Mechanisms of Glaucoma in Exfoliation Syndrome
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Abstract:
The most important characteristic of exfoliation syndrome (XFS) is that it involves a greater risk of developing glaucoma. In comparison with other forms of open-angle glaucoma, exfoliation glaucoma is more resistant to medical therapy and progresses faster. Possible pathologic mechanisms of glaucoma development in XFS comprise: (1) elevated intraocular pressure (IOP) caused by functional impairment of aqueous humor outflow due to deposition of exfoliation material in the trabecular meshwork and trabecular cell dysfunction, (2) XFS-associated connective tissue elastosis leading to structural and functional alterations of the lamina cribrosa which increases the vulnerability toward elevated IOP and development of glaucomatous optic neuropathy, (3) elevated IOP due to closure of the anterior chamber angle accompanied by forward displacement of the crystalline lens due to zonular weakness, (4) presumable primary functional impairment of retinal ganglion cells. In addition to the discovery of lysyl oxidase-like 1, further genetic associations have been identified and knowledge related to XFS etiology and pathophysiology has markedly increased over the past 10 years. Further cell biological investigations navigated by the molecular genetics underlying XFS will eventually lead to a better understanding of the complex mechanisms of exfoliation glaucoma.Primary (astronomy)
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To observe open angle glaucoma in the presence of low intra-ocular pressure. Methods: A descriptive cross-sectional study was done on 150 patients who attended the glaucoma clinic during one year from January 2005 to January 2006. A detailed history was obtained and a thorough ophthalmic examination was performed, including gonioscopy, ophthalmoscopy, applanation tonometery and automated perimetery. Results: Out of 150 patients of Primary open angle glaucoma 33 patients (22%) were found to have glaucoma at intra-ocular pressure level below normal (low pressure glaucoma), with mean age 56±9.21 years. Mean age of Primary open angle glaucoma group was 52.5±8.7%. Of the 33 cases of low-pressure glaucoma (22 patients) 66.6% were male and (11 patients) 33.4% were female, while in Primary open angle glaucoma (82 patients) 70% were male and (35 patients) 30% were female. Mean intra ocular pressure was 15.13±3.60 mm Hg in low-pressure glaucoma and 28±6.5 mm Hg) in Primary open angle glaucoma. Maximum intra ocular pressure in Low-pressure glaucoma group was 21 mm Hg and minimum Intra ocular pressure was observed as 8 mm Hg, while these values observed as 50 mm Hg and 10 mm Hg respectively in primary open angle glaucoma. Conclusions: Low pressure glaucoma remains a difficult diagnosis for ophthalmologist who favors the argument that raised Intra ocular pressure is essential for the diagnosis of Primary open angle glaucoma. Low pressure glaucoma changes the definition of glaucoma and our concept of intra ocular pressure as a sole etiological factor is now out dated.
Gonioscopy
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Glaucoma has been one of the world’s greatest challenges in medicine. Glaucoma is a group of eye related diseases which causes damage to the optic nerve and in the long run affecting vision or causing vision loss. Open angle glaucoma is damage to the optic nerve, usually caused by high intraocular pressure. Open angle glaucoma falls under the types of glaucoma. There are typically no early warning signs or painful symptoms of open angle glaucoma. It develops slowly and sometimes without noticeable sight loss for many years. Open angle glaucoma is the most common form of eye diseases.
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Achievement of target intraocular pressure is the goal of every efficient antiglaucoma therapy. Target intraocular pressure is the level of intraocular pressure which is associated with minimal likelihood of visual field or optic nerve lesion, or an existing lesion progression due to elevated intraocular pressure. Results of large clinical studies which have offered some new concepts on target intraocular pressure in the management of glaucoma are reviewed. An association between the curve of intraocular pressure decrease and glaucoma progression was demonstrated in these studies. Generally, a lower value of target intraocular pressure implies better protection from the loss of vision and visual field impairment in glaucoma patients. In advanced glaucoma, the greatest possible reduction from the initial intraocular pressure should be attempted. A 20% reduction from the initial intraocular pressure or decrease to < 18 mmHg in advanced glaucoma has been recognized as a favorable strategy to reach target intraocular pressure. In normal tension glaucoma, a lower value of target intraocular pressure is associated with a slower disease progression. In patients with initial glaucoma, 25% reduction from the initial intraocular pressure will slow down the disease progression by 45%. The value of target intraocular pressure depends on the pretreatment level of intraocular pressure, optic nerve condition, glaucoma disease state, rate of glaucoma progression, patient's age, and other risk factors for the development of glaucoma.
