Effects of Pentoxifylline on Peri-Implant Capsule Cellularity and Thickness: A Controlled Experimental Study in a Rat Silicone Implant Model.

Capsular contracture is a fibrotic foreign-body response to silicone implants, driven primarily by TGF-β1-mediated myofibroblast activation and profibrotic signaling, with no established pharmacological prophylaxis. Pentoxifylline (PTX), an antifibrotic agent acting on these pathways, has rarely been evaluated for peri-implant capsule formation. Twenty-eight male Sprague Dawley rats received a 2 cm × 1 cm smooth silicone block in a dorsal sub-panniculus carnosus pocket. After pre-specified exclusions, 20 animals were analyzed in two equal groups: control (saline) and PTX (25 mg/kg/day intraperitoneally) for six weeks. Intracapsular fibroblast/myofibroblast density and capsule thickness were quantified by H&E histology with digital image analysis. PTX reduced fibroblast/myofibroblast density by 35.7% (36.28 ± 9.80 vs. 56.46 ± 16.69 cells/HPF; p = 0.004; d = 1.47). Capsule thickness was reduced by 33.0% (340.10 ± 199.88 vs. 507.78 ± 170.72 µm; d = 0.90), which did not reach significance (Student's t p = 0.059); the Mann-Whitney U sensitivity analysis gave p = 0.045. Systemic PTX reduced intracapsular fibroblast/myofibroblast density, with a directionally consistent but statistically inconclusive secondary signal for capsule thickness. Consistent with the antifibrotic profile of PTX, these findings identify a candidate signal warranting confirmation in a mechanistically powered follow-up, within the limitations of a single-dose, single-sex, H&E-based design.