The fetal ophthalmic artery is a branch of the internal carotid artery and terminates into the hyaloid artery. The hyaloid artery enters the optic cup via the optic fissures and stalk (developing optic nerve) (see Fig. 1-12). At approximately 6 weeks gestation, the ophthalmic artery becomes entrapped in the optic cup as the optic fissure closes. The portion of the hyaloid artery within the optic stalk eventually becomes the central retinal artery, while the more terminal parts of the hyaloid artery arborize around the posterior aspect of the developing lens. The hyaloid artery gradually atrophies and regresses as branches of the hyaloid artery become sporadically occluded by macrophages.52,54 Regression of the hyaloid vasculature is usually complete by the fifth month of human gestation. Bergmeister's papilla represents a remnant of the hyaloid vasculature that does not regress; this is a benign anomaly consisting of a small fibrous glial tuft of tissue that emanates from the center of the optic disc.
The hyaloid vasculature is the primary source of nutrition to the embryonic retina. Regression of the hyaloid vasculature serves to stimulate retinal vessel angiogenesis. Spindle-shaped mesenchymal cells from the wall of the hyaloid vein at the optic disc form buds that invade the nerve fiber layer during the fourth month of gestation.6 Subsequently, solid cords of mesenchymal cells within the inner retina canalize and contain occasional red blood cells at approximately 5 months gestation. In situ differentiation of craniofacial angioblasts has been demonstrated in avian species using polyclonal antibodies to quail endothelial cells.75 Vascular budding and further differentiation form the deeper capillary network in the retina.73 The primitive capillaries have laminated walls consisting of mitotically active cells secreting basement membrane.95 Those cells in direct contact with the bloodstream differentiate into endothelial cells while the outer cells become pericytes. Tissue culture experiments have demonstrated that the primitive capillary endothelial cells are multipotent and can redifferentiate into fibroblastic, endothelial, or muscle cells, possibly illustrating a common origin of these different tissue types.6 Pigment epithelium derived factor (PEDF) has been demonstrated to inhibit angio-genesis of the cornea and vitreous. Inadequate levels may play a permissive role in ischemia-driven aberrant vascularization.33 The central retinal artery grows from the optic nerve to the periphery, forming the temporal and nasal retinal arcades. By approximately 5 months, the retinal arcades have progressed to the equator of the eye. At this time, the long and short posterior ciliary arteries are well developed, with the long posterior artery supplying the anterior segment and the short posterior artery supplying the choroid. The retinal arteries grow from the optic nerve toward the ora serrata and reach the nasal periphery first (by 8 months).73 Even at birth, however, there is usually a crescent of avascular retina in the temporal periphery. The fact that a newborn infant has an immature temporal retina without complete vascularization may explain why there have been scattered cases of retinopathy of prematurity in full-term infants. Oxygen affects angiogenesis and seems to play a role in stimulating and retarding vessel growth.83 In immature kitten retinas, increased oxygen concentration causes atrophy and regression of capillaries whereas hypoxia increases capillary arborization.79 Endothelial cell growth is also promoted by low oxygen tension, and endothelial growth is inhibited by high oxygen tension.7 Vasoendothelial growth factor (VEGF) both stimulates and maintains normal vessel growth to the peripheral retina. High oxygen downregulates VEGF, stopping the normal process of peripheral vascularization.2,58,84 These findings give rise to the hypothesis that retinopathy of prematurity (ROP) is secondary to initial increased oxygen concentration, which results in inhibition or retraction of peripheral capillary networks (vaso-obliteration).5 This lack of peripheral capillary network subsequently results in retinal hypoxia increased VEGF then secondary endothelial cell growth and neovascularization (i.e., ROP).82 There is evidence that strict curtailment of O2 dose early in a premature infants course reduces the incidence of severe ROP.112a
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