Jean Marc Perone1, Jean Baptiste Conart, Pierre-Jean Bertaux, Nicolas Sujet-Perone, Nadia Ouamara, Maxime Sot, Jean Jacques Henry. 1. *Department of Ophthalmology, Regional Hospital Center of Metz-Thionville, Mercy Hospital, Metz, France; †Ophthalmology Department, University Hospital Center of Nancy Brabois, Nancy, France; ‡Clinical Research Department, Regional Hospital Center of Metz-Thionville, Mercy Hospital, Metz, France; and §Technological Universitary Institut, GMP Department, Lorraine University, Metz, France.
Abstract
PURPOSE: We created a laboratory model of a cornea that was subjected to various pressures and thermal and mechanical factors to better understand the genesis of keratoconus deformation. METHODS: A steel base allowed for fixation of circular multilaminated patches of araldite (10 cm in diameter, 5 mm thick) in which the corneal anatomy was modeled. The model was plunged into a steam room (374°F/3 bars of pressure for 1 h) to ensure thermal homogeneity and was subjected to pressure using compressed air. Three models were assessed: a fault-free model with no lesion (model 1), and 2 models with a defect. The first of the defective models (model 2) had an external crack-type lesion (1 cm long; 1 mm deep). The second defective model (model 3) had one quarter thinned down using abrasive sandpaper (thickness reduced by 30%-40%). RESULTS: For model 1, which represented a healthy cornea, homogeneous modification was noted when examined under polarized light. In model 2, no excessive deformation was noticed, but there were stress lines at the edge of the lesion. Model 3 had a deformity, similar to keratoconic deformation. CONCLUSIONS: Our findings suggest that the disease progresses under environmental stresses, but only when there is an initial defect, and especially when there is a thinning down defect. This thinning down defect may be induced by continual eye rubbing.
PURPOSE: We created a laboratory model of a cornea that was subjected to various pressures and thermal and mechanical factors to better understand the genesis of keratoconus deformation. METHODS: A steel base allowed for fixation of circular multilaminated patches of araldite (10 cm in diameter, 5 mm thick) in which the corneal anatomy was modeled. The model was plunged into a steam room (374°F/3 bars of pressure for 1 h) to ensure thermal homogeneity and was subjected to pressure using compressed air. Three models were assessed: a fault-free model with no lesion (model 1), and 2 models with a defect. The first of the defective models (model 2) had an external crack-type lesion (1 cm long; 1 mm deep). The second defective model (model 3) had one quarter thinned down using abrasive sandpaper (thickness reduced by 30%-40%). RESULTS: For model 1, which represented a healthy cornea, homogeneous modification was noted when examined under polarized light. In model 2, no excessive deformation was noticed, but there were stress lines at the edge of the lesion. Model 3 had a deformity, similar to keratoconic deformation. CONCLUSIONS: Our findings suggest that the disease progresses under environmental stresses, but only when there is an initial defect, and especially when there is a thinning down defect. This thinning down defect may be induced by continual eye rubbing.