decrease the risk of capsular contracture. Further investigation is needed to determine the mechanism by which HADM inhibits these inflammatory cells, whether HADM reduces the incidence of breast capsular contracture, and if so, the longevity of this effect.
人脱细胞真皮基质（HADM；以前称为“脱细胞尸体真皮”）可能会限制被认为在包膜挛缩中起作用的炎症变化，包膜挛缩是基于植入物的乳房重建的常见并发症。
通过对参与包膜形成的关键炎症标志物进行免疫组化分析，评估HADM与天然乳房包膜标本之间的差异。
连续20例患者接受了基于双平面HADM的即刻两阶段植入物乳房重建。在组织扩张器-植入物置换期间，从组织扩张器包膜获取生物整合的HADM和天然乳房包膜（内部对照）的全层活检标本。对内皮细胞（CD31）、B细胞（CD20）、T细胞（CD3）、巨噬细胞（CD68）、I型和III型胶原蛋白以及肌成纤维细胞（α-平滑肌肌动蛋白）进行免疫组化分析。由一位不知情的组织病理学家对观察到的标志物标记水平进行半定量评分，从0（无）到3（严重），并使用Wilcoxon秩和检验进行统计分析。
从1例患者获得双侧样本；所有其他样本均为单侧。与天然乳房组织的包膜样本相比，HADM样本中所有炎症标志物的水平均显著较低（P <.001）。
这些较低水平的炎症标志物支持了先前证据，即HADM可能抑制乳房包膜发育的炎症和促纤维化信号特征，并降低包膜挛缩的风险。需要进一步研究以确定HADM抑制这些炎症细胞的机制、HADM是否降低乳房包膜挛缩的发生率，以及如果是这样，这种效果的持续时间。
