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PubMed This is a summary of 25 peer-reviewed journal articles Updated
Ophthalmology

Biology & Types of Open-Angle Glaucoma

At a Glance

Open-angle glaucoma occurs when the eye’s drainage angle stays open but fluid outflow meets resistance, allowing pressure or other stress to damage the optic nerve. It includes primary, normal-tension, and secondary forms, each requiring individualized evaluation.

Understanding the biology of open-angle glaucoma (OAG) is the first step toward managing it effectively. While you may hear “glaucoma” used as a single term, it actually describes a group of conditions that share a common outcome: damage to the optic nerve [1].

The Biology of Drainage

Your eye is a pressurized system. It produces a clear fluid called aqueous humor that circulates through the front of the eye and exits through a specialized drainage tissue called the trabecular meshwork ™ [2].

In a healthy eye, this fluid flows out easily, maintaining a stable pressure. In OAG, the “drainage angle”—the space where the fluid exits—remains physically open, but the fluid faces internal resistance. This happens for several reasons:

  • Structural Changes: The trabecular meshwork cells can change, becoming more rigid or “contractile,” which reduces their ability to filter fluid [3][4].
  • Molecular “Clogging”: Proteins and fibers can build up in the drainage tissue, effectively “clogging” the pipes at a microscopic level [5][6].
  • Drainage Canal Issues: The Schlemm’s canal, which carries fluid away from the meshwork, can also narrow or become less efficient [7][8].

How Your Sight Is Affected

When drainage slows down, pressure builds up inside the eye. This pressure puts physical stress on the optic nerve head, the sensitive spot where the nerve leaves the eye to go to the brain [9].

The damage occurs specifically to retinal ganglion cells (RGCs) and their long fibers, called axons. Think of these like the individual wires inside a fiber-optic cable [9]. Pressure can physically pinch these fibers or cut off their supply of energy and nutrients [10][11]. Over time, these “wires” die, and the information from your eye can no longer reach your brain, leading to vision loss [10][12].

Open-Angle vs. Angle-Closure

Doctors make a critical distinction between “open-angle” and “angle-closure” glaucoma using a test called gonioscopy, where a special lens is used to look directly at the drainage angle [13].

  • Open-Angle (OAG): The iris (the colored part of the eye) is in its proper position, and the drainage angle is clear and visible. The problem is deep inside the drainage tissue [14].
  • Primary Angle-Closure (PACG): The iris physically bunches up and blocks the drainage angle, like a piece of paper covering a sink drain [15]. This can cause a sudden, painful spike in pressure (acute) or happen slowly over time (chronic) [16][17].

Primary Open-Angle Glaucoma and the Pressure Spectrum

Primary Open-Angle Glaucoma (POAG) is the most common form of the disease. It is important to know that a pressure reading of 21 mmHg is simply a statistical reference, not a strict cutoff line for a diagnosis [1].

  • POAG with Elevated Pressure: Many people with POAG have intraocular pressure (IOP) readings consistently above 21 mmHg, which contributes to their nerve damage [18].
  • Normal-Tension Glaucoma (NTG): This is a subtype of POAG where optic nerve damage occurs even though eye pressure measurements are repeatedly within the statistical “normal” range (10–21 mmHg) [1]. This suggests the optic nerve may be exceptionally sensitive. Some evidence links NTG to vascular issues like migraines, poor blood flow, or low nighttime blood pressure, but these are potential contributors, not definitive diagnostic tests [19][20]. Never alter your blood pressure medications without consulting your prescribing doctor.

Secondary Open-Angle Glaucomas

In these types, a specific “secondary” cause triggers the drainage problem. Your doctor will examine you for signs of these conditions, as they can sometimes progress faster or require different treatments.

  • Pseudoexfoliative Glaucoma (PEXG): An abnormal, dandruff-like flaky material is produced throughout the eye. This material gets caught in the trabecular meshwork, causing high and often fluctuating eye pressure [21][22]. It often affects one eye more than the other [23][24].
  • Pigmentary Glaucoma (PG): The iris pigment (the “paint” that gives your eye color) rubs off and floats into the eye fluid. These tiny pigment granules can settle into the drainage meshwork, blocking the outflow [25].
  • Steroid-Induced Glaucoma: Long-term use of corticosteroids (eye drops, inhalers, nasal sprays, creams, or pills) can raise eye pressure. Do not start or stop steroid medications without speaking to your doctor.
  • Other Secondary Causes: Glaucoma can also develop secondary to severe eye inflammation (uveitic), physical trauma (traumatic), or abnormal blood vessel growth in the eye (neovascular).

By identifying your specific type, your doctor can better predict how your eye will behave and tailor a treatment plan to keep your vision stable.

