title: Altering the way the optic nerve head responds to intraocular pressure-a potential approach to glaucoma therapy.
abstract: Over the past decade, engineering principles have been used to explain why a mechanical load, intraocular pressure, can lead to the development of glaucomatous optic neuropathy. This has led to the 'biomechanical theory' of glaucoma, which posits that the behavior of optic nerve head connective tissues (specifically within the peripapillary sclera and lamina cribrosa) in response to intraocular pressure (regardless of its magnitude) can directly and indirectly influence the physiology and pathophysiology of the optic nerve head. Given that the biomechanics of the sclera and lamina cribrosa probably influence retinal ganglion cell loss in glaucoma, the idea that altering biomechanical behavior might be protective against glaucoma is an appealing notion. There is some evidence to suggest that stiffening the peripapillary sclera may be protective against the development of glaucoma in an animal model. It is technically possible to stiffen the sclera in vivo using collagen cross-linking techniques already applied in vivo to the cornea in the treatment of keratoconus. It has yet to be established whether scleral cross-linking is safe in humans and that it confers anything more than a theoretical advantage in terms of reducing the risk of glaucomatous damage.
authors.affiliation: NIHR Biomedical Research Centre at Moorfields Eye Hospital NHS Foundation Trust and UCL Institute of Ophthalmology, London, EC1 V 2PD, UK. nick.strouthidis@moorfields.nhs.uk
authors.forename: Nicholas G
authors.initials: NG
authors.lastname: Strouthidis
authors.forename: Michael J A
authors.initials: MJ
authors.lastname: Girard
mesh_terms: D000818:Animals; D001696:Biomechanical Phenomena; D005901:Glaucoma / Q000150:complications / Q000503:physiopathology / Q000628:therapy*; D006801:Humans; D007429:Intraocular Pressure / Q000502:physiology*; D009898:Optic Disk / Q000502:physiology*; D009901:Optic Nerve Diseases / Q000209:etiology / Q000503:physiopathology; D012590:Sclera / Q000502:physiology