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Endocytosis by keratocytes (corneal fibroblasts) is an important part of the host defense system. To investigate the long-term fate of endocytosed materials, we injected polystyrene latex beads into the corneal stroma of four rabbits. The corneal stroma was observed under a transmission electron microscope 4 and 800 days after the injection. After 4 days, the beads were found not only between the collagen fibers of the stroma, but also in some keratocytes. After 800 days, no extracellular beads were seen, but endocytosed beads remained, surrounded by limiting membranes, in the cytoplasm of keratocytes. These observations demonstrate that keratocytes endocytose latex beads and store them for a long time, isolating these foreign materials from the corneal stroma. These observations suggest that keratocytes, like some other fibroblasts perform a noninflammatory and nonimmunological defense function.

A 39-year-old man suffered from corneal neovascularization, through to result from hypoxia caused by improper use of polymethylmethacrylate (PMMA) hard contact lenses. The condition was successfully treated by oxygenation of the corneas under swimming goggles.

The migration and spreading of the corneal epithelial cells adjacent to a wound is the first step in successful epithelial resurfacing. To understand the role of actin filaments and microtubules of the cytoskeletal system in the spreading of corneal epithelial cells, we plated rabbit corneal epithelial cells on a fibronectin matrix and studied the effects of cytochalasin B, which inhibits actin filaments assembly, and colchicine, which inhibits microtubules assembly, on the ability of individual cells to spread. Changes in the morphology of actin filaments and microtubules were also studied using immunofluorescent microscopy. The area of spread epithelial cells depended on the concentration of fibronectin used to coat the surface. In spread cells, stress fibers of actin filaments were evenly distributed throughout the cytoplasm, whereas microtubules were observed only at the perinuclear region. The presence of cytochalasin B during the cell attachment and spreading decreased the area of the spread cells more than did colchicine. However, once the epithelial cells were spread on a fibronectin matrix, cytochalasin B and colchicine each decreased the cell area only slightly, and to the same extent. These results indicate that formation of actin filaments is more important than formation of microtubules to the spreading of corneal epithelial cells.

The natural course of corneal epithelial erosions was studied retrospectively in patients who had undergone cataract extraction. Postsurgical epithelial defects occurred in 41 of 796 eyes (5.2%). No difference was noted in the incidence of corneal epithelial defects in eyes after intracapsular and extracapsular cataract extraction. Of the 41 eyes with postsurgical corneal erosion, 26 (63.4%) showed corneal epithelial defects by the fourth postoperative day. Two types of healing patterns were noticed: rapid healing, in which there was complete epithelial resurfacing within 4 days after the onset of corneal erosion, and prolonged healing, in which the period for complete epithelial resurfacing ranged from 6 days to 34 days. Since fibronectin has been reported to facilitate corneal epithelial migration and adhesion, we administered autologous fibronectin eyedrops in five cases in which corneal epithelial erosion developed after cataract surgery and epithelial defects persisted more than 7 days (except case 2). In all cases receiving fibronectin treatment, complete epithelial resurfacing occurred. In four of five eyes, fibronectin eye drops were effective in epithelial resurfacing within 3-9 days; in one eye, complete epithelial resurfacing took 23 days. The present results indicate that there are two types of epithelial erosion and that fibronectin eye drops might be one of the possible therapeutic approaches for the treatment of persistent epithelial defects. The weak adhesion of epithelial cells underlying basement membrane may be one of the causes of persistent epithelial defects after cataract surgery.