Today eyes with massive periretinal proliferation which are often seen after uncured retinal detachments or after perforating injuries can be cured at least in 25 to 35% of the cases, even with modern surgical techniques. This is due to proliferation of cells, which enter through different pathways--retinal tears, perforating wounds of sclera and chorioidea, damaged retina or retinal vessels--into the vitreous and form membranes, which prevent the retina to attach. In the vitreous gel these cells of different origin can transform into fibroblast-like or myofibroblast-like cells. They also behave in the same way like fibroblasts or myofibroblasts and cause a kind of excessive wound healing and scar formation in the vitreous cavity. With the use of modern vitreous techniques we could cure nearly 43% of 14 patients with MPP after uncured retinal detachments or after perforating injuries. Because mechanical removal of intravitreal and periretinal membranes alone turned out to be unsuccessful in nearly 60%, methods of medical therapy to suppress this cell-activity seemed to be rather needed. By animal experiment we tried to produce retinal detachments by transplantation of homologue fibroblasts into the vitreous cavity of rabbit eyes, and observed traction detachments in 55% of the eyes. Histologic examination showed a rapid change of loose, round fibroblasts into elongated cells with long nuclei, which formed strands and caused vasoproliferation, especially where the strand reached the rabbit retina. By means of autoradiography the peak of cell activity turned out to be in the 3rd week after cell-transplantation and further examinations of the optic disc showed, that the vascular endothelium cell might be one source of the proliferation. There was no difference between the number of eyes which developed retinal detachment in the aphakic eyes and in the lentectomized and vitrectomized eyes, but we observed the clinical appearance of MPP earlier and more pronounced in the lentectomized and vitrectomized eyes. In the last experiment we tried to inhibit intraocular proliferation with intravitreal dexamethasone alcohol. This leaded to a significant reduce of the number of experimental detachments and vasoproliferations.