A brief review of the histopathology of proliferative vitreoretinopathy (PVR).

Proliferative vitreoretinopathy (PVR) is thought to represent an exaggerated and protracted scarring process following rhegmatogenous retinal detachment (RD) and following RD surgery. Following detachment, a combination of retinal ischaemia, inflammation and cell proliferation lead to the formation of tractional membranes on the epiretinal and subretinal surfaces and to marked gliosis within the retina that leads to retinal shortening. Both of these factors convert a rhegmatogenous RD into a tractional one are a major feature of RD surgery failure. The major cell types that are involved in PVR are retinal pigment epithelium (RPE), glial cells (principally Muller cells) and inflammatory cells (macrophages and lymphocytes). These cells interact with numerous growth factors and cytokines derived from the breakdown of the blood-retinal barrier and from vitreous contact that trigger a cascade of cellular processes, such as epithelial-mesenchymal transition (EMT), cell migration, chemotaxis, proliferation, elaboration of basement membrane and collagen and cellular contraction, that lead to overt retinal pathology. This review covers the histopathology of PVR and touches upon the cellular processes involved in the pathogenesis of PVR.