[Pathogenesis of traumatic proliferative vitreoretinopathy]

Proliferative vitreoretinopathy is the main cause of loss of vision following posterior penetrating eye injury. Clinically, it can range from macular epiretinal membrane to total retinal detachment and phthisis bulbi. To gain more knowledge of its pathogenesis, the author performed morphologic studies using a primate model and also studied the distribution of fibronectin in 13 enucleated patient eyes using immunofluorescent histochemical techniques. Results indicate this disease process represents an overstimulated response to retinal injury. Posterior vitreous detachment at the level of internal limiting membrane appears to be a predisposing factor. During the active phase of the disease process, there is selective increase of fibronectin in the choroid. This increase is not merely due to the passive leakage of plasma caused by the injury, but the choroid itself produces cellular fibronectin. Fibronectin is known to enhance wound healing and may be an important factor in the pathogenesis of proliferative vitreoretinopathy.