Measuring the Biaxial Stress-Strain Characteristics of Human Sclera

2007 ◽  
Author(s):  
C. G. Olesen ◽  
I. Tertinegg ◽  
A. Eilaghi ◽  
G. W. Brodland ◽  
C. Horst ◽  
...  
Keyword(s):  
Risk Factor ◽  
Intraocular Pressure ◽  
Optic Nerve ◽  
Ganglion Cell ◽  
Mechanical Strain ◽  
Biaxial Stress ◽  
Retinal Ganglion ◽  
Irreversible Loss ◽  
Elevated Intraocular Pressure ◽  
Primary Risk Factor

Glaucoma is a common ocular disease that causes irreversible loss of vision. Elevated intraocular pressure (IOP) is the primary risk factor for developing glaucoma. It is believed that increased IOP causes mechanical strain on the glial cells that support the retinal ganglion cell axons and thereby causes ganglion cell apoptosis [1,2]. This damage occurs in the optic nerve head (ONH) region of the eye, and is important for understanding ONH biomechanics.

scholarly journals An Overview of Glaucoma: Bidirectional Translation between Humans and Pre-Clinical Animal Models

2021 ◽  
Author(s):  
Sophie Pilkinton ◽  
T.J. Hollingsworth ◽  
Brian Jerkins ◽  
Monica M. Jablonski
Keyword(s):  
Risk Factor ◽  
Intraocular Pressure ◽  
Optic Nerve ◽  
Animal Models ◽  
Retinal Ganglion Cells ◽  
Optic Nerve Head ◽  
Ganglion Cells ◽  
Treatment Modalities ◽  
Retinal Ganglion ◽  
Glaucomatous Damage

Glaucoma is a multifactorial, polygenetic disease with a shared outcome of loss of retinal ganglion cells and their axons, which ultimately results in blindness. The most common risk factor of this disease is elevated intraocular pressure (IOP), although many glaucoma patients have IOPs within the normal physiological range. Throughout disease progression, glial cells in the optic nerve head respond to glaucomatous changes, resulting in glial scar formation as a reaction to injury. This chapter overviews glaucoma as it affects humans and the quest to generate animal models of glaucoma so that we can better understand the pathophysiology of this disease and develop targeted therapies to slow or reverse glaucomatous damage. This chapter then reviews treatment modalities of glaucoma. Revealed herein is the lack of non-IOP-related modalities in the treatment of glaucoma. This finding supports the use of animal models in understanding the development of glaucoma pathophysiology and treatments.

Interactions Between Factors Influencing Optic Nerve Head Biomechanics

2007 ◽  
Author(s):  
Ian A. Sigal ◽  
John G. Flanagan ◽  
C. Ross Ethier
Keyword(s):  
Optic Nerve ◽  
Optic Nerve Head ◽  
Mechanical Response ◽  
Ganglion Cells ◽  
Cell Damage ◽  
Mechanical Strain ◽  
Lamina Cribrosa ◽  
Retinal Ganglion ◽  
The Finite Element Method ◽  
Primary Risk Factor

Glaucoma is the second most common cause of blindness worldwide, and elevated intraocular pressure (IOP) is the primary risk factor for developing this disease. It has been postulated that IOP-induced mechanical strain on optic nerve head (ONH) glial cells leads to retinal ganglion cell damage and the consequent loss of vision in glaucoma. To better evaluate this theory it is important to understand the biomechanical environment within the ONH. Unfortunately it is very difficult to make measurements in the ONH, and it is particularly difficult to access the region in the ONH where the ganglion cells are thought to be injured, namely the lamina cribrosa. We have therefore developed models of the ONH and used the finite element method (FEM) to predict ONH mechanical response to changes in IOP [1].

