Ultrastructural change of age-related debris in bruch's membrane analyzed in laser scars of human retina

Purpose. To further elucidate the mechanism of action of laser treatment for diffuse retinal edema or drusen. Especially the mechanism of action of lasers using a wavelength in the near infra-red region of the spectrum is still unclear. However it has been shown that diabetic macular edema and drusen respond to such laser treatment. As a hypothesis there may be interference with accumulated Hpid deposits at the level of RPE and Bruchs membrane, which block active fluid transport from the sensory retina to the choroid. It has been shown previously by means of light microscopy that Hpid components in Bruch's membrane are reduced by laser treatment. Methods. Four eyes with a malignant choroidal melanoma were lasered using a diode laser with 810 nm prior to enucleation. Eight diabetic donor eyes with laser scars were also included (2 eyes with 9-monthold pigmented laser scars, 6 eyes with already depigmented lesions). Sections of lasered areas were stained with Oil-red-0 for light microscopy or were processed for electron microscopy. Results. In all laser scars the staining intensity for Oilred-0 was reduced, whereas the immediate laser burns revealed persistence of lipid debris.Ultrastructurally there was thinning of the inner collagenous layer with a reduced amount of age-related debris. This effect was more pronounced in 9-month-old pigmented lesions in the area with overlying phagocytic RPE cells. At the margins of the scars the decrease of debris was gradual and patchy, whereas the center of the lesion and areas adjacent to phagocytic RPE cells were almost completely denuded. Conclusions. Laser-induced reduction of lipid components was evident in all examined laser scars, independently from the laser source or the age of the lesion. This may explain why laser treatment for macular edema or drusen is sufficient with different types of lasers and wavelengths. Besides removal of the debris by phagocytosis other mechanisms of action, such as involvement of endothelial intrusions or destruction of rod outer segments are discussed.