Mechanisms of maculopathy.

This article will review the cellular constituents of the macula and speculate on their contribution to the pathogenesis of macular disease. The retinal pigment epithelium (RPE) has been implicated in senile macular degeneration (SMD). Over time, RPE dysfunction and death may result from the cumulative effect of light and free radical damage. Inherited metabolic abnormalities or the degree of uveal pigmentation could increase the RPE's susceptibility to environmental stress. In exudative SMD, the excessive production of extracellular matrix material by the RPE may contribute to sub-RPE neovascularization and disciform scar formation. Macular edema reflects a breakdown in the blood-retinal barrier. Inflammatory mediators produced in the anterior segment may cause aphakic cystoid macular edema (CME). Recent observations suggest that Müller cell dysfunction is important in CME. Vascular incompetence, as well as capillary occlusion characterize diabetic retinopathy. Angiogenic factors elaborated by ischemic retina are thought to be the stimulus for neovascularization. Diabetic tractional macular detachment results from neovascular proliferation on the partially detached vitreous. Posterior vitreous detachment predisposes to epiretinal gliosis. Endogenous infections and metastatic neoplasms have a predilection for the macula, reflecting the region's high blood flow.