Submitted Successfully!
To reward your contribution, here is a gift for you: A free trial for our video production service.
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Version Summary Created by Modification Content Size Created at Operation
1 -- 408 2022-12-01 06:40:08 |
2 formatted Meta information modification 408 2022-12-01 06:41:48 |

Video Upload Options

Do you have a full video?

Confirm

Are you sure to Delete?
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Macanian, J.;  Sharma, S.C. Pathogenesis of Glaucoma. Encyclopedia. Available online: https://encyclopedia.pub/entry/37531 (accessed on 24 April 2024).
Macanian J,  Sharma SC. Pathogenesis of Glaucoma. Encyclopedia. Available at: https://encyclopedia.pub/entry/37531. Accessed April 24, 2024.
Macanian, Jason, Sansar C. Sharma. "Pathogenesis of Glaucoma" Encyclopedia, https://encyclopedia.pub/entry/37531 (accessed April 24, 2024).
Macanian, J., & Sharma, S.C. (2022, December 01). Pathogenesis of Glaucoma. In Encyclopedia. https://encyclopedia.pub/entry/37531
Macanian, Jason and Sansar C. Sharma. "Pathogenesis of Glaucoma." Encyclopedia. Web. 01 December, 2022.
Peer Reviewed
Pathogenesis of Glaucoma

Glaucoma, a neurodegenerative disease, has a varied pathogenesis scenario, including elevated intraocular pressure (IOP), and hypoxic conditions in the retina. Consequently, degenerating optic axons at the optic nerve head are observed clinically when extensive damage has already occurred. Following elevated IOP, changes in retinal ganglion cells lead to apoptosis immediately followed by degeneration of their optic axons. Degradation of axons leads to cupping of the optic nerve head and visual field losses. Here we emphasize that it is the retinal ganglion cells that are initial targets of elevated IOP, and, together with hyperactivity of retinal astrocytes, create the ischemic conditions which represent the earliest sign in the pathogenesis of glaucoma.

elevated IOP reactive astrocytes apoptosis retinal ganglion cells glaucoma
Glaucoma is a group of progressive eye disorders that is characterized by damage to the optic nerve head because of the breakdown of retinal ganglion cells and their axons which merge to form the optic nerve. Glaucoma is the leading cause of irreversible blindness, with more than 80 million people estimated to be affected by the disease worldwide. This number is projected to exceed 110 million by 2040 [1].
Glaucoma is associated with numerous risk factors including, but not limited to, age, gender, smoking history, race, and elevated intraocular pressure. Reports show a 36% greater prevalence of glaucoma in males than in females [2]. Risk of developing glaucoma has also been shown to increase with age [3]. Of individuals aged 40 years and above, 5.7% of Blacks have glaucoma whereas only 2.2% of white people do [4]. It is worth noting that, perhaps due to lack of access to glaucoma screening and to treatment, glaucoma is often undiagnosed. Previous reports have indicated that more than 50% of people with glaucoma are undiagnosed [5][6]. In an effort to address this public health crisis, it is important to establish methods for screening patients for risk factors of glaucoma worldwide.
Glaucoma is strongly associated with increased intraocular fluid pressure (IOP), as the aqueous humor exerts increased force per area than usual on the internal surface of the eye. This may occur in glaucoma because of blockages in the trabecular meshwork (TM) of the eye, which normally functions to drain aqueous humor from the anterior chamber. Poor drainage results in the accumulation of aqueous humor and causes IOP elevation. Glaucomatous eyes with elevated intraocular pressure have been shown to exhibit abnormalities in both the extracellular matrices of the retina and lamina cribrosa, which result in decreased function of the optic nerve and therefore lower visual acuity [7].

References

  1. Allison, K.; Patel, D.; Alabi, O. Epidemiology of Glaucoma: The Past, Present, and Predictions for the Future. Cureus 2020, 12, e11686.
  2. Tham, Y.-C.; Li, X.; Wong, T.Y.; Quigley, H.A.; Aung, T.; Cheng, C.-Y. Global Prevalence of Glaucoma and Projections of Glaucoma Burden through 2040: A Systematic Review and Meta-Analysis. Ophthalmology 2014, 121, 2081–2090.
  3. McMonnies, C.W. Glaucoma history and risk factors. J. Optom. 2017, 10, 71–78.
  4. Kelly, E.; Wen, Q.; Haddad, D.; O’Banion, J. Effects of an Aging Population and Racial Demographics on Eye Disease Prevalence: Projections for Georgia Through 2050. Am. J. Ophthalmol. 2020, 210, 35–40.
  5. Topouzis, F.; Coleman, A.L.; Harris, A.; Koskosas, A.; Founti, P.; Gong, G.; Yu, F.; Anastasopoulos, E.; Pappas, T.; Wilson, M.R. Factors Associated with Undiagnosed Open-Angle Glaucoma. Am. J. Ophthalmol. 2008, 145, 327–335.
  6. Quigley, H.A. Number of people with glaucoma worldwide. Br. J. Ophthalmol. 1996, 80, 389–393.
  7. Wallace, D.M.; O’Brien, C.J. The role of lamina cribrosa cells in optic nerve head fibrosis in glaucoma. Exp. Eye Res. 2016, 142, 102–109.
More
Information
Subjects: Ophthalmology
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register : ,
View Times: 765
Entry Collection: Encyclopedia of Glaucoma
Online Date: 01 Dec 2022
1000/1000