[Vitreoretinal proliferation. II. Pathogenic hypotheses]

The pathogenesis of proliferative vitreoretinopathy remains poorly understood and a large variety of hypotheses have been developed in an attempt to investigate cellular proliferations that follow rhegmatogenous retinal detachment. Several growth promoting factors have been identified within the vitreous body and proliferative membranes from patients with PVR. Their enzymatic, chemotactic, mitogenic or proinflammatory properties make them good candidates, either alone or more probably in a synergistic manner. They may be involved at different levels in the successive stages of PVR, cell migration, proliferation or vitreoretinal contraction. Numerous ocular and even extra-ocular structures may be involved as retina, pigment epithelium, ciliary body and serum, contain large amounts of these growth factors. Immune mediated inflammatory reactions have also been described and vitreoretinal strands exert additional mechanical effects. Current pathogenetic hypotheses suggest that PVR results from a wound healing process induced by retinal breaks and detachment of the neuroepithelium, when is reached a threshold of biological stimulation. Cell proliferation is unfortunately often overstimulated and the proliferating cells invade the vitreous cavity. If surgery is not capable of efficiently blocking the proliferation, it will be autostimulated and lead to a complete vitreoretinal retraction.