Scleral Biomechanics in the Glaucomatous Monkey Eye

2009 ◽  
Author(s):  
Michaël J. A. Girard ◽  
Jun-Kyo F. Suh ◽  
Michael Bottlang ◽  
Claude F. Burgoyne ◽  
J. Crawford Downs
Keyword(s):  
Intraocular Pressure ◽  
Optic Nerve ◽  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Nutritional Support ◽  
Lamina Cribrosa ◽  
Collagen Fibers ◽  
Type I ◽  
Retinal Ganglion ◽  
The Brain

The sclera is the outer shell and principal load-bearing tissue of the eye, and consists primarily of avascular lamellae of collagen fibers. Ninety percent of the collagen fibers in the sclera are Type I, which provide the eye with necessary mechanical strength to withstand intraocular pressure (IOP). A small hole pierces the posterior sclera, known as the scleral canal, through which the retinal ganglion cell axons turn and pass out of the eye on their path to the brain. The scleral canal is spanned by a fenestrated connective tissue called the lamina cribrosa that provides structural and nutritional support to the axons as they leave the eye. This region, including the peripapillary sclera (the sclera closest to the canal), the lamina cribrosa, and the contained retinal ganglion cell axons, is collectively known as the optic nerve head or ONH.

scholarly journals Elevated Intraocular Pressure Causes Abnormal Reactivity of Mouse Retinal Arterioles

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Adrian Gericke ◽  
Carolina Mann ◽  
Jenia Kouchek Zadeh ◽  
Aytan Musayeva ◽  
Ismael Wolff ◽  
...  
Keyword(s):  
Intraocular Pressure ◽  
Ganglion Cell ◽  
Blood Vessels ◽  
Retinal Ganglion Cell ◽  
Ganglion Cell Layer ◽  
Cell Layer ◽  
Retinal Ganglion ◽  
Retinal Arterioles ◽  
Retinal Ganglion Cell Layer ◽  
Elevated Intraocular Pressure

Objective. Glaucoma is a leading cause of severe visual impairment and blindness. Although high intraocular pressure (IOP) is an established risk factor for the disease, the role of abnormal ocular vessel function in the pathophysiology of glaucoma gains more and more attention. We tested the hypothesis that elevated intraocular pressure (IOP) causes vascular dysfunction in the retina. Methods. High IOP was induced in one group of mice by unilateral cauterization of three episcleral veins. The other group received sham surgery only. Two weeks later, retinal vascular preparations were studied by video microscopy in vitro. Reactive oxygen species (ROS) levels and expression of hypoxia markers and of prooxidant and antioxidant redox genes as well as of inflammatory cytokines were determined. Results. Strikingly, responses of retinal arterioles to stepwise elevation of perfusion pressure were impaired in the high-IOP group. Moreover, vasodilation responses to the endothelium-dependent vasodilator, acetylcholine, were markedly reduced in mice with elevated IOP, while no differences were seen in response to the endothelium-independent nitric oxide donor, sodium nitroprusside. Remarkably, ROS levels were increased in the retinal ganglion cell layer including blood vessels. Expression of the NADPH oxidase isoform, NOX2, and of the inflammatory cytokine, TNF-α, was increased at the mRNA level in retinal explants. Expression of NOX2, but not of the hypoxic markers, HIF-1α and VEGF-A, was increased in the retinal ganglion cell layer and in retinal blood vessels at the protein level. Conclusion. Our data provide first-time evidence that IOP elevation impairs autoregulation and induces endothelial dysfunction in mouse retinal arterioles. Oxidative stress and inflammation, but not hypoxia, appear to be involved in this process.

scholarly journals Natural Products: Evidence for Neuroprotection to Be Exploited in Glaucoma

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3158
Author(s):  
Annagrazia Adornetto ◽  
Laura Rombolà ◽  
Luigi Antonio Morrone ◽  
Carlo Nucci ◽  
Maria Tiziana Corasaniti ◽  
...  
Keyword(s):  
Natural Products ◽  
Risk Factor ◽  
Intraocular Pressure ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Main Risk Factor ◽  
Number Of Patients ◽  
Elevated Intraocular Pressure ◽  
Underlying Mechanisms

Glaucoma, a leading cause of irreversible blindness worldwide, is an optic neuropathy characterized by the progressive death of retinal ganglion cells (RGCs). Elevated intraocular pressure (IOP) is recognized as the main risk factor. Despite effective IOP-lowering therapies, the disease progresses in a significant number of patients. Therefore, alternative IOP-independent strategies aiming at halting or delaying RGC degeneration is the current therapeutic challenge for glaucoma management. Here, we review the literature on the neuroprotective activities, and the underlying mechanisms, of natural compounds and dietary supplements in experimental and clinical glaucoma.

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