Hospital de Sao Joao, Servico de Cirurgia Plastica, Porto, Portugal.
Aesthet Surg J. 2011 May;31(4):420-8. doi: 10.1177/1090820X11404400.
The etiology and ideal clinical treatment of capsular contracture (CC) remain unresolved. Bacteria, especially coagulase-negative staphylococci, have been previously shown to accelerate the onset of CC. The role of fibrin in capsule formation has also been controversial.
The authors investigate whether fibrin and coagulase-negative staphylococci (CoNS) modulate the histological, microbiological, and clinical outcomes of breast implant capsule formation in a rabbit model and evaluate contamination during the surgical procedure.
Thirty-one New Zealand white female rabbits were each implanted with one tissue expander and two breast implants. The rabbits received (1) untreated implants and expanders (control; n = 10), (2) two implants sprayed with 2 mL of fibrin and one expander sprayed with 0.5 mL of fibrin (fibrin; n = 11), or (3) two implants inoculated with 100 µL of a CoNS suspension (10(8)CFU/mL-0.5 density on the McFarland scale) and one expander inoculated with a CoNS suspension of 2.5 × 10(7) CFU/mL (CoNS; n = 10). Pressure/volume curves and histological and microbiological evaluations were performed. Operating room air samples and contact skin samples were collected for microbiological evaluation. The rabbits were euthanized at four weeks.
In the fibrin group, significantly decreased intracapsular pressures, thinner capsules, loose/dense (<25%) connective tissue, and negative/mild angiogenesis were observed. In the CoNS group, increased capsular thicknesses and polymorph-type inflammatory cells were the most common findings. Similar bacteria in capsules, implants, and skin were cultured from all the study groups. One Baker grade IV contracture was observed in an implant infected with Micrococcus spp.
Fibrin was associated with reduced capsule formation in this preclinical animal model, which makes fibrin an attractive potential therapeutic agent in women undergoing breast augmentation procedures. Clinical strategies for preventing bacterial contamination during surgery are crucial, as low pathogenic agents may promote CC.
包膜挛缩（Capsular Contracture，CC）的病因和理想的临床治疗方法仍未得到解决。先前的研究表明，细菌，尤其是凝固酶阴性葡萄球菌（Coagulase-negative Staphylococci，CoNS），会加速 CC 的发生。纤维蛋白在囊袋形成中的作用也存在争议。
作者通过兔模型研究纤维蛋白和凝固酶阴性葡萄球菌（Coagulase-negative Staphylococci，CoNS）是否会调节乳房植入物囊袋形成的组织学、微生物学和临床结果，并评估手术过程中的污染情况。
31 只新西兰白兔每只均植入一个组织扩张器和两个乳房植入物。将兔子分为三组：（1）未处理的植入物和扩张器（对照组；n=10）；（2）两个植入物喷洒 2mL 纤维蛋白，一个扩张器喷洒 0.5mL 纤维蛋白（纤维蛋白组；n=11）；（3）两个植入物接种 100µL CoNS 悬浮液（10⁸CFU/mL-0.5 麦氏浊度），一个扩张器接种 2.5×10⁷ CFU/mL CoNS 悬浮液（CoNS 组；n=10）。进行压力/容积曲线和组织学及微生物学评估。采集手术室空气样本和接触皮肤样本进行微生物学评估。兔子在四周时安乐死。
纤维蛋白组囊内压力显著降低，囊袋较薄，结缔组织疏松/致密（<25%），血管生成阴性/轻度。CoNS 组则以囊袋厚度增加和多形核炎性细胞为最常见表现。所有研究组均从囊袋、植入物和皮肤中培养出相同的细菌。一枚植入物感染微球菌属（Micrococcus spp.）后出现 1 例 Baker 分级Ⅳ级挛缩。
纤维蛋白与该临床前动物模型中的囊袋形成减少有关，这使得纤维蛋白成为乳房隆乳术妇女有吸引力的潜在治疗药物。在手术过程中防止细菌污染的临床策略至关重要，因为低致病性病原体可能会促进 CC 的发生。
