Proliferative vitreoretinopathy (PVR) is a disease that develops as a complication of rhegmatogenous retinal detachment.

[1][2] A number of studies have explored various possible adjunctive agents for the prevention and treatment of PVR, such as methotrexate, although none have yet been licensed for clinical use.

[4] Predisposing factors for Postoperative PVR are preoperative PVR, aphakia, high levels of vitreous proteins,[5] duration of retinal detachment before corrective surgery, the size of the retinal hole or tear, intra-ocular inflammation, vitreous hemorrhage, and trauma to the eye.

The accumulation of fluid in the subretinal space and the tractional force of the vitreous on the retina result in rhegmatogenous retinal detachment.

The RPE cells undergo epithelial-mesenchymal transition (EMT) and develop the ability to migrate out into the vitreous.

Lornoxicam not only normalized the expression of cyclooxygenases in both models of PVR, but also neutralized the changes of the retina and the choroid thickness caused by the injection of pro-inflammatory agents.

These are opaque and block the light falling on the retina so the retinal reattachment surgery needs to be performed after manually peeling the membrane off.

HGF stimulates RPE cell migration and its presence is also strongly detected in retinal membranes.