Common questions in this guide

What does open-angle glaucoma mean?
Open-angle glaucoma means the drainage angle in the eye remains physically open, but the drainage tissue resists the normal flow of aqueous humor. The resulting pressure or stress can damage the optic nerve and lead to vision loss.
How is open-angle glaucoma different from angle-closure glaucoma?
In open-angle glaucoma, the drainage angle is visible and open while the problem is deeper in the drainage tissue. In angle-closure glaucoma, the iris blocks or crowds the angle and may cause a sudden rise in pressure, eye pain, or halos around lights.
What is the difference between primary open-angle and normal-tension glaucoma?
Primary open-angle glaucoma is the most common form of glaucoma and may occur with eye pressure above 21 mmHg. Normal-tension glaucoma is a subtype in which optic nerve damage occurs even though repeated pressure readings remain within the statistical normal range of 10–21 mmHg.
What are pseudoexfoliative and pigmentary glaucoma?
Pseudoexfoliative glaucoma occurs when flaky material builds up in the eye and blocks the drainage tissue, often causing high or fluctuating pressure and affecting one eye more than the other. Pigmentary glaucoma occurs when pigment from the iris collects in the drainage tissue and reduces fluid outflow.
Can steroid medicines cause open-angle glaucoma?
Long-term corticosteroid use can raise eye pressure and contribute to steroid-induced glaucoma. Steroids may be found in eye drops, inhalers, nasal sprays, creams, or pills, so do not start or stop one without discussing it with the prescribing clinician.
What is gonioscopy, and why is it used for glaucoma?
Gonioscopy uses a special lens to let an eye doctor examine the drainage angle directly. It helps distinguish open-angle glaucoma from angle-closure glaucoma and can show whether the angle is open, narrowed, or blocked.

Questions to Ask Your Doctor

Curated prompts to bring to your next appointment.

  1. 1.During my exam, was the drainage angle clearly open or did you see any signs of 'crowding' or narrowing?
  2. 2.Based on my optic nerve appearance and visual field, do I have Primary Open-Angle Glaucoma or Normal-Tension Glaucoma?
  3. 3.Did you see any signs of flaky material or pigment rubbing off during my slit-lamp exam?
  4. 4.What is my target eye pressure, and how does it relate to the specific type of glaucoma I have?
  5. 5.Are there any secondary factors, like my blood pressure or history of steroid use, that might be contributing to my condition?

Questions For You

Tap a prompt to share your answer — we'll use it plus this page's context to start a tailored conversation.

References

References (25)
  1. 1

    Primary open-angle glaucoma.

    Weinreb RN, Leung CK, Crowston JG, et al.

    Nature reviews. Disease primers 2016; (2()):16067 doi:10.1038/nrdp.2016.67.

    PMID: 27654570
  2. 2

    [The trabecular meshwork: Structure, function and clinical implications. A review of the littérature (French translation of the article)].

    Buffault J, Labbé A, Hamard P, et al.

    Journal francais d'ophtalmologie 2020; (43(8)):779-793 doi:10.1016/j.jfo.2020.04.022.

    PMID: 32807552
  3. 3

    The exit strategy: Pharmacological modulation of extracellular matrix production and deposition for better aqueous humor drainage.

    Pattabiraman PP, Toris CB

    European journal of pharmacology 2016; (787()):32-42.

    PMID: 27112663
  4. 4

    Intraocular Pressure and the Mechanisms Involved in Resistance of the Aqueous Humor Flow in the Trabecular Meshwork Outflow Pathways.

    Tamm ER, Braunger BM, Fuchshofer R

    Progress in molecular biology and translational science 2015; (134()):301-14.

    PMID: 26310162
  5. 5

    Smad-independent TGF-β2 signaling pathways in human trabecular meshwork cells.

    Pervan CL

    Experimental eye research 2017; (158()):137-145 doi:10.1016/j.exer.2016.07.012.

    PMID: 27453344
  6. 6

    TIMP1, TIMP2, and TIMP4 are increased in aqueous humor from primary open angle glaucoma patients.

    Ashworth Briggs EL, Toh T, Eri R, et al.

    Molecular vision 2015; (21()):1162-72.

    PMID: 26539028
  7. 7

    Impaired angiopoietin/Tie2 signaling compromises Schlemm's canal integrity and induces glaucoma.

    Kim J, Park DY, Bae H, et al.

    The Journal of clinical investigation 2017; (127(10)):3877-3896.

    PMID: 28920924
  8. 8

    A ROCK inhibitor suppresses the transforming growth factor-beta-2-induced endothelial-mesenchymal transition in Schlemm's canal endothelial cells.

    Fujimoto T, Inoue-Mochita M, Inoue T

    Scientific reports 2023; (13(1)):9655 doi:10.1038/s41598-023-36808-8.

    PMID: 37316554
  9. 9

    Impaired axonal transport contributes to neurodegeneration in a Cre-inducible mouse model of myocilin-associated glaucoma.

    Kaipa BR, Kasetti R, Sundaresan Y, et al.

    JCI insight 2025; (10(5)).

    PMID: 39836483
  10. 10

    Life under pressure: The role of ocular cribriform cells in preventing glaucoma.

