Retinopathy is a common cause of blindness in all age groups. There are 15 million people in the United States with age-related macular degeneration (AMD)—20% of those aged 65 to 74 years and 30% aged 74 years—and 1.6 million of those have neovascular (wet) AMD. In the working age population there are 20 million (7% of the population) with diabetes, and 50% of patients with diabetes mellitus have diabetic retinopathy (DR) after 25 years. In children, retinopathy of prematurity (ROP) is a major cause of vision loss. Approximately 460,000 (11%) of infants per year are born prematurely, and there are 2000 infants per year with severe ROP, even with treatment. There is a high impact of blindness in children (0–70 years).

Although fewer children are affected by retinal neovascularization than adults, ROP offers a window into understanding the pathophysiology of retinopathy. The study of ROP has helped to develop nondestructive therapy for retinopathy. Research in ROP is easier in theory than that in DR or AMD, as there are clear and distinct comparisons to be made: normal in utero development versus development after premature birth. If we understand what factors change between the in utero retina where vascularization proceeds normally without retinopathy and the retina of infants born prematurely, then we may better understand normal vascular development, vessel loss, vessel repair, and neovascularization. ROP occurs over a much shorter time line (10–20 weeks) than does DR or AMD. 1