Capillary closure secondary to retinal vein occlusion - A morphological, histopathological, and immunohistochemical study

Background: The mechanisms underlying capillary closure leading to neovascularisation in retinal disease are unknown. In order to further characterize these mechanisms morphological, histopathological, and immunohistochemical changes in areas of capillary closure secondary to retinal vein occlusion were studied. Material: The retina from four eyes of two patients with evidence of previous retinal vein occlusion were cast for demonstrating the morphology of capillary closure. Subsequent histological sections through these areas were stained with periodic acid Schiff, Sirius red, and Alcian blue (basement membranes), and by immunohistochemistry to type IV collagen (basement membranes), von Willebrand factor (endothelial cells), glial fibrillary acid protein (GFAP) and vimentin (glial cells), S-100 protein (perivascular glial cells), carbonic anhydrase isoenzyme IT (CAH-II) and CD-57 antigen (Muller cells), and CD-68 antigen (microglia). Results: Retinal capillary closure was most prominent on the venous side of microvascular units. The material which was accumulated to occlude the lumen of retinal capillaries displayed immunoreactivity to GFAP, vimentin, CD-57 antigen, and CAM-II, but not to S-100 protein, suggesting that this material represents invaded Muller cells. The perivascular glial cells displayed continuous bands of immunoreactivity to S-100 protein corresponding to border zones of retinal areas affected by retinal vein occlusion, but this immunoreactivity was absent inside areas of capillary closure. The histopathological and immunohistochemical appearance of vascular basement membranes was similar in areas of capillary occlusion and outside these areas. Conclusions: The findings in areas of capillary closure secondary to retinal vein occlusion showed both similarities to and differencies from capillary closure in other retinal disease such as diabetic retinopathy, This evidence may act as a basis for further elucidation of the pathophysiology of capillary closure in retinal disease.