PURPOSE: The purpose of this study was to examine the expression of cyclo-oxygenase (COX)-2 in the idiopathic epiretinal membrane (IERM), inner limiting membrane (ILM), and proliferative diabetic retinopathy membrane. METHODS: Twenty membranes, consisting of eight IERMs, four ILMs, and eight proliferative diabetic retinopathy membranes, were surgically removed. Formalin-fixed, paraffin-embedded tissue sections were processed for immunohistochemistry using anti-COX-2 antibody. The nuclear density showing the density of cells situated in IERM and ILM specimens was calculated under high-power fields using a light microscope. RESULTS: The IERM comprised flattened cells with oval nuclei constituting a monolayer. The ILM contained a few cells with abundant collagenous tissues. Neither endothelial nor inflammatory cells were observed in the IERM and ILM. COX-2 immunoreactivity was markedly detected in cells located in the IERM. In contrast, COX-2 immunoreactivity was faintly detected in the ILM. The COX-2-positive rate was 65.4 +/- 15.5% and 34.3 +/- 20.3% in the IERM and ILM, respectively, being significantly higher in the former (P = 0.046). The nuclear density was 39.3 +/- 10.3 and 8.6 +/- 7.2 in the IERM and ILM, respectively, being significantly higher in the former (P = 0.0003). The proliferative diabetic retinopathy membranes consisted of many vascular endothelial and stromal cells. Cytoplasmic immunoreactivity for COX-2 was detected in endothelial and stromal cells in the proliferative diabetic retinopathy membranes. CONCLUSION: These results suggest that COX-2 plays a potential role in the formation of avascular and vascularized epiretinal membranes if an epiphenomenon of COX-2 expression within these epiretinal membranes has been ruled out in future studies.
PURPOSE: The purpose of this study was to examine the expression of cyclo-oxygenase (COX)-2 in the idiopathic epiretinal membrane (IERM), inner limiting membrane (ILM), and proliferative diabetic retinopathy membrane. METHODS: Twenty membranes, consisting of eight IERMs, four ILMs, and eight proliferative diabetic retinopathy membranes, were surgically removed. Formalin-fixed, paraffin-embedded tissue sections were processed for immunohistochemistry using anti-COX-2 antibody. The nuclear density showing the density of cells situated in IERM and ILM specimens was calculated under high-power fields using a light microscope. RESULTS: The IERM comprised flattened cells with oval nuclei constituting a monolayer. The ILM contained a few cells with abundant collagenous tissues. Neither endothelial nor inflammatory cells were observed in the IERM and ILM. COX-2 immunoreactivity was markedly detected in cells located in the IERM. In contrast, COX-2 immunoreactivity was faintly detected in the ILM. The COX-2-positive rate was 65.4 +/- 15.5% and 34.3 +/- 20.3% in the IERM and ILM, respectively, being significantly higher in the former (P = 0.046). The nuclear density was 39.3 +/- 10.3 and 8.6 +/- 7.2 in the IERM and ILM, respectively, being significantly higher in the former (P = 0.0003). The proliferative diabetic retinopathy membranes consisted of many vascular endothelial and stromal cells. Cytoplasmic immunoreactivity for COX-2 was detected in endothelial and stromal cells in the proliferative diabetic retinopathy membranes. CONCLUSION: These results suggest that COX-2 plays a potential role in the formation of avascular and vascularized epiretinal membranes if an epiphenomenon of COX-2 expression within these epiretinal membranes has been ruled out in future studies.