BACKGROUND: Capsular contracture (CC) remains a very common complication and the main cause of reoperation following a mammary implant surgery. Leukotrienes play an important role in the inflammatory cascade linked to the development of the periprosthetic capsule. The aim of this paper is to evaluate the incidence of recurrence of capsular contracture in female patients who underwent a secondary mammary augmentation due to this etiology, with and without treatment with leukotriene inhibitors during postoperative care.
METHODS: Sixty-four women submitted to a secondary mammary augmentation due to CC were evaluated retrospectively. Out of these patients, 20 (31%) were treated with Montelukast for 3 months. The remaining 44 (69%) did not receive antileukotriene. The presence of capsular contracture was measured using the Baker classification and magnetic resonance imaging a year after postoperative care. The median follow-up period was 15 months.
RESULTS: The patients receiving Montelukast (n = 20) presented a 15% CC rate (n = 1). The women that did not receive antileukotriene therapy (n = 44) presented a 16% CC rate (n = 7).
CONCLUSIONS: The results of our study show that treatment with Montelukast for 3 months after the operation is associated with lower rates of capsular contracture when compared to patients that did not receive the treatment.
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Capsular contracture is an important complication after silicone mammary implant surgery. Fibroblasts and macrophages play critical roles in the pathogenesis of capsular contracture, making these two cell types therapeutic targets. It has been reported that inhibiting histamine receptors results attenuates fibrosis, but the role of roxatidine (a histamine receptor 2 inhibitor) in preventing fibrosis caused by breast implant materials remains unknown. The aim of the present study was to assess the hypothesis that roxatidine might have a prophylactic effect in capsular contracture induced by implant material. Inflammation induced by breast implant materials was mimicked by co‑culturing macrophages or fibroblasts with these materials in vitro. Capsular contracture was modeled in mice by planting breast implant materials in a subcutaneous pocket. Roxatidine was added in the culture medium or administered to mice bearing breast implant materials. By co‑culturing macrophages or fibroblasts with common breast implant materials (micro‑textured or smooth breast implants), the present study demonstrated that macrophages respond to these materials by producing pro‑inflammatory cytokines, a process that was abolished by addition of roxatidine to the culture medium. Although fibroblasts did not respond to implant surface materials in the same way as macrophages, the conditioned media of macrophages induced proliferation of fibroblasts. Mechanistically, administration of roxatidine inhibited activation of NF‑κB and p38/mitogen‑activated protein kinase (MAPK) signaling in macrophages. Furthermore, treatment with roxatidine in implant‑bearing mice reduced serum concentrations of transforming growth factor‑β and the abundance of fibroblasts around the implant. The present study concluded that roxatidine plays an important role in preventing fibrosis by inhibiting activation of NF‑κB and p38/MAPK signaling in macrophages.