In this article the authors review present knowledge concerning the pathogenesis of proliferative vitreoretinopathy (PVR). The function of cells such as macrophages, fibroblasts, retinal pigment epithelial cells, and glial cells, as well as their interaction with constituents of the extracellular matrix such as fibronectin, vitronectin, and factor XIII, are described. Current data on growth factor involvement in the pathogenesis of PVR are explained. Attention is focused on the histopathological differences between traumatic and idiopathic membranes, "young" and "old" membranes, and PVR and diabetic membranes. On the basis of the findings presented, the importance of the breakdown of the blood-retinal barrier, the participation of the coagulation system, and immunological aspects of membrane formation are discussed. Conceivable new strategies for medical treatment of PVR are proposed.