Effects of Fibrin, Thrombin, and Blood on Breast Capsule Formation in a Preclinical Model

Abstract

Fibrin application during breast implantation may reduce rates of CC, but the presence of staphylococci is associated with increased capsule pressure even in the presence of fibrin, so care should be taken to avoid bacterial contamination.

Capsular Contracture after Breast Augmentation: An Update for Clinical Practice

“…Other immunological agents have also been reported as having a role in the development of capsular contracture. These include connective tissue growth factor factor and interleukins 4, 6, 10, 13, and 21 amongst others, all of which promote fibrosis [ 30 ]. However, more research on their individual roles needs to be conducted before their influence can be fully evaluated.…”

Animal Model of Implant Capsular Contracture: Effects of Chitosan

“…We previously reported complementary studies in which the same protocol is used to analyze silicone breast implants with ports impregnated with LMWC and those sprayed with Tissucol/Tisseel (Baxter International, Deerfield, Illinois). 87,88 conclusions Baker grade III/IV CC was observed in a rabbit model when implants were impregnated with chitosan; the CC was not due to a bacterial infection. This preclinical study may provide a model to test various mechanistic hypotheses of breast capsule formation and subsequent CC and suggests an approach of studying CC with a preclinical animal model.…”

Histologic, Molecular, and Clinical Evaluation of Explanted Breast Prostheses, Capsules, and Acellular Dermal Matrices for Bacteria

“…Several semi-quantitative methods of assessing capsular contracture histologically on the basis of cellularity, 4,9,23,29,39 vascularity, 39,40 fibrosis, 39 or collagen distribution or orientation are reported. 4,9,23,29 However, in the absence of a widely-recognized histologic grading system, we chose to study capsule cellularity and collagen distribution, which have previously been linked to capsular contracture, and about which we have recently reported. 41…”

“…1 Proposed mechanisms for CC continue to evolve, usually implicating an upstream inflammatory event leading to abnormal downstream collagen or myofibroblast deposition. [2][3][4][5][6][7][8][9][10] While several CC studies investigated signaling pathways mediated by transforming growth factor-ß (TGF-ß), 3 tumor necrosis factor-stimulated gene-6 (TSG-6), 5 or leukotriene antagonist-mediated immunomodulation, 8,11,12 others focused on the impact of subclinical infection or biofilms. [13][14][15][16][17][18][19][20][21] An association between bacteria and CC is supported by studies implementing increasingly sophisticated culture techniques, 19 recently accompanied by electron and confocal microcopy, and molecular biology.…”