Abstract

Alterations in the molecular composition, organization, and structure of the human vitreous are an inevitable consequence of aging. Complete and innocuous posterior vitreous detachment (PVD) is the most common ultimate consequence of vitreous aging [see chapter II.C. Vitreous aging and PVD], but this can often be disturbed by anomalies in this complex process. Insufficient dehiscence at the vitreoretinal interface, excessive gel liquefaction, or both can result in an anomalous PVD (APVD), sometimes associated with vitreoschisis (VS), which is a lamellar split in the posterior vitreous cortex. APVD and VS are associated