%0 Journal Article
%T Mechanisms of Inflammation in Proliferative Vitreoretinopathy: From Bench to Bedside
%A Stavros N. Moysidis
%A Aristomenis Thanos
%A Demetrios G. Vavvas
%J Mediators of Inflammation
%D 2012
%I Hindawi Publishing Corporation
%R 10.1155/2012/815937
%X Proliferative vitreoretinopathy (PVR) is a vision-threatening disease and a common complication of surgery to correct rhegmatogenous retinal detachment (RRD). Several models of the pathogenesis of this disease have been described with some of these models focusing on the role of inflammatory cells and other models focusing on the role of growth factors and cytokines in the vitreous which come into contact with intraretinal and retinal pigment epithelial cells. New experiments have shed light on the pathogenesis of PVR and offer promising avenues for clinical intervention before PVR develops. One such target is the indirect pathway of activation of platelet-derived growth factor receptor alpha (PDGR¦Á), which plays an important role in PVR. Clinical trials assessing the efficacy of 5-fluorouracil (5-FU) and low-molecular-weight heparin (LMWH), daunorubicin, and 13-cis-retinoic acid, among other therapies, have yielded mixed results. Here we review inflammatory and other mechanisms involved in the pathogenesis of PVR, we highlight important clinical trials, and we discuss how findings at the bench have the potential to be translated to the bedside. 1. Introduction Proliferative vitreoretinopathy (PVR) is a vision-threatening disease that can occur secondary to retinal detachment (RD). RD allows macrophages, retinal pigment epithelial (RPE) cells, glial cells, and fibroblasts to migrate to the vitreous, where they proliferate, survive, form extracellular matrix proteins and assemble into a membrane [1]. This membrane can attach to the retina and subsequently contract, which can cause a new retinal detachment or failure of a surgically corrected detachment [2]. PVR occurs most commonly as a complication of surgery to correct rhegmatogenous retinal detachment (RRD) and is the most common reason for the failure of this operation [3, 4]. In one study of 119 patients with RRD and no previous vitreoretinal surgery, there was a 52.9% prevalence of PVR and 26.9% prevalence of severe PVR with mean retinal detachment duration of days [5]. Visual outcomes and the anatomical success of surgery are worse for RD that is complicated by PVR and may require twice as many resources to care for as those cases of RD without PVR [6]. Here we review inflammatory and other mechanisms involved in the pathogenesis of PVR, we highlight important clinical trials, and we discuss how findings at the bench have the potential to be translated to the bedside. 2. The Macrophage Hypothesis for Development of PVR Some of the hypotheses regarding the pathogenesis of PVR have focused on the
%U http://www.hindawi.com/journals/mi/2012/815937/