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Background: Glaucoma is one of the most common causes of blindness and is usually associated with elevated intraocular pressure. In patients with primary open angle glaucoma the number of trabecular meshwork cells is decreased. Death of the trabecular meshwork cells may be a result of apoptosis. Objective: To investigate the aqueous humor levels of soluble Fas (sFas) and Fas-Ligand (sFasL) in glaucomatous patients. Methods: Concentration of sFas and sFasL were measured by ELISA in 41 eyes with glaucoma (21 with pseudoexfoliation and 20 with primary open angle glaucoma) and 39 eyes with cataract as controls. Results: The sFas concentration was lower in the primary open angle than the pseudoexfoliation glaucoma and the cataract groups (p=0.002 and p= 0.004, respectively). The sFasL level did not show any significant difference in the three groups. Conclusion: A lower level of sFas may provide proper microenvironment for increased apoptosis of trabecular meshwork cells in primary open angle glaucoma.
Pseudoexfoliation syndrome
Pseudoexfoliation
Aqueous humour
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To determine if the expression of endothelial leukocyte adhesion molecule 1 (ELAM-1) in the trabecular meshwork system of the porcine eye, when subjected to experimental glaucoma, is increased as it does in human glaucoma.Immunohistochemistry using a specific mouse antihuman ELAM-1 antibody was performed on the trabecular meshwork system of five pigs. The episcleral veins of the left eyes were cauterized as reported elsewhere to induce glaucoma. Immunodetection of ELAM-1 was assayed in human trabecular meshwork samples obtained from trabeculectomy as a positive control.Pig eyes exhibiting elevated intraocular pressure (IOP) and damage to retinal ganglion cells (RGCs) due to experimental glaucoma as reported elsewhere, were found to exhibit ELAM-1 immunoreactivity in their trabecular meshwork.ELAM-1 protein, the first molecular marker for human glaucoma, can also be considered a candidate molecular marker of induced glaucoma in the pig model of experimental glaucoma. The results of our study further validated the pig eye as an animal model of glaucoma, since increased expression of ELAM-1, which has been found in the trabecular meshwork of human eyes with glaucoma, is also found in pig eyes subjected to experimental glaucoma via episcleral vein cauterization.
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Ocular corticosteroids are commonly used clinically. Unfortunately, their administration frequently leads to ocular hypertension, i.e., elevated intraocular pressure (IOP), which, in turn, can progress to a form of glaucoma known as steroid-induced glaucoma. The pathophysiology of this condition is poorly understood yet shares similarities with the most common form of glaucoma. Using nanotechnology, we created a mouse model of corticosteroid-induced ocular hypertension. This model functionally and morphologically resembles human ocular hypertension, having titratable, robust, and sustained IOPs caused by increased resistance to aqueous humor outflow. Using this model, we then interrogated the biomechanical properties of the trabecular meshwork (TM), including the inner wall of Schlemm's canal (SC), tissues known to strongly influence IOP and to be altered in other forms of glaucoma. Specifically, using spectral domain optical coherence tomography, we observed that SC in corticosteroid-treated mice was more resistant to collapse at elevated IOPs, reflecting increased TM stiffness determined by inverse finite element modeling. Our noninvasive approach to monitoring TM stiffness in vivo is applicable to other forms of glaucoma and has significant potential to monitor TM function and thus positively affect the clinical care of glaucoma, the leading cause of irreversible blindness worldwide.
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Glaucoma is the second leading cause of irreversible blindness in the world according to the World Health Organization. It is characterized by the progressive degeneration of the optic nerve and despite the significant advances in the field, a cure for glaucoma remains to be found. The trabecular meshwork (TM) has been identified as the key tissue that drives pressure regulation in eye. In this review, we look over the main role of the aforementioned meshwork, as well as its outflow physiology and pathology. Research in the field of glaucoma has mostly progressed by employing animal models. However, these models are often expensive, cumbersome and exhibit a high intra-species variability. The lack of 3D in vitro models complicates the study of TM pressure regulation mechanisms, which makes it difficult to make progress in glaucoma research. In this paper, we review the time evolution of glaucoma models and discuss the ways in which tissue engineering fabrication techniques can be applied to create an artificial TM that serves as a 3D in vitro model. We also study possible outflow evaluation systems that are valid for both scaffold testing and drug screening, which may improve the understanding of TM biology.
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