Proliferative vitreoretinopathy (PVR) remains the most commonly observed failure in the surgery of rhegmatogenous retinal detachment (RRD), albeit substantial efforts have been taken to better understand and manage the condition in the past. Basic research indicates that proliferative vitreoretinopathy illustrates scarring – end-stage of wound healing process, which occurs post-retinal detachment surgery. Current medical treatment for PVR has been directed toward the prevention of inflammation – first stage of wound-healing process, and inhibition of cell proliferation – second stage.
Surgery for proliferative vitreoretinopathy, at present, demonstrates high anatomical success rate, despite disappointing visual results. Utilization of adjunctive treatments for preventing cellular proliferation has been deemed effective in the treatment & prevention of PVR, or post-surgery recurrences. Proliferation control and strategies directed toward the improvement of visual outcome are imperative focus areas for future studies in PVR. In addition, researches on the peri-retinal and intra-retinal pathology of proliferative vitreoretinopathy have illustrated characteristic alterations, which will significantly influence surgical management and visual outcome.
Proliferative Vitreoretinopathy Market: New PVR Development Suppression & Prevention Methods to Underpin Growth
Proliferative vitreoretinopathy, an inflammatory fibrotic disease, stems from inflammatory milieu post-RRD, which in turn prevents retinal healing. Several studies aimed at suppressing or preventing the development of PVR are being conducted worldwide, with some of the recent ones elucidating effect of “substance P (SP),” and targeted use of non-steroidal anti-inflammatory drugs such as “lornoxicam.”
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Research carried out on lornoxicam has not only demonstrated successful improvement in the condition of retina and choroid, but also reduced frequency of membrane formation significantly. Studies conducted on substance P have revealed that SP has the capability of inhibiting apoptosis, and epithelial-mesenchymal transition (EMT) induced by TNFα caused, thereby suppressing or preventing development of proliferative retinopathy.