Role of Low Molecular Weight Heparin and other Adjunctive Medical Treatement in Management of Proliferative Vitroreotinopathy

Abstract

Despite the substantial progress that has been made during the past 30 years, the pathogenesis of PVR is incompletely understood. At present PVR can be considered as an excessive vitreoretinal wound healing process characterized by the phases of inflammation, proliferation, and remodeling. Once the vicious cycle of detachment resulting in a disintegration of the interphotoreceptor matrix and dissociation of RPE cells from Bruch’s membrane and a dispersion of the cells into the vitreal cavity, accompanied by breakdown of the blood–retinal barrier (BRB) and an influx of blood-derived cells and soluble factors including growth and inflammatory factors, serum fibrin, and metalloproteinases into the vitreous and retina. These “storm of cytokines” has started a permanent functional failure due to structural retinal changes is initiated. These factors stimulate the scattering, migration and proliferation of the cells of retinal and extraretinal origins followed by periretinal membrane formation. Myofibroblastic transdifferentiation of cells within the fibroproliferative membranes during epithelial- mesenchymal transition and extracellular matrix remodelling cause membrane contraction resulting in fixed redetachment of the retina (Fig.20). Potentially, growth factor mechanisms may hold the key to the imbalance of wound healing regulation seen in PVR. However, the exact roles of individual growth factors remain uncertain in what is likely to be a complex network of growth factor activity in the various stages of the evolution of PVR.