    Paula JS, O'Brien C, Stamer WD

    Experimental eye research 2016; (151()):150-9.

    PMID: 27567558
  11. 11

    Pathophysiology of primary open-angle glaucoma from a neuroinflammatory and neurotoxicity perspective: a review of the literature.

    Evangelho K, Mogilevskaya M, Losada-Barragan M, Vargas-Sanchez JK

    International ophthalmology 2019; (39(1)):259-271 doi:10.1007/s10792-017-0795-9.

    PMID: 29290065
  12. 12

    Protein misfolding and mitochondrial dysfunction in glaucoma.

    Venkatesan A, Bernstein AM

    Frontiers in cell and developmental biology 2025; (13()):1595121 doi:10.3389/fcell.2025.1595121.

    PMID: 40385286
  13. 13

    Low Sensitivity of the Van Herick Method for Detecting Gonioscopic Angle Closure Independent of Observer Expertise.

    Johnson TV, Ramulu PY, Quigley HA, Singman EL

    American journal of ophthalmology 2018; (195()):63-71 doi:10.1016/j.ajo.2018.07.026.

    PMID: 30071210
  14. 14

    The genetic basis for adult onset glaucoma: Recent advances and future directions.

    Wang Z, Wiggs JL, Aung T, et al.

    Progress in retinal and eye research 2022; (90()):101066 doi:10.1016/j.preteyeres.2022.101066.

    PMID: 35589495
  15. 15

    Management of Primary Angle-Closure Glaucoma.

    Lai J, Choy BN, Shum JW

    Asia-Pacific journal of ophthalmology (Philadelphia, Pa.) 2016; (5(1)):59-62 doi:10.1097/APO.0000000000000180.

    PMID: 26886121
  16. 16

    Beyond the optic nerve: Genetics, diagnosis, and promising therapies for glaucoma.

    Kaushik M, Tiwari P, Dada T, Dada R

    Gene 2024; (894()):147983 doi:10.1016/j.gene.2023.147983.

    PMID: 37952746
  17. 17

    Blindness in glaucoma: primary open-angle glaucoma versus primary angle-closure glaucoma-a meta-analysis.

    George R, Panda S, Vijaya L

    Eye (London, England) 2022; (36(11)):2099-2105 doi:10.1038/s41433-021-01802-9.

    PMID: 34645961
  18. 18

    Glaucoma.

    Jonas JB, Aung T, Bourne RR, et al.

    Lancet (London, England) 2017; (390(10108)):2183-2193 doi:10.1016/S0140-6736(17)31469-1.

    PMID: 28577860
  19. 19

    Vascular and autonomic dysregulation in primary open-angle glaucoma.

    Pasquale LR

    Current opinion in ophthalmology 2016; (27(2)):94-101 doi:10.1097/ICU.0000000000000245.

    PMID: 26720776
  20. 20

    Normal tension glaucoma in Asia: Epidemiology, pathogenesis, diagnosis, and management.

    Chen MJ

    Taiwan journal of ophthalmology 2020; (10(4)):250-254 doi:10.4103/tjo.tjo_30_20.

    PMID: 33437596
  21. 21

    The clinical features in patients with newly diagnosed pseudoexfoliative glaucoma in Serbia.

    Maric VD, Grgurevic AD, Cirkovic AM, et al.

    European journal of ophthalmology 2020; (30(3)):513-524 doi:10.1177/1120672119831532.

    PMID: 30808180
  22. 22

    Molecular Portraits of Aqueous Humor in Primary and Pseudoexfoliative Open-Angle Glaucoma.

    Shebardina NG, Petrov SY, Iomdina EN, et al.

    Journal of proteome research 2026; (25(3)):1700-1713 doi:10.1021/acs.jproteome.5c00982.

    PMID: 41665634
  23. 23

    Long Term Results of Visual Field Progression Analysis in Open Angle Glaucoma Patients Under Treatment.

    Kocatürk T, Bekmez S, Katrancı M, et al.

    The open ophthalmology journal 2015; (9()):116-20 doi:10.2174/1874364101509010116.

    PMID: 26311586
  24. 24

    Visual Subfield Progression in Glaucoma Subtypes.

    Su WW, Hsieh SS, Cheng ST, et al.

    Journal of ophthalmology 2018; (2018()):7864219 doi:10.1155/2018/7864219.

    PMID: 29750123
  25. 25

    Patterns of Retinal Nerve Fiber Layer Loss in Different Subtypes of Open Angle Glaucoma Using Spectral Domain Optical Coherence Tomography.

    Baniasadi N, Paschalis EI, Haghzadeh M, et al.

    Journal of glaucoma 2016; (25(10)):865-872 doi:10.1097/IJG.0000000000000534.

    PMID: 27599175

This page is for informational purposes only and does not constitute medical advice. Your eye doctor should interpret your eye pressure, optic nerve findings, and test results and recommend care for your situation.

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