Morphology of surgical ILM‐specimens in epiretinal membranes, macular holes, and diabetic retinopathy

Purpose Myofibroblasts play a major role in the production of retractile phenomena causing contraction or shrinkage of the epiretinal membranes (ERM) in proliferative vitreoretinopathy and diabetic retinopathy. The purpose of our study was to evaluate the expression of myofibroblasts on epiretinal tissues in eyes with epiretinal membranes, diabetic macular edema (DME) or macular holes. Methods Samples of ERM and ILMs (internal limiting membranes) following macular epiretinal membrane removal in eyes with diabetic maculopathy, refractory to conservative treatment, idiopathic epiretinal membrane and macular holes, were collected. Double immunofluorescence staining, with antibodies recognizing a smooth muscle actin (a‐SMA) and fibronectin (ED‐A FN) or vimentin in myofibroblasts, followed by confocal and electronic microscopy was performed. Results a‐SMA in association with either ED‐A FN or vimentin were detected in all ERM specimens. a‐SMA and ED‐A FN were also detected in ILMs removed in cases of stage IV macular holes. ED‐A FN was expressed in close relation to a‐SMA–positive myofibroblasts, predominately located close to the border of the macular hole area. In all idiopathic ERMs, ED‐A FN was expressed in close relation to a‐SMA–positive myofibroblasts. In those cases, no a‐SMA staining was observed in ILM specimens. Conclusion Scanning electron microscopy indicated that active contraction mechanisms are always expressed in epiretinal macular membrane and underling ILM tissues in eyes with diabetic maculopathy and late stages of macular hole.ILM folding seems to be myofibroblast‐independent in idiopathic epiretinal membrane cases.