Corneal biomechanics, natural geometry, and intraocular pressure (IOP) determine corneal topography and consequently optical quality. For corneas affected by the ectatic disorder of keratoconus (KC), more factors need to be considered. One of the principal challenges that KC presents to clinicians is not fully understanding the etiology of the disease, although, some progress has been achieved in exploring structural changes and using cross-linking (CXL) to halt the progression of the disease. The focus of this dissertation was to develop a finite element model (FEM) of the cornea to investigate the impact of KC and CXL on optical aberrations.

First, we developed a finite element model of the human cornea that can capture the biomechanics of keratoconus and crosslinking through localized material property changes to test the impact of different input variables. We concluded that input variables such as degree of asymmetry of the natural geometry, depth dependence of material properties, and fibers' degree of dispersion play a key role in the outcomes of the model. All the variables deemed most important were incorporated into the model following their most realistic settings while variables with less impact were treated through a simpler approach based on the principles of DOE and ANOVA.

The KC model captures the thinning and bulging typical of early stages of the ectatic disorder, by altering material properties locally, without superimposing thickness change. This is relevant because the localized thinning is a key indicator of KC and previous FEM have imposed the thickness change in the model. In addition, optical features associated with KC were observed in our model of KC such as the increment in curvature (+4 D), as well as the significant increments in vertical coma and HOAs. Clinical references confirmed the trend observed in aberrations computed from our model agreed with the observed in KC. Especially, the increment in vertical coma (and total coma), as well as HOAs which percent relative to the total aberrations increases considerably for KC corneas.

With the FEM of keratoconic corneas, studies of further weakening of the tissue and increment of the KC region were conducted. The stress plots and relative worsening of aberrations were more significant when the KC region size increased. These particular results suggest that progression might be linked to the stresses concentrated around the limits of the KC region causing healthy tissue to deteriorate expanding the KC region.

In addition, crosslinking treatment was simulated on the keratoconic cornea models. The CXL treatment was imposed as a local change in material properties (C10). The stiffening effect was confirmed through curvature flattening, reduction of strain and stresses, particularly the concentrated stresses in the limits of the KC region, as well as changes in optical aberrations. Furthermore, two variants of the potential stiffening gradient across depth were evaluated. Both profiles maintain a gradient where anterior layers of the cornea are stiffer than posterior layers. For these cases, no significant differences in stress, or aberrations were observed.