Etiology of Keratoconus: proposed biomechanical pathogenesis

Abstract

Abstract Background The etiology of keratoconus most likely involves substantial biomechanical interactions. The goal of this study was to characterize corneal biomechanics using computer modeling techniques in order to elucidate the pathogenesis of keratoconus in biomechanical terms. Methods Finite element models of the cornea that are based on anatomical dimensions were developed. Cases comprising of thinned regions as well as regions with degraded isotropic mechanical properties and a case of gradual stiffening towards the limbus were subjected to normal intraocular pressures. The resulting deformations and dioptric power maps were analyzed and compared. Three additional cases that are based on a model of a thin plate were used to demonstrate the effect a transition from orthotropic to isotropic mechanical properties would have in terms of deformations and diopteric power maps. Results Results show that under 10mmHg intraocular pressure, decreasing the modulus of elasticity and thinning have opposite effects on the dioptric power maps of a homogenous isotropic cornea. When the thickness was maintained at 500 microns and the stiffness was decreased from 0.4 MPa to 0.04 MPa there was an increase of more than 40 diopters. For a cornea with a constant modulus of elasticity value of 0.4 MPa, 350 microns decrease in thickness resulted in a decrease of approximately 25 diopters. The anisotropic non-homogenous characteristics of the cornea have shown to be critical for maintaining the morphology of a healthy corneal. Conclusions Degradation of the circumferential fibers may very well be an initiating factor of a biomechanical process in which a bulge is gradually created from a presumably healthy cornea under normal underlying pressures and therefore, the identification of the early stages of keratoconus might be achievable by monitoring the in-vivo corneal fiber distribution.