Abstract

Previous concepts for the pathogenesis of proliferative vitreoretinopathy (PVR) have focused on the central role of retinal pigment epithelium cells only, potentially contributing to the lack of clinical advances. More recent studies have demonstrated the essential role of retinal glial cells in the PVR healing response but failed to identify a consistent triggering mechanism.

We propose a revised concept for the pathogenesis of PVR based on retinal injury and response. A posterior vitreous detachment (PVD) is invariably present in patients with rhegmatogenous retinal detachment and PVR. There is evidence to suggest that the shearing forces of acute PVD can cause mechanical injury to the inner retina and trigger a subsequent intraretinal glial healing response. That response is characterised by subclinical glial cell activation and proliferation that may then be amplified into full-blown PVR by coexisting pathology such as retinal breaks and detachment.

Whether a PVD causes interface pathology depends on the plane of separation of the posterior vitreous and areas of increased vitreoretinal adhesions. If the vitreous separates in a plane or location that damages the inner retina then glial cell activation and proliferation are likely to develop. The severity of the subclinical inner retinal damage may then represent one of the missing links in our understanding of the pathogenesis of PVR and would explain many of the findings we encounter in clinical practice. Controlling the process of acute PVD and subsequent intraretinal response may be essential in the prevention and management of PVR.