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