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. No data are available.

中文翻译：

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增生性玻璃体视网膜病变：修订后的视网膜损伤和反应概念


以前关于增生性玻璃体视网膜病变 （PVR） 发病机制的概念仅集中在视网膜色素上皮细胞的核心作用上，这可能导致缺乏临床进展。最近的研究表明，视网膜神经胶质细胞在 PVR 愈合反应中起着重要作用，但未能确定一致的触发机制。我们提出了一个基于视网膜损伤和反应的 PVR 发病机制的修订概念。玻璃体后脱离 （PVD） 总是存在于孔源性视网膜脱离和 PVR 患者中。有证据表明，急性 PVD 的剪切力可对视网膜内造成机械损伤，并触发随后的视网膜内神经胶质细胞愈合反应。这种反应的特征是亚临床神经胶质细胞活化和增殖，然后可能通过共存的病理（如视网膜破裂和脱离）扩增成全面的 PVR。PVD 是否会导致界面病变取决于玻璃体后部和玻璃体视网膜粘连增加区域的分离平面。如果玻璃体在损害视网膜内部的平面或位置分离，则可能会发生神经胶质细胞活化和增殖。亚临床视网膜内损伤的严重程度可能代表了我们对 PVR 发病机制的理解中缺失的环节之一，并可以解释我们在临床实践中遇到的许多发现。控制急性 PVD 的过程和随后的视网膜内反应对于预防和管理 PVR 可能至关重要。没有可用的数据。