Abstract

SA.10.03

Update on new insights in the pathophysiology of proliferative vitreoretinopathy (PVR) – from bench to bedside

Stephan Hoffmann, Berthold Seitz
Klinik für Augenheilkunde, Universitätskliniken des Saarlandes, Homburg/Saar

Proliferative vitreoretinopathy (PVR) is a common cause of blindness after failed retinal reattachment surgery and trauma. Retinal pigment epithelial cells (RPE) are considered as a cellular main compound in the disease. These cells are released after eye trauma through retinal holes and are dispersed into the vitreous cavity. After attachment onto the inferior part of the retina, these cells form in concordance with glial cells and fibroblasts contractile membranes under the influence of growth factors and extracellular matrices. The formation of these contractile membranes is considered as a form of pathologic wound healing in the eye. The membranes are mostly formed in the inferior part of the eye and the membrane proliferation and contraction leads to tractive retina detachment and possible blindness. Despite progress in the field of vitreoretinal surgery, PVR is still a tremendous complication of the disease treatment. A deciphering of the pathobiology of PVR is still needed for a selective treatment of the disease. Proliferation, migration and contraction of the RPE-cells is stimulated by growth factors as ”transforming growth factor-beta” (TGF-beta), “basic fibroblast growth factor” (bFGF) and the inflammatory growth factor “tumor necrosis factor-alpha” (TNF-alpha). Current research also shows an involvement of the multiligand receptor system RAGE and its ligands in the inflammatory processes in PVR and the mesenchymal transformation of the RPE-cell. An overview on new insights into the pathobiology of PVR will be given as also the link between these new pathobiological insights and clinical work in retinology.

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