Department of Plastic and Reconstructive Surgery, Faculty of Medicine, University of Oporto, Hospital of São João, Portugal.
Aesthet Surg J. 2011 Mar;31(3):302-9. doi: 10.1177/1090820X11398351.
The root cause of capsular contracture (CC) associated with breast implants is unknown. Recent evidence points to the possible role of fibrin and bacteria in CC formation.
The authors sought to determine whether fibrin, thrombin, and blood modulated the histological and microbiological outcomes of breast implant capsule formation in a rabbit model.
The authors carried out a case-control study to assess the influence of fibrin, thrombin, and blood on capsule wound healing in a rabbit model. Eighteen New Zealand white rabbits received four tissue expanders. One expander acted as a control, whereas the other expander pockets received one of the following: fibrin glue, rabbit blood, or thrombin sealant. Intracapsular pressure/volume curves were compared among the groups, and histological and microbiological evaluations were performed (capsules, tissue expanders, rabbit skin, and air). The rabbits were euthanized at two or four weeks.
At four weeks, the fibrin and thrombin expanders demonstrated significantly decreased intracapsular pressure compared to the control group. In the control and fibrin groups, mixed inflammation correlated with decreased intracapsular pressure, whereas mononuclear inflammation correlated with increased intracapsular pressure. The predominant isolate in the capsules, tissue expanders, and rabbit skin was coagulase-negative staphylococci. For fibrin and thrombin, both cultures that showed an organism other than staphylococci and cultures that were negative were associated with decreased intracapsular pressure, whereas cultures positive for staphylococci were associated with increased intracapsular pressure.
Fibrin application during breast implantation may reduce rates of CC, but the presence of staphylococci is associated with increased capsule pressure even in the presence of fibrin, so care should be taken to avoid bacterial contamination.
与乳房植入物相关的包膜挛缩（CC）的根本原因尚不清楚。最近的证据表明纤维蛋白和细菌可能在 CC 的形成中起作用。
作者试图确定纤维蛋白、凝血酶和血液是否会影响兔模型中乳房植入物胶囊形成的组织学和微生物学结果。
作者进行了一项病例对照研究，以评估纤维蛋白、凝血酶和血液对兔模型中胶囊伤口愈合的影响。18 只新西兰白兔接受了四个组织扩张器。一个扩张器作为对照，而其他扩张器口袋接受了以下一种治疗：纤维蛋白胶、兔血或凝血酶密封剂。比较了各组的囊内压/体积曲线，并进行了组织学和微生物学评估（胶囊、组织扩张器、兔皮和空气）。兔子在两周或四周时被安乐死。
在四周时，纤维蛋白和凝血酶扩张器与对照组相比，囊内压显著降低。在对照组和纤维蛋白组中，混合炎症与囊内压降低相关，而单核炎症与囊内压升高相关。胶囊、组织扩张器和兔皮中的主要分离物为凝固酶阴性葡萄球菌。对于纤维蛋白和凝血酶，除了葡萄球菌以外的其他生物体的培养物和阴性培养物均与囊内压降低相关，而葡萄球菌阳性的培养物与囊内压升高相关。
在乳房植入物期间应用纤维蛋白可能会降低 CC 的发生率，但即使存在纤维蛋白，葡萄球菌的存在也与囊内压升高相关，因此应注意避免细菌污染。
