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.


METHODS
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 II (CAH-II) and CD-57 antigen (Müller 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 CAH-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 differences 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.
Bek
T
T
Department of Ophthalmology, Arhus University Hospital, Denmark.
D000368:Aged; D000369:Aged, 80 and over; D015703:Antigens, CD / Q000378:metabolism; D002196:Capillaries / Q000378:metabolism / Q000473:pathology; D002256:Carbonic Anhydrases / Q000378:metabolism; D003094:Collagen / Q000378:metabolism; D005260:Female; D005451:Fluorescein Angiography; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006801:Humans; D007124:Immunoenzyme Techniques; D008297:Male; D012164:Retinal Diseases / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D012170:Retinal Vein Occlusion / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D012171:Retinal Vessels / Q000378:metabolism / Q000473:pathology*; D009418:S100 Proteins / Q000378:metabolism; D014746:Vimentin / Q000378:metabolism; D014841:von Willebrand Factor / Q000378:metabolism
D015703:Antigens, CD; D005904:Glial Fibrillary Acidic Protein; D009418:S100 Proteins; D014746:Vimentin; D014841:von Willebrand Factor; D003094:Collagen; D002256:Carbonic Anhydrases