Use of the transforming growth factor-beta1 inhibitor peptide in periprosthetic capsular fibrosis: experimental model with tetraglycerol dipalmitate

BACKGROUND
Capsular contracture is the most common specific complication associated with silicone prostheses. It is thought to be caused by the gradual retraction of the fibrous scar tissue that forms around the prosthesis. Molecular biology has made it possible to determine the role of transforming growth factor beta (TGF-beta) in the scar physiopathology of any fibrotic process, including periprosthetic capsular fibrosis. The effects on the inhibition of TGF-beta have also been demonstrated in experimental models of scar formation and fibrosis, which opens the way for new therapeutic alternatives in the treatment of capsular contracture.

METHODS
Three experimental groups of 10 rats each were formed to evaluate periprosthetic fibrosis after its modulation with a newly synthesized TGF-beta1 peptide inhibitor in a tetraglycerol dipalmitate matrix. In the first group, subcutaneously and submuscularly placed, smooth, solid silicone prostheses were left untreated; in the second group, the prostheses were left after being immersed in a solution of tetraglycerol dipalmitate; and in the third group, following the same protocol as in the second group, the solution contained tetra-glycerol dipalmitate mixed with the inhibitor peptide of TGF-beta1. The animals were euthanized 8 weeks after implantation, and the capsules were assessed both macroscopically and histologically.

RESULTS
Inhibition of capsular thickness and cellularity was significantly more effective in the group of animals treated with the inhibitor peptide of TGF-beta1.

CONCLUSIONS
The TGF-beta1 inhibitor peptide applied in a matrix with tetraglycerol dipalmitate is significantly effective in achieving a reduction in periprosthetic fibrosis after placement of silicone implants, either subcutaneously or submuscularly. This result suggests new therapeutic approaches.

CITATION  Plast Reconstr Surg. 2005 Oct;116(5):1370-8.  doi: 10.1097/01.prs.0000181694.07661.0d