Miller Katherine E, Hontanilla Bernardo, Cabello Alvaro, Marre Diego, Armendariz Leticia, Leiva Jose
Department of Plastic and Reconstructive Surgery, Clinica Universidad de Navarra, Pamplona, Spain.
Department of Plastic and Reconstructive Surgery, Clinica Universidad de Navarra, Pamplona, Spain.
J Plast Reconstr Aesthet Surg. 2016 Jan;69(1):70-6. doi: 10.1016/j.bjps.2015.08.027. Epub 2015 Sep 6.
The effect of late infection on capsular contracture has yet to be established, leaving a gap in clinical guidelines for the treatment patients with breast implants. This trial is the first to assess if the treatment of these infections can reverse this effect in an in vivo rat model and whether late distant infections increase the incidence of capsular contracture.
Three groups of female Wistar rats (n = 42) received two silicone implants in separate dorsal, subcutaneous pockets. All groups except control underwent injection of a human strain of methicillin-sensitive Staphylococcus aureus (MSSA) at least 30 days after implantation, allowing for physiologic capsule formation. The infection group received a peritoneal injection, inducing a transient bacteremia, the treated group received a course of antibiotics following bacterial inoculation, and a final group received no intervention and served as control.
Implants were removed 4 months after insertion, and capsules measured for thickness and sent for bacterial quantification. Compared to both the control and treated groups, capsule thickness in the infection group was statistically greater (p < 0.05), a difference not observed between treated and control groups. In addition, a statistically significant positive correlation was found between capsule thickness and bacterial count (R = 0.614, p < 0.01).
The difference in thickness between the control capsules and those from the infection group is an indication that bacterial contamination of a capsule from a remote late infection may increase the incidence of capsular contracture suggesting that treating late infections could in fact prevent capsular contracture.
晚期感染对包膜挛缩的影响尚未明确，这使得乳房植入患者的临床治疗指南存在空白。本试验首次评估在体内大鼠模型中治疗这些感染是否能逆转这种影响，以及晚期远处感染是否会增加包膜挛缩的发生率。
三组雌性Wistar大鼠（n = 42）在背部皮下不同部位植入两个硅胶假体。除对照组外，所有组在植入后至少30天接受人源甲氧西林敏感金黄色葡萄球菌（MSSA）注射，以形成生理性包膜。感染组接受腹腔注射，诱导短暂菌血症，治疗组在细菌接种后接受一个疗程的抗生素治疗，最后一组不进行干预作为对照组。
植入4个月后取出假体，测量包膜厚度并进行细菌定量检测。与对照组和治疗组相比，感染组的包膜厚度在统计学上更大（p < 0.05），治疗组和对照组之间未观察到差异。此外，包膜厚度与细菌计数之间存在统计学上显著的正相关（R = 0.614，p < 0.01）。
对照组包膜与感染组包膜厚度的差异表明，远处晚期感染导致的包膜细菌污染可能会增加包膜挛缩的发生率，这表明治疗晚期感染实际上可以预防包膜挛缩。
