Scleral biomechanics in the normal, glaucomatous and aging eye
Description
Glaucoma is the second leading cause of blindness worldwide and is characterized by an irreversible damage to the retinal ganglion cell axons within the optic nerve head (ONH). Once thought to only occur at elevated levels of intraocular pressure (IOP), glaucoma can develop at normal levels without distinct etiology. Since IOP alone cannot explain the development and progression of the disease, we have theorized that the biomechanics of the ONH plays a central role in driving several pathologic mechanisms that can lead to the neuropathy The ONH is embedded within the posterior scleral shell - the white outer coat of the eye. From a biomechanical perspective, the sclera directly transmits IOP-induced stress and strain to the ONH, and we therefore hypothesize that the biomechanical behavior of the sclera contributes to the development and progression of glaucoma Our objective is to use state-of-the-art experimental and computational tools to characterize scleral biomechanics in normal and glaucomatous monkey eyes. Because the prevalence of glaucoma increases exponentially with age, we additionally characterize scleral biomechanics in the aging monkey eye to investigate the underlying mechanisms for the age-related increased susceptibility to glaucoma We introduce a constitutive model for the posterior sclera that includes stretch-induced stiffening and multi-directionality of the collagen fibers. Application of this model to an idealized eye geometry shows that scleral collagen fibers have a strong impact on ONH deformations. By experimentally measuring IOP-induced 3-D scleral deformations, and regional variations in scleral topography and thickness, we characterize the mechanical properties of individual scleral shells using an inverse finite element (FE) method. We show that monkey posterior sclera (1) is a nonlinear, anisotropic, inhomogeneous tissue, (2) stiffens with age, (3) is biomechanically altered in some, but not all, glaucomatous eyes. In normal eyes, we suggest that the sclera shields the ONH from biomechanical insult by resisting large deformations (nonlinearity), and scleral canal expansion (anisotropy). We suggest that age-related scleral stiffening could dramatically impact the homeostasis of the ONH. Finally, we suggest that scleral remodeling occurs in glaucomatous eyes to prevent further increase in ONH deformations and thus inhibits progression of the disease