Purpose. To investigate the effects of Fuchs’ corneal dystrophy (FCD) on corneal biomechanical properties and the results of IOP readings in relation to changes in corneal hysteresis (CH) and central corneal thickness (CCT). methods. Corneal biomechanical properties, including CH, corneal resistance factor (CRF), and CCT, were measured with the ocular response analyzer (ORA) in 11 eyes of 11 patients with clinically confirmed FCD and 12 eyes of 12 healthy subjects. The ORA was also used to determine the values of intraocular pressure (IOP_g) and corneal compensated IOP (IOP_cc). Goldmann applanation tonometry (GAT) was also measured. results. CH measured 10.3 ± 1.6 mm Hg (range, 8.7–13.8) in normal eyes and 6.9 ± 1.8 mm Hg (range, 4.6–11.7) in FCD eyes (P = 0.001). CRF in the normal and FCD eyes was 10.5 ± 1.5 mm Hg (range, 8.5–13.3) and 8.1 ± 1.9 (range, 4.5–11.2), respectively (P = 0.005). CCT was higher in FCD eyes (606 ± 20 μm; range, 578–635) than in normal eyes (538.4 ± 24.9 μm; range, 495–575; P = 0.0001). IOP_g was 16.2 ± 2.2 mm Hg (range, 13.5–18.7) in control eyes compared with 17.6 ± 2.7 mm Hg (range, 12.8–18.6) in FCD eyes (P = 0.201). However, IOP_cc in the FCD group (21.8 ± 4.6 mm Hg; range, 12.8–29.0) was higher than in the control group (16.5 ± 3.4 mm Hg; range, 11.9–23.9; P = 0.006). GAT in the normal and FCD eyes was 16.7 ± 2.1 mm Hg (range, 12.8–18.6) and 16.9 ± 2.3 mm Hg (range, 13.1–19.0), respectively (P = 0.205). conclusions. FCD led to a change of corneal biomechanical properties. CH and CRF were significantly lower in FCD eyes than in normal eyes. IOP_cc was significantly higher in FCD eyes than in control eyes. These values may be useful in addition to CCT when assessing corneal rigidity. Thus, FCD may cause an underestimation error in IOP measurement.

The modification of the mechanical properties of the human crystalline lens with age can be a major cause of presbyopia. Since these properties cannot be measured in vivo, numerical simulation can be used to estimate them. We propose an inverse method to determine age-dependent change in the material properties of the tissues composing the human crystalline lens. A finite element model of a 30-year-old lens in the accommodated state was developed. The force necessary to achieve full accommodation in a 30-year-old lens of known external geometry was computed using this model. Two additional numerical models of the lens corresponding to the ages of 40 and 50 years were then built. Assuming that the accommodative force applied to the lens remains constant with age, the material properties of nucleus and cortex were estimated by inverse analysis. The zonular force necessary to reshape the model of a 30-year-old lens from the accommodated to the unaccommodated geometry was 0.078 newton (N). Both nucleus and cortex became stiffer with age. The stiffness of the nucleus increased with age at a higher rate than the cortex. In agreement with the classical theory of Helmholtz, on which we based our model, our results indicate that a major cause of presbyopia is that both nucleus and cortex become stiffer with age; therefore, a constant value of the zonular forces with aging does not achieve full accommodation, that is, the accommodation capability decreases.

In the last decade, we have witnessed substantial progress in our understanding of corneal biomechanics and architecture. It is well known that diabetes is a systemic metabolic disease that causes chronic progressive damage in the main organs of the human body, including the eyeball. Although the main and most widely recognized ocular effect of diabetes is on the retina, the structure of the cornea (the outermost and transparent tissue of the eye) can also be affected by the poor glycemic control characterizing diabetes. The different corneal structures (epithelium, stroma, and endothelium) are affected by specific complications of diabetes. The development of new noninvasive diagnostic technologies has provided a better understanding of corneal tissue modifications. The objective of this review is to describe the advances in the knowledge of the corneal alterations that diabetes can induce.