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Commentary: Interfere with the Interface?

It was observed that fewer patients with wet or dry age related macular degeneration (AMD) have complete posterior vitreous detachment (PVD) as compared with controls.[2,3] There are four important principles one needs to keep in mind when understanding the role of VMI in the disease pathogenesis.[1] First, the presence of vitreo‐macular traction (VMT) promotes a low‐grade inflammation that potentiates the disease activity. In addition, VMT can also damage the retinal pigment epithelium (RPE) cells thus increasing the RPE VEGF. Second, when there is an absence of PVD, it is hypothesized that there is decreased oxygenation at the retinal surface, which can lead to higher VEGF levels. Third, the presence of PVD allows cytokines sequestered close to the retina to easily diffuse away, thus decreasing the concentration of VEGF for disease activity. Last, based on a similar logic, the injected anti‐VEGF drugs are able to diffuse better when there is a presence of PVD, thus achieving higher therapeutic levels at the location of disease activity.