Cellular activity at the vitreoretinal interface after full-thickness retinal wounds was studied in rabbit eyes, using light and electron microscopy. Glial cell extensions grew initially on the retinal surface around the wound site. This brief period of glial proliferation was associated with the posttraumatic inflammatory response and, more specifically, with phagocytic monocyte accumulation at the vitreoretinal interface. Once the inflammation subsided, this abortive attempt to grow membranes on the retinal surface stopped and true epiretinal membranes did not develop. Our observations suggest that intraocular inflammation and macrophage response determine the extent of healing and scarring on an injured retinal surface, and thus may play a key role in the pathogenesis of epiretinal membranes.