Pathogenesis of retinopathy of prematurity and possible preventive strategies

• Published in: Early human development 2008-02, Vol.84 (2), p.83-88
• Main Authors: Fleck, Brian W, McIntosh, Neil
• Format: Article
• Language: English
• Subjects: Advanced Basic Science; Animals; Humans; Infant, Newborn; Infant, Premature; Neonatal and Perinatal Medicine; Neovascularization, Pathologic - pathology; Neovascularization, Pathologic - prevention & control; Oxygen; Oxygen - adverse effects; Oxygen - therapeutic use; Pathogenesis; Rats; Retinopathy of Prematurity; Retinopathy of Prematurity - etiology; Retinopathy of Prematurity - pathology; Retinopathy of Prematurity - prevention & control
• ISSN: 0378-3782; 1872-6232
• DOI: 10.1016/j.earlhumdev.2007.11.008

Abstract Retinopathy of Prematurity (ROP) occurs when premature birth interrupts normal retinal vascular development. Postnatal tissue oxygen levels are significantly higher than those present in utero. Oxygen therapy further increases oxygen levels in the developing retina. Hypoxia driven, VEGF mediated, retinal endothelial cell proliferation is reduced. Low IGF-1 levels may also contribute to delayed retinal vascular development. The neural structures of the peripheral avascular retina continue to develop, and become more metabolically active. Complex, as yet poorly understood abnormalities of structural and molecular interactions between immature endothelial cells and immature astrocytes at the anterior “leading edge” of retinal vascular development leads to the development of an ROP ridge. VEGF produced by the hypoxic peripheral retina, along with structural abnormalities of cell relationships within, and at the vitreoretinal interface of the ROP ridge, results in extraretinal angiogenesis – stage 3 ROP. Stage 3 ROP may resolve spontaneously, or may progress to traction retinal detachment and blindness.