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Proliferative vitreoretinopathy (PVR) is the most common complication after repair of a retinal detachment. It is a clinical syndrome characterized by fibrocellular proliferation resulting in the formation of fibrotic epiretinal (i.e., preretinal and subretinal) membranes. Despite improvements in surgical techniques and anatomical outcomes, the treatment of PVR remains a challenge to preserve functional vision. PVR represents a wound healing response and multiple cytokines and growth factors may play a key role in its development. One of the most critical steps in the development of PVR is transformation of retinal pigment epithelium cells into fibroblastic and myofibroblastic phenotypes, which results in proliferation of fibrocellular membranes. Contraction of the membranes causes tractional retinal detachment. Treatment of PVR includes meticulous removal of fibrocellular membranes, relieving traction on all retinal breaks and intraocular tamponade. Several pharmacologic agents have demonstrated effectiveness in preventing the contraction of fibrocellular membranes in experimental models of PVR.
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Jusufbegovic et al. (2015) studied this question.
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