Panagiotis Kallinikos1, Nathan Efron. 1. Eurolens Research, Department of Optometry and Neuroscience, University of Manchester Institute of Science and Technology, Manchester, United Kingdom. p.kallinikos@student.umist.ac.uk
Abstract
PURPOSE: To employ confocal microscopy to investigate the etiology of keratocyte loss after short-term contact lens wear by monitoring quantitative changes in keratocyte density. METHODS:Twenty neophyte subjects aged 26 +/- 3 years participated in the study, which was conducted over the course of three experimental sessions. In the first session, one eye of each subject was fitted with a silicone hydrogel contact lens, and the other eye served as the control. Both corneas were exposed to an anoxic environment for 2 hours. Ultrasound pachometry and confocal microscopy were performed on both eyes at baseline, immediately after the experiment and 2 hours post experiment. This procedure was repeated after 72 hours, but in this case one eye of each subject was fitted with a hyper-Dk rigid contact lens, and the fellow eye served again as the control. In the third experimental session, each subject was asked to periodically rub one eye only. Tear samples collected from the rubbed and control eyes were assayed for epidermal growth factor (EGF), hepatocyte growth factor (HGF), and interleukin (IL)-8. RESULTS: The increase in corneal thickness was similar in the experimental and control eyes. Both anterior and posterior keratocyte densities decreased in the experimental eyes compared with the control eyes, in all sessions. EGF and IL-8 concentrations were increased in the rubbed eyes compared with the control eyes. CONCLUSIONS: It is hypothesized that the mechanical stimulation of the corneal surface, due to the physical presence of a contact lens, induces the release of inflammatory mediators that cause keratocyte dysgenesis or apoptosis. Copyright Association for Research in Vision and Ophthalmology
RCT Entities:
PURPOSE: To employ confocal microscopy to investigate the etiology of keratocyte loss after short-term contact lens wear by monitoring quantitative changes in keratocyte density. METHODS: Twenty neophyte subjects aged 26 +/- 3 years participated in the study, which was conducted over the course of three experimental sessions. In the first session, one eye of each subject was fitted with a silicone hydrogel contact lens, and the other eye served as the control. Both corneas were exposed to an anoxic environment for 2 hours. Ultrasound pachometry and confocal microscopy were performed on both eyes at baseline, immediately after the experiment and 2 hours post experiment. This procedure was repeated after 72 hours, but in this case one eye of each subject was fitted with a hyper-Dk rigid contact lens, and the fellow eye served again as the control. In the third experimental session, each subject was asked to periodically rub one eye only. Tear samples collected from the rubbed and control eyes were assayed for epidermal growth factor (EGF), hepatocyte growth factor (HGF), and interleukin (IL)-8. RESULTS: The increase in corneal thickness was similar in the experimental and control eyes. Both anterior and posterior keratocyte densities decreased in the experimental eyes compared with the control eyes, in all sessions. EGF and IL-8 concentrations were increased in the rubbed eyes compared with the control eyes. CONCLUSIONS: It is hypothesized that the mechanical stimulation of the corneal surface, due to the physical presence of a contact lens, induces the release of inflammatory mediators that cause keratocyte dysgenesis or apoptosis. Copyright Association for Research in Vision and Ophthalmology