Clinical and histologic response of subcutaneous expanded polytetrafluoroethylene (Gore-Tex) and porous high-density polyethylene (Medpor) implants to acute and early infection.

OBJECTIVE: To examine the responses of subcutaneously implanted expanded polytetrafluoroethylene (e-PTFE, Gore-Tex) and porous high-density polyethylene (PHDPE, Medpor) to experimentally induced infection.
DESIGN: Sprague-Dawley rats were implanted subcutaneously with either e-PTFE or PHDPE implants. Inocula of Staphylococcus aureus were injected directly over the implants and the wounds were observed for clinical signs of infection. After the animals were killed, the implants were harvested and underwent Histologic examination.
SUBJECTS: Twenty-eight adult male Sprague-Dawley rats weighing 200 to 250 g. INTERVENTION: A 8-mm diameter, 1-mm-thick implant of either e-PTFE or PHDPE was placed in a subcutaneous pocket over each animal's dorsum. Either at the time of implantation or 14 days afterward, an inoculum of 10(9) colony-forming units of S aureus was injected transcutaneously directly over each implant. The animals were observed for 7 days before being killed. The implants were harvested and examined by both conventional light and scanning electron microscopy, and the degree of capsule reaction, infection, inflammation, and implant degradation was evaluated.
RESULTS: Implants inoculated at the time of implantation were more likely to become clinically infected. Results for e-PTFE and PHDPE implants were similar in this group (5 of 5 e-PTFE and 5 of 5 PHDPE implants infected). The PHDPE implants inoculated 14 days after implantation were less likely to become infected (1 of 4 infected) than e-PTFE implants (3 of 4 infected), and were statistically less likely to become infected than PHDPE implants inoculated immediately after implantation (25% vs 100%; P < .02). Histologically, this resistance to infection correlated with increasing fibrovascular ingrowth into the PHDPE implants. The infected PHDPE implant had little to no ingrowth compared with PHDPE control implants. The uninfected e-PTFE implant had evidence of early fibrovascular ingrowth into the peripheral pores of the implant.
CONCLUSIONS: Because of differences in pore size, PHDPE promotes faster fibrovascular ingrowth. The presence of vascularized host tissue in and around the implant lends stability and resistance to experimentally induced infection. Conservative management of clinical implant infections should be considered if bacterial seeding occurs after substantial fibrovascular ingrowth is present. Future alloplast designs should include pore sizes that will encourage invasion of the implant by host tissue.