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Editors Selection IGR 11-1

Experimental Glaucoma: Scleral biomechanics and RGC

Comment by Crawford Downs on:

52697 Studies of scleral biomechanical behavior related to susceptibility for retinal ganglion cell loss in experimental mouse glaucoma, Nguyen C; Cone FE; Nguyen TD et al., Investigative Ophthalmology and Visual Science, 2013; 54: 1767-1780

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Optic nerve head (ONH) biomechanics likely plays an important role in the development and progression of glaucoma, but it is not well understood. Experimental and numerical studies indicate that the peripapillary sclera is influential in determining ONH biomechanics, as this ring of sclera defines the mechanical boundary condition for the contained ONH at the scleral canal. Nguyen, Quigley and colleagues induced chronic IOP elevations with anterior chamber bead injection in 43 eyes of CD1 mice and 42 eyes of B6 mice. They then compared scleral shell size, thickness, and estimated mechanical strains in the experimental glaucoma eyes to 126 and 128 control eyes from CD1 and B6 mice, respectively. The peripapillary sclera thinned, and axial length and width increased in the elevated IOP eyes compared with fellow control eyes. Mechanical scleral strains were lower in the elevated IOP eyes, indicating an increased structural stiffness in the glaucoma eyes. These results together suggest that the sclera exhibits a strong connective tissue remodeling response when exposed to chronically elevated IOP, which is the most important contribution of the work, and mimics results seen in previous studies of human donor eyes and the nonhuman primate model of experimental glaucoma. When compared to the B6 mice, CD1 mice exhibited greater axial length, higher strains in the temporal region, and thinning of the peripheral sclera in the glaucoma eyes. The CD1 mice also exhibited greater axonal loss than B6 mice, which the authors attribute to scleral biomechanics as stated in the manuscript title. However, the majority of the murine ONH is surrounded by a vascular plexus at the scleral canal that shields the axons from direct mechanical insult from peripapillary scleral strain. Also, it may be that differences between the strains in some other factor underlie the observed differences in axonal susceptibility. There are no data in the study that link peripapillary scleral biomechanics to axonal damage, so direct evidence of the biomechanical mechanisms of ONH axon loss in glaucoma remains elusive.

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