Background. Breast implants are commonly placed postbreast cancer reconstruction, cosmetic augmentation, and gender-affirming surgery. Breast implant illness (BII) is a systemic complication associated with breast implants. Patients with BII may experience autoimmune symptoms including fatigue, difficulty concentrating, hair loss, weight change, and depression. BII is poorly understood, and the etiology is unknown. The purpose of this literature review is to characterize BII autoimmune disorders and determine possible causes for its etiology. Methods. The PubMed, Google Scholar, Embase, Web of Science, and OVID databases were interrogated from 2010 to 2020 using a query strategy including search term combinations of implants, breast implant illness, autoimmune, and systemic illness. Results. BII includes a spectrum of autoimmune symptoms such as fatigue, myalgias/arthralgias, dry eyes/mouth, and rash. A review of epidemiological studies in the past ten years exhibited evidence affirming an association between breast implants and autoimmune diseases. The most commonly recognized were Sjogrens syndrome, rheumatoid arthritis, systemic sclerosis, chronic fatigue syndrome, and Raynauds syndrome. Explantation resulted in alleviation of symptoms in over 50 of patients, strengthening the hypothesis linking breast implants to BII. Studies have shown that silicone is a biologically inert material and unlikely to be the cause of these symptoms. This is supported by the fact that increased risk of autoimmune disease was also reported in patients with other implantable biomaterials such as orthopedic implants. Recent studies shed light on a possible role of bacterial biofilm and subsequent host-pathogen interactions as a confounding factor to this problem. Conclusion. BII could be dependent on biofilm infection and the microenvironment around the implants. The true pathophysiology behind these complaints must be further investigated so that alternative treatment regimens other than explantation can be developed. Translational significance of these studies is not limited to breast implants but extends to other implants as well.

This study investigates a mechanistic link of bacterial biofilm–mediated host-pathogen interaction leading to immunological complications associated with breast implant illness (BII). Over 10 million women worldwide have breast implants. In recent years, women have described a constellation of immunological symptoms believed to be related to their breast implants. We report that periprosthetic breast tissue of participants with symptoms associated with BII had increased abundance of biofilm and biofilm-derived oxylipin 10-HOME compared with participants with implants who are without symptoms (non-BII) and participants without implants. S. epidermidis biofilm was observed to be higher in the BII group compared with the non-BII group and the normal tissue group. Oxylipin 10-HOME was found to be immunogenically capable of polarizing naive CD4⁺ T cells with a resulting Th1 subtype in vitro and in vivo. Consistently, an abundance of CD4⁺Th1 subtype was observed in the periprosthetic breast tissue and blood of people in the BII group. Mice injected with 10-HOME also had increased Th1 subtype in their blood, akin to patients with BII, and demonstrated fatigue-like symptoms. The identification of an oxylipin-mediated mechanism of immune activation induced by local bacterial biofilm provides insight into the possible pathogenesis of the implant-associated immune symptoms of BII.

Lymphedema is chronic swelling from lymphatic dysfunction. The vascular delay phenomenon is used in flap reconstruction to increase flap viability through staged selective partial disruption of blood supply to enhance flap survival, followed by flap transfer 7–10 days later. A similar corollary for lymphatics remains unknown. The purpose of this study was to evaluate whether lymphatic preconditioning with staged disruption of lymphatics in the murine hindlimb lymphedema model can be protective against lymphedema. C57BL/6 mice underwent 20 Gy hindlimb irradiation. Group 1 (immediate lymphatic disruption) underwent a circumferential skin incision, complete lymphatic disruption, and popliteal lymph node excision in a single-stage operation. Group 2 (delayed lymphatic disruption) underwent a semi-circumferential inguinal skin incision and dominant lymphatic transection and, 7 days later, received a circumferential skin incision, complete lymphatic transection, and popliteal lymphadenectomy. Paw thickness was measured weekly. Near-infrared laser lymphangiography and immunohistochemistry were performed on D35. Group 2 had a lower average paw thickness (p = 0.0008) and greater lymphatic clearance signal intensity at 24 h (p = 0.0035). Immunohistochemistry indicated an abundance of the lymphatic endothelial-specific marker podoplanin in Group 2 compared to Group 1 (p = 0.03). This study demonstrates evidence for a novel concept of a lymphatic delay phenomenon parallel to the well-known vascular delay phenomenon.