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R.R. Peddada, R.A. Linsenmeier; Diminished Oxygen Diffusion to Outer Retina in the Presence of Drusen in Age–Related Macular Degeneration (AMD): Computational Model and Histopathologic Correlation . Invest. Ophthalmol. Vis. Sci. 2005;46(13):1215.
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Purpose: To describe changes in oxygen partial pressure in outer retina in the presence of drusen and correlate these changes with observed histopathologic changes in AMD. Background: Drusen in AMD have been shown to be associated with decreased transport of water and proteins between choroid and outer retina. Hypothesis: Oxygen diffusion to outer retina may also be compromised in the presence of drusen. This may lead to atrophic changes in retina overlying the drusen. Methods: An axisymmetric diffusion computational model is employed to calculate the oxygen partial pressures in the outer retina in a four layer composite diffusion model. Boundary conditions imposed include partial pressure of oxygen in the choriocapillaris (62 mm Hg) and outer nuclear layer (15 mm Hg). Oxygen diffusivity of drusen is assumed to be 35 % of retina corresponding to the lower limit of biological tissues. The resulting oxygen partial pressure profiles are compared with previously published histopathologic changes in the outer retina in the presence of drusen. Results: Drusen that are 20 µm thick and 50 µm in diameter can lower oxygen consumption of retina to 60 % of normal (without drusen). Wider and thicker drusen are associated with greater reduction in oxygen consumption. Oxygen partial pressure is lowest centrally along the axis of the drusen and increases towards the periphery of the drusen. These results correlate well with previously reported histopathologic changes seen in photoreceptors in AMD. Specifically, thicker drusen produce greater damage to photoreceptors. This damage is most prominent immediately over the druse and less in the periphery similar to the oxygen partial pressure distribution. Conclusions: Drusen may compromise oxygen diffusion to photoreceptors and this may be one explanation for the observed histologic changes in the photoreceptors in AMD.
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