Glaucoma is a progressive optic neuropathy that results in structural changes in the optic nerve head and visual field defects that may lead to severe visual impairment or blindness. Glaucoma may arise secondary to other causes such as trauma, steroid therapy, or inflammatory processes such as uveitis. Most cases of glaucoma, however, have no identifiable etiology and are termed primary glaucoma. Glaucoma is also classified as either open-angle glaucoma, in which the angle between the cornea and the pupil is normal, or closed-angle glaucoma, in which this angle is narrowed. Primary open-angle glaucoma (POAG) is the most prevalent type in the U.S. population. The pathogenesis of optic nerve damage in POAG is not well understood, but is likely multifactorial. The primary risk factor for development of POAG is an increase of intraocular pressure (IOP) above 21 mm Hg, which is considered to be the upper limit of normal for IOP. In population studies, increasing IOP is associated with an increased prevalence of POAG. Increased IOP was once considered a defining feature of POAG. However, a significant proportion (25-50%) of individuals with primary glaucomatous optic disc changes and visual field deficits have normal IOP measurements, a condition known as normal tension glaucoma (NTG). As a result, increased IOP is no longer considered to be part of the definition of POAG. Race is also an important risk factor for POAG. The incidence and prevalence of POAG also increase with age. Family history is also an important risk factor, indicating that glaucoma is partly attributable to genetic factors. For example, there is an approximately four-fold increase in risk of POAG in siblings of patients with glaucoma. Additional risk factors may include decreased central cornea thickness; low diastolic perfusion pressures (diastolic blood pressure -intraocular pressure); diabetes; and severe myopia. There have been no long-term, prospective studies of untreated patients with POAG. As a result, the natural history of POAG is not well understood. Overall progression of visual field deficits develops in a linear fashion over time, although progression is faster with higher levels of IOP. Although glaucoma is a frequent cause of blindness, estimated rates of progression do not appear sufficient to lead to complete blindness during the lifetime of the majority of those affected. Since IOP is the only modifiable risk factor in POAG, the cornerstone of glaucoma therapy is IOP reduction. Treatment options include topical medications, systemic medications, laser surgery, and incisional surgery, alone or in combination. In recent years, several large randomized clinical trials have examined the benefits of various treatment strategies for both increased IOP without glaucoma (ocular hypertension), and glaucoma, with and without increased IOP. To update prior USPSTF recommendations, we critically reviewed these recent studies for quality and strength of evidence to support treatment and screening for POAG. Key Questions addressed include (but are not limited to): KQ1. Is There New Evidence That Screening for Open-angle Glaucoma Reduces Severe Visual Impairment? KQ3. Is There New Evidence That Feasible Screening Tests are Accurate and Reliable in Detecting Increased Intracular Pressure or Open-angle Glaucoma? KQ4. Is There New Evidence That Treating Increased Intraocular Pressure Reduces the Incidence of Primary Open-angle Glaucoma? KQ5. Is There New Evidence That Treating Increased Intraocular Pressure Reduces Severe Visual Impairments? KQ6. Is There New Evidence That Treating Open-angle Glaucoma with Drugs, Laser, and/or Surgery Reduces Severe Visual Impairment? KQ7. Is There New Evidence That Screening Results in Adverse Effects? Is Screening Acceptable to Patients? KQ8. Is There New Evidence That Treatment of Increased Intraocular Pressure and/or Open-angle Glaucoma Results in Adverse Effects?