PURPOSE: To evaluate the effect of the sustained-release of ethylenediaminetetraacetic acid (EDTA) chelating Ca++ on lens epithelial cell (LEC) migration. SETTING: Nishi Eye Hospital, Jinshikai Medical Foundation, Osaka, Japan. METHODS: Polylactic-glycolic acid disks containing 10% EDTA were placed in saline solution for about 2 weeks in vitro. About 60% (7 micrograms/hour) of the EDTA was released during that time. The disks with a posterior chamber intraocular lens placed above were implanted in the capsular bag in five rabbit eyes after continuous curvilinear capsulorhexis and phacoemulsification. A disk without EDTA and the same lens type were placed in the bag in the contralateral eyes, which served as controls. RESULTS: After 2 to 3 months, opacification in the central posterior capsule was significantly reduced in all eyes that received the disk with EDTA. CONCLUSION: The deprivation of Ca++ disrupted interaction between the posterior capsule and migrating LECs by inactivating the adhesion molecule integrin synthesized by LECs, significantly reducing LEC migration onto the posterior capsule.
PURPOSE: To evaluate the effect of the sustained-release of ethylenediaminetetraacetic acid (EDTA) chelating Ca++ on lens epithelial cell (LEC) migration. SETTING: Nishi Eye Hospital, Jinshikai Medical Foundation, Osaka, Japan. METHODS:Polylactic-glycolic acid disks containing 10% EDTA were placed in saline solution for about 2 weeks in vitro. About 60% (7 micrograms/hour) of the EDTA was released during that time. The disks with a posterior chamber intraocular lens placed above were implanted in the capsular bag in five rabbit eyes after continuous curvilinear capsulorhexis and phacoemulsification. A disk without EDTA and the same lens type were placed in the bag in the contralateral eyes, which served as controls. RESULTS: After 2 to 3 months, opacification in the central posterior capsule was significantly reduced in all eyes that received the disk with EDTA. CONCLUSION: The deprivation of Ca++ disrupted interaction between the posterior capsule and migrating LECs by inactivating the adhesion molecule integrin synthesized by LECs, significantly reducing LEC migration onto the posterior capsule.