Pharmacological approach to treatment of proliferative vitreoretinopathy

Proliferative vitreoretinopathy (PVR) is the major cause of persistent loss of vision after retinal detachment surgery and is characterized by the formation of scar-like fibrocellular membranes on the neuroretina giving rise to tractional retinal (re-)detachment. Epithelial-mesenchymal transition, adhesion, migration and proliferation of retinal pigment epithelial (RPE) cells disseminated from the normal site at Bruch's membrane in concert with an activation of glial cells, hyalocytes and immune cells are key cellular events in the onset of the disease. The interplay between the cellular events and various growth factors, cytokines and matrix proteins thereby drives the undesirable formation of PVR membranes. Blocking these pathological events would greatly enhance the overall prognosis of surgical treatment. Clinical trials assessing the efficacy of antiproliferative and anti-inflammatory substances have yielded mixed results. Thus no safe or sufficiently effective pharmacological agent has so far been established in the clinical routine. Recent advances in the fundamental understanding of the pathogenesis of PVR aided in the identification of several new therapeutic targets to block the cellular events intrinsic to the disease. This article gives an overview of the results for adjunct therapies already tested in clinical studies and highlights experimental concepts for novel treatment strategies.