Follistatin and the Breast Implant Capsule

Frenkiel, Brett A.; Temple-Smith, Peter; Kretser, David de; Southwick, Graeme

doi:10.1097/gox.0000000000001258

Cited by 8 publications

(6 citation statements)

References 69 publications

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“…Our data now show that serum concentration levels of Activin A and follistatin in patients with capsular contracture differ from the standard serum level determined by us and the values that occur in long-term patients asymptomatic with regard to capsular contracture. 34,35 Contrary to Dohi et al and Frenkiel et al 25,36 , we could not observe that higher follistatin concentrations were also associated with higher Activin A concentrations. We observed normal Activin A serum levels and below standard follistatin levels in capsular fibrosis patients.…”

Section: Discussioncontrasting

confidence: 95%

“…This assumption is confirmed in the animal experiments with regard to capsular fibrosis as a pathological fibrotic process, where it could be demonstrated that the local application of follistatin in the implant pocket led to a significant reduction in pericapsular inflammation and fibrosis. 25 The aim of this study was to determine whether and how the serum concentrations of Activin A and follistatin changes after breast augmentation with silicone implants. This is intended to provide insights into the possible influence of the activin-follistatin axis in the development of the capsular contracture.…”

Section: Introductionmentioning

confidence: 99%

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Activin A and Follistatin Serum Concentrations in Breast Augmentation Patients

Zeplin

2021

Plast Surg (Oakv)

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Background: Capsular contracture is caused by an excessive fibrotic reaction similar as observed in other progressive fibrotic disorders. For their pathogenesis, several studies confirmed the importance of activins and follistatin. The aim of this study was to determine and analyze serum levels of Activin A and follistatin in patients with capsular contracture after aesthetic breast augmentation. Methods: The study included 361 female patients who underwent primary aesthetic breast augmentation, came for control examination after breast augmentation or for revision operation because of capsular contracture. Blood samples were taken and using a specific ELISA to determine the serum concentration levels of Activin A and Follistatin. Results: Ninety-six patients (n = 96), who developed a capsular contracture Baker ≥°III and underwent revision surgery were collected (capsular fibrosis group). One-hundred and fourteen patients (n = 114) were asymptomatic for capsular fibrosis Baker ≥°III after primary breast augmentation and 33 (n = 33) of them had developed no capsular fibrosis after more than 10 years (long-term group). For control group, blood samples were taken from 167 patients (n = 167) before primary aesthetic breast augmentation. Serum Activin A levels were significantly higher in the long-term Group compared with those in the capsular fibrosis- and the control groups. Follistatin levels were significantly lower in the capsular fibrosis group compared to the control- and the long-term groups. A small amount of control group patients (n = 16) developed a capsular fibrosis within 2 years after primary breast augmentation with significant lower follistatin levels. Retrospectively, they showed significantly lower serum follistatin levels than the control group even before the onset of capsular contracture. Conclusions: Capsular fibrosis has no effect on Activin A serum levels. In contrast, follistatin serum levels are lower in patients with capsular fibrosis. These results show that besides many other factors, a dysregulation of the Activin–follistatin axis may have importance on the pathogenesis of capsular contracture.

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Section: Discussioncontrasting

confidence: 95%

Section: Introductionmentioning

confidence: 99%

Activin A and Follistatin Serum Concentrations in Breast Augmentation Patients

Zeplin

2021

Plast Surg (Oakv)

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“…The pathogenesis of breast prosthetic implant-associated SCC is not clear. Metaplastic squamous epithelialization of the capsular lining or entrapment of skin or adnexal elements has been acknowledged [15]. The most common histological characterization in implant capsules was collagen bre alignment and brous capsule [16,17].…”

Section: Discussionmentioning

confidence: 99%

Breast prosthetic implant-associated Squamous Cell Carcinoma: A case report and Literature Review

Liu

Zhao

et al. 2021

Preprint

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BackgroundBreast reconstruction is widely used for women undergoing mastectomy. Prosthetic implants have become a common technique performed for these women because of their safety, flexibility and adjustable size. There are few reports of implant-associated squamous cell carcinoma. In addition to this report, only 8 reports including 11 cases have been reported in the English literature.Case presentationWe report the case of a patient with breast prosthetic implant-associated squamous cell carcinoma who received mastectomy and prosthetic implants 10 years ago. She was recently hospitalized with unilateral breast enlargement. Surgical pathology showed squamous cell carcinoma around the breast implant. There was no evidence of primary squamous cell carcinoma at any other anatomic site. We analysed all 11 patients with breast implant-derived squamous cell carcinoma (SCC) from a thorough literature search to identify studies. The median age of patients at SCC diagnosis was 56.8 years old. The average time from initial breast augmentation until SCC diagnosis was 21.9 years. The prognosis was poor; 4 of the 11 patients eventually progressed or died within 1 year, 3 of the 11 patients were disease free during the follow-up period, and 4 of the 11 patients were lost to follow-up. The most widespread opinion is that chronic inflammation from breast implants plays a substantial role in the disease progression of SCC.ConclusionsWe reported the rare complications associated with breast prosthetic implants and reviewed the literature. This malignancy should be taken into account in patients with breast prosthetic implants who have acute breast pain and enlargement.

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“…Prepared breast implant surface materials were seeded into 8-week old Balb/c female mice (weight ~20 g, Jackson Laboratory), according to a published paper (25). Mice were maintained in the specific-pathogen-free environment (control at constant 23°C and 40–60% humidity) with a 12-h light/dark cycle.…”

Section: Methodsmentioning

confidence: 99%

Roxatidine inhibits fibrosis by inhibiting NF‑κB and MAPK signaling in macrophages sensing breast implant surface materials

Wang

Tian

et al. 2019

Mol Med Report

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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.

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Follistatin and the Breast Implant Capsule

Abstract: Supplemental Digital Content is available in the text.

Cited by 8 publications

References 69 publications

Activin A and Follistatin Serum Concentrations in Breast Augmentation Patients

Activin A and Follistatin Serum Concentrations in Breast Augmentation Patients

Breast prosthetic implant-associated Squamous Cell Carcinoma: A case report and Literature Review

Roxatidine inhibits fibrosis by inhibiting NF‑κB and MAPK signaling in macrophages sensing breast implant surface materials

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