**3. ERM-pathogenesis**

The diagnosis of PVD, which is defined as separation between the posterior vitreous cortex and the internal limiting membrane (ILM) of the retina, has been described in up to 95% of cases of idiopathic ERM [9]. Residual cortical vitreous secondary to a PVD or anomalous PVD leading to vitreoschisis with only partial separation of the posterior hyaloid remain to be factors allowing proliferation of glial cells. Inflammation is a central component of disorders leading to secondary ERMs, with increased inflammatory mediators promoting fibrocellular growth. Retinal glial cells, hyalocytes, fibroblasts, myofibroblasts are the predominant cell types found in the ERMs. Retinal pigment epithelial cells, macrophages, T-, and, B-cells are identified in secondary ERMs [6]. Extracellular matrix production and remodeling are predominant. The extracellular matrix components that have been described in ERMs include collagen types I, II, III, IV, and VI, fibronectin, and laminin [10–12]. Extracellular fibrils are thin in cellophane macular reflex and are much thicker in preretinal macular fibrosis [10].
