Macrophage Depletion Ameliorates Posterior Capsule Opacification in Rodents

Abstract

Purpose: : To investigate whether macrophages play a role in the development of posterior capsule opacification (PCO) in rodents.

Methods: : An extracapsular lens extraction was performed in 13 consecutive Sprague–Dawley rats. Animals were treated intravenously with liposomal clodronate (Cl₂MDP–lip) or phosphate–buffered saline (PBS) liposomes (PBS–lip) one day preoperatively and on the first day postoperatively, and sacrificed 3 days postoperatively. Eyes were examined clinically prior to enucleation, and then processed for light microscopy and immunohistochemistry. PCO was evaluated clinically and histopathologically in a masked fashion. Student t–test and Chi–square were used to assess differences between groups.

Results: : A statistically significant reduction in the number of macrophages (ED1+, ED7+, ED8+) was found in the Cl₂MDP–lip–treated group compared with the PBS–lip–treated group (p = 0.03, p = 0.001, p = 0.03, respectively). There was a trend towards less central opacification and capsular wrinkling detected clinically in the Cl₂MDP–lip–treated group, but differences were not statistically significant (p = 0.16 and p = 0.06, respectively). No statistically significant differences were observed between groups with respect to qualitative histopathologic scores of PCO. However, a quantitative analysis of lens epithelial cells (LEC) in the center of the posterior capsule disclosed statistically significant differences between groups, with fewer cells detected in the Cl₂MDP–lip–treated group (p= 0.03).

Conclusions: : Depletion of macrophages was accompanied by a reduction in LEC proliferation and PCO in rodents. This finding supports the role of macrophages in the pathogenesis of PCO and has therapeutic implications for the most common complication of cataract surgery.

Keywords: posterior capsular opacification (PCO) • inflammation • proliferation