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Preventive Effect of Synthetic Tryptophan Metabolite on Silicone Breast Implant–Induced Capsule Formation

Kang, Shin, Hyuk, MD*; Jang, Suk, Yoon, MD*; Ryou, Jeong, Hyun, MD, PhD; Kim, Woo, Seob, MD, PhD*; Kim, Han, Koo, MD, PhD*; Bae, Tae, Hui, MD, PhD*; Kim, Mi, Kyung, MD, PhD

doi: 10.1097/SAP.0000000000001335

Background In the field of plastic surgery, capsular contracture after silicone breast implant surgery is a major clinical problem. This experimental study confirms that the synthetic tryptophan metabolite N-(3′,4′-dimethoxycinnamonyl) anthranilic acid (Tranilast) reduces capsule formation and prevents capsular contracture.

Methods Eighteen New Zealand white rabbits were divided into 2 groups. In the experimental group, implants were inserted into each rabbit, and oral synthetic tryptophan metabolite was administered daily at a dose of 5 mg/kg in 10 mL of saline. In the control group, rabbits received implants and the same amount of saline without the metabolite. After 2 months, peri-implant tissues were harvested and analyzed.

Results The thickness of the capsules and the inflammatory cell counts were decreased in the experimental group (P < 0.001). The collagen fibers in the experimental group were thinner, less dense, and more organized than in control group. The results of reverse transcription quantitative polymerase chain reaction analysis showed that the genes for transforming growth factor β1 (P = 0.002), alpha smooth muscle actin (P < 0.001), and collagen types I (P = 0.002) and III (P = 0.004) were underexpressed in the experimental groups. Furthermore, the counts of T-cell immunity-related cytokine presenting cells were decreased in the experimental groups (CD3, 4, 25, 45RA, 45RO, 69, interleukin-2, 4 [P < 0.001], and interferon γ [P = 0.028]).

Conclusions This study confirms that a synthetic derivative of a tryptophan metabolite decreases capsule formation and prevents capsular contracture by inhibiting the differentiation of fibroblasts to myofibroblasts, selectively inhibiting collagen synthesis, and decreasing specific T-cell immune responses by changing anti-inflammatory cytokine expression.

From the *Department of Plastic and Reconstructive Surgery, Chung-Ang University Hospital, Heuksuk-Dong, Dongjak-Gu, Seoul; †Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon; and ‡Department of Pathology, Chung-Ang University Hospital, Heuksuk-Dong, Dongjak-Gu, Seoul, Korea.

Received July 28, 2017, and accepted for publication, after revision November 16, 2017.

Conflicts of interest and sources of funding: The authors have no financial interest in any of the products, devices, or drugs mentioned in this article.

Reprints: Woo Seob Kim, MD, PhD, Department of Plastic and Reconstructive Surgery, Chung-Ang University Hospital, 102, Heuksuk-Ro, Dongjak-Gu, Seoul, 156-755, Korea. E-mail:

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