[The vitreoretinal interface and its role in the pathogenesis of vitreomaculopathies].

The vitreoretinal interface consists of the inner limiting membrane of the retina, the posterior vitreous cortex, and an intervening extracellular matrix. Hyalocytes are mononuclear phagocytes embedded in the posterior vitreous cortex, in a single layer of sparse density. At the macula, anomalous posterior vitreous detachment (PVD) results in either full-thickness vitreous cortex adhesion with vitreomacular traction syndrome, or partial-thickness adhesion due to vitreoschisis, a split in the posterior vitreous cortex. Anomalous PVD with vitreoschisis splitting behind the level of the monolayer of hyalocytes leaves a relatively thin hypocellular membrane attached to the macula. Vitreoschisis anterior to the level of the hyalocytes leaves a thicker cellular membrane. Persistent vitreopapillary adhesion promotes outward (from the fovea) tangential traction and is therefore associated with macular holes. Inward (centripetal) tangential traction results in macular pucker, almost always in the absence of persistent vitreopapillary adhesion. The English full-text version of this article is available at SpringerLink (under supplemental).