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Botulinum Toxin A Affects Early Capsule Formation Around Silicone Implants in a Rat Model

Kim, Young Seok MD, PhD; Hong, Jong Won MD; Yoon, Jung Ho MD; Hwang, Yong Seok MD; Roh, Tai Suk MD, PhD; Rah, Dong Kyun MD, PhD

doi: 10.1097/SAP.0b013e318295de95
Research
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Summary Capsular contracture is one of the most common complications resulting from implants placed during mammoplasty and rhinoplasty, and there is no definitive solution or a method for preventing it. Recent reports suggest that botulinum toxin A (BoTA) is effective at reducing keloid scars clinically. Peri-implant capsules are histologically similar to keloid scars and hypertrophic scars. Therefore, we hypothesized that BoTA may reduce peri-implant capsule formation.

To test our hypothesis, we divided 24 male Sprague-Dawley rats into an experiment group and a control group. We created two 15 × 15-mm subpanniculus pockets in each rat. Botulinum toxin A (0.5 mL; 5 U) was injected into the carnosa layer of the experimental group’s pockets and 0.5 mL normal saline was similarly injected in the control group. Hemispherical silicone implants, 15 mm in diameter, were inserted into the pockets. After 6 weeks, the peri-implant capsule was excised and examined by histologic evaluation, immunohistochemical stain, scanning electron microscope, and real-time polymerase chain reaction.

Capsular thickness, number of inflammatory cells, number of vessels, and transforming growth factor β1 expression were reduced in the experimental group compared to the control group (P < 0.01). The experimental group’s collagen pattern was loose and well organized. The total myofibroblast content was lower in the experimental group than in the control group; however, this difference was not statistically significant (P = 0.32). Additionally, the experimental group had a smaller fibrosis index than the control group (P < 0.05).

Our results suggest that BoTA may provide an alternative treatment for reducing capsule formation and preventing contracture, and further studies may reveal the mechanism of action.

From the Department of Plastic and Reconstructive Surgery, Institute for Human Tissue Restoration, Yonsei University College of Medicine, Seoul, Korea.

Received September 26, 2012, and accepted for publication, after revision, April 5, 2013.

Conflicts of interest and sources of funding: Supported by grants from a Faculty Research Grant from Yonsei University College of Medicine (6-2010-0038, TS Roh) and by the Basic Science Research Program through the National Research Foundation of Korea (NRF), funded by the Ministry of Education, Science, and Technology (2012-0003180, YS Kim).

Reprints: Tai Suk Roh, MD, PhD, Department of Plastic and Reconstructive Surgery, Gangnam Severance Hospital, Yonsei University College of Medicine 211 Eonju-ro, Gangnam-gu, Seoul 135-720, Korea. E-mail: rohts@yuhs.ac.

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