Background: The etiology and clinical treatment of capsular contracture remain unresolved as the causes may be multifactorial. Triamcinolone acetonide applied in the pocket during surgery was reported to be ineffective in prevention of capsular contracture. However, if injected 4-6 weeks after surgery or as a treatment for capsular contracture, decreased applanation tonometry measurements and pain were observed. It was assumed that intraoperative application of triamcinolone was not effective because its effect does not last long enough. However, betadine, antibiotics, and fibrin were found to be effective in preventing capsular contracture with intraoperative applications and are more effective in the early phases of wound healing than in later stages. The role of triamcinolone acetonide in capsule formation is unknown. The purpose of this study was to determine if triamcinolone acetonide modulates breast capsule formation or capsular contracture in the early phases of wound healing in a rabbit model.
Methods: Rabbits (n=19) were implanted with one tissue expander and two breast implants and were killed at 4 weeks. Implant pocket groups were (1) Control (n=10) and (2) Triamcinolone (n=9). Pressure/volume curves and histological, immunological, and microbiological evaluations were performed. Operating room air samples and contact skin samples were collected for microbiological evaluation.
Results: In the triamcinolone group, a decreased capsular thickness, mild and mononuclear inflammation, and negative or mild angiogenesis were observed. There were no significant differences in intracapsular pressure, fusiform cell density, connective tissue, organization of collagen fibers, and microbiological results between the groups. There was no significant difference in the dialysate levels of IL-8 and TNF-α, but correlation between IL-8 and TNF-α was observed.
Conclusion: Triamcinolone acetonide during breast implantation influences early capsule formation and may reduce capsular contracture.
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