Normal and abnormal vitreoretinal interface conditions

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AbstractPathologic changes at the vitreoretinal interface and vitreomacular traction, lead to the phenotypic lesions as epiretinal membranes (ERMs), idiopathic macular holes, vitreomacular traction syndrome (VMTS) and myopic foveoschisis. Remnants of vitreous collagen fibers in the presence of clinically evident posterior vitreous detachment (PVD) and/or cellular proliferations of fibrous astrocytes or glial cells growing outward from the retina to the inner retinal surface through the internal limiting membrane (ILM) , in the presence of growth factors as laminin, fibronectin, may contribute to fibrocellular proliferation at the retinal surface. Most studies of idiopathic of diabetic or macular holes related epiretinal membranes, described the presence of fibrocytes or myofibroblasts and more recent studies confirmed these observations using antibodies against alpha smooth muscle actine (a‐SMA). Based on the mechanistic association between a‐SMA expression and tractional force generation, there is little doubt that these cells represented the source of traction during the evolution of those pathologies.