Tumor necrosis factor-α (TNF-α) is a multifunctional, proinflammatory cytokine that mediates pleiotropic biological functions, especially inflammation and immunoregulation. We hypothesized that blocking TNF-α with a monoclonal antibody would decrease inflammation and subconjunctival scarring in an animal model of experimental filtration surgery.
In a randomized, prospective, masked-observer study, 30 New Zealand albino rabbits underwent glaucoma filtration surgery. The animals were allocated to receive either intraoperative application of infliximab (group A) or mitomycin C (MMC) at a concentration of 0.2 mg/ml (group B) or balanced salt solution (BSS, control) (group C). Different infliximab doses, namely 1.0, 2.0, 3.0, 4.0, 5.0 mg in 0.1 ml, were applied. Bleb survival and characteristics were evaluated over a 30-day period. The animals were killed on postoperative day 15 or 30. Histology of the operated eyes was performed to evaluate and grade the amount of scarring in each group. Cellular density was evaluated in each case.
Infliximab did not appear to improve outcomes in this model of glaucoma filtration surgery. Bleb survival was significantly higher in the MMC group compared to the other groups (p < 0.001 for both comparisons). Vascularity was also significantly lower in the MMC group compared to the other groups (p = 0.018 for both comparisons). There was a significant decrease in cellular density in the MMC group compared to the control (p = 0.0352) and the infliximab group (p < 001).
Our results have shown that trabeculectomies in the infliximab group failed faster and displayed more scarring, compared to the control and MMC groups. This outcome suggests that the infliximab doses used in this pilot study resulted in a subconjunctival TNF-α concentration, which acted as a stimulator to fibroblasts.