Toll-Like Receptors (TLRs) Expression in Contracted Capsules Compared to Uncontracted Capsules

Abstract

Introduction The etiology of capsular contracture after surgical implantation of breast implants remains unclear, but an important role is seen for the immune system. Toll-like receptors are immune receptors recognizing both pathogen-associated molecular patterns and damage-associated molecular patterns. The former are present on bacteria such as Staphylococcus epidermidis (bacteria earlier associated with capsular contracture), and the latter are released after (mechanical) stress. The aim of this study was to investigate the expression of TLRs 1–10 in relation to capsular contracture. Materials and Methods Fifty consecutive breast capsules were collected during implant removal or replacement. The extent of capsular contracture was scored according to the Baker score. A sample specimen (0.5 cm 3 ) was obtained from all tissues. cDNA was synthesized from isolated mRNA from the collected specimens. PCR analyses were conducted to test for cDNA presence and to quantify concentration. TLR1–10 expression was measured for each of the Baker scores separately and compared to all Baker scores. Results Expression of all TLRs in all Baker scores was seen. TLR2 and TLR6 were more often present in contracted samples (Baker 3 or 4) compared to uncontracted samples (Baker 1 or 2) [Baker 2 vs. 3 ( p = 0.034) and Baker 2 vs. 3 ( p = 0.003), respectively]. None of the TLRs displayed a significantly higher expression in contracted capsules compared to uncontracted capsules. Conclusion This study shows that TLR2 and TLR6 are more often expressed in contracted capsules compared to non-contracted capsules however not in higher concentrations. Level of Evidence III This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

The State of the Art about Etiopathogenetic Models on Breast Implant Associated–Anaplastic Large Cell Lymphoma (BIA-ALCL): A Narrative Review

“…Bachour et al in 2019 compared the expression of toll-like receptors in contracted and noncontracted capsules: they found a higher expression of TLR in contracted capsules than uncontracted, and the differences were significant for TLR-2, TLR-6 and TLR-8 [ 85 ]. The macrophage activation leads to cytokines and chemokines secretion such as IL-8 and TNF-alpha, producing an increased inflammatory response usually founded in contracted capsules [ 86 , 87 , 88 , 89 , 90 , 91 , 92 , 93 , 94 , 95 , 96 ].…”

Subclinical Infection of the Silicone Breast Implant Surface as a Possible Cause of Capsular Contracture: A Follow-Up

“…Investigation of the role of toll-like receptors in peri-implant implant tissue is a very logical step forward in an attempt to establish the pathophysiology and molecular evidence behind BII. This study and others aimed to dissect molecular mechanisms behind the condition would perhaps allow us to determine whether indeed there are patients who should not be recipients of breast implants [20][21][22][23].…”

“…Considering the fact that immune alterations and chronic inflammatory profiles may have a similar pathophysiology regardless of whether reactions are considered ''local'', and limited to the surrounding breast environment, or systemic; the hypothesis that capsular contracture and breast implant illness share the same initial pathogenesis and are on a continuum of the same chronic inflammatory spectrum is reasonable [22][23][24][25][26]. The combination of the presence of toxic or immunizing-capable detachment molecules from Staphylococcus epidermidis biofilms as well as some silicone gel adjuvant potency may lead to different reactions ranging from local-in some circumstances unilateralfibrosis (capsular contracture) through systemic ones (fibromyalgia, BII) [10, [22][23][24][25][26][27].…”

“…Considering the fact that immune alterations and chronic inflammatory profiles may have a similar pathophysiology regardless of whether reactions are considered ''local'', and limited to the surrounding breast environment, or systemic; the hypothesis that capsular contracture and breast implant illness share the same initial pathogenesis and are on a continuum of the same chronic inflammatory spectrum is reasonable [22][23][24][25][26]. The combination of the presence of toxic or immunizing-capable detachment molecules from Staphylococcus epidermidis biofilms as well as some silicone gel adjuvant potency may lead to different reactions ranging from local-in some circumstances unilateralfibrosis (capsular contracture) through systemic ones (fibromyalgia, BII) [10, [22][23][24][25][26][27]. Therefore, it should not be surprising that the outcomes from implant explanation or periprosthetic capsulectomy are inconsistent and often not permanent-once the systemic inflammatory cascade is activated, it tends to have its own dynamic course and the elimination of antigens and the site of local inflammation may not result in the resolution of the multitude of symptoms and problems that may be present [4,17,18,[22][23][24][25][26].…”

“…The combination of the presence of toxic or immunizing-capable detachment molecules from Staphylococcus epidermidis biofilms as well as some silicone gel adjuvant potency may lead to different reactions ranging from local-in some circumstances unilateralfibrosis (capsular contracture) through systemic ones (fibromyalgia, BII) [10, [22][23][24][25][26][27]. Therefore, it should not be surprising that the outcomes from implant explanation or periprosthetic capsulectomy are inconsistent and often not permanent-once the systemic inflammatory cascade is activated, it tends to have its own dynamic course and the elimination of antigens and the site of local inflammation may not result in the resolution of the multitude of symptoms and problems that may be present [4,17,18,[22][23][24][25][26].…”