Macular degeneration is the leading cause of central or reading vision loss in the United States. A reproducible model of subretinal neovascularization (SRN) and disciform degeneration is of great importance in the study of the pathogenesis, which is at present poorly understood. Our current model of SRN is a promising step in the investigation of the pathogenic mechanisms and natural history. In this experimental model, intense argon laser photocoagulation is used to produce breaks in Bruch's membrane, which results in an inflammatory response with macrophage infilatration. This is followed by proliferation of the retinal pigment epithelial cells, endothelial cells, and fibroblasts with the formation of both active and inactive new vessels. Involution of the active vessels eventually occurs. Although we have determined many of the steps in the pathogenesis of SRN, the exact role and relative importance of each stage is still unknown. The hypotheses that the macrophage is the prime initiator of angiogenesis and that proliferation of the retinal pigment epithelium is responsible for the involution of SRN will be investigate both clinically and morphologically. This model lends itself to manipulation, and the experiments are designed to test these hypotheses by altering the progression and speed of events by enhancing, depressing, activating, and inactivating specific cellular and extracellular components. The significance of retinal necrosis, non-thermal injury, and therapeutic laser will be investigated in the same way. A better understanding of the pathogenesis may ultimately provide the basis for successful therapy.
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