Proliferative vitreoretinopathy (PVR) is a disease entity related to a number of intraocular diseases, including retinal detachment (RD). Several studies have confirmed the hypothesis that PVR occurs as a reparative process induced by retinal breaks and excessive infl ammatory reaction. A survey of recently published series suggested that the frequency of PVR remains largely unchanged in primary RD, with the incidence ranging from 5.1 to 11.7%. PVR is the most common cause of failed repair of rhegmatogenous RD and risk factors for PVR are related to several, well-known pre-, intra-, and postoperative clinical situations. Currently, surgery such as pneumatic retinopexy, scleral buckling, and pars plana vitrectomy (PPV) is the mainstream therapeutic modality for RD and PVR. The goal of surgery is to create chorioretinal adhesion around all the retinal breaks and to relive all the tractional force. Single-operation reattachment rates were 73% for pneumatic retinopexy and 82% for scleral buckling after 6 months, and multipleoperation reattachment rates at 2 years were 99% for pneumatic retinopexy and 98% for scleral buckling for RD. Surgical success rates for PVR have improved as techniques and instruments of vitrectomy evolved. The introduction of ancillary techniques such as longeracting gases and long-term vitreous substitutes like silicone oil elevated the success rate from 35 – 40% to approximately 60 – 75% at 6 months. Despite these advances, more than one-fourth of initially successful cases results
in redetachment due to recurrent retinal traction. Furthermore, visual results are less satisfactory and only 40 – 80% of cases with anatomic success achieve ambulatory vision. As a result, PVR remains a diffi cult problem to manage and continuing efforts have been made to develop other forms of therapy to inhibit the pathologic response causing traction. Recent efforts have been directed toward the chemical inhibition of cellular proliferation and membrane contraction in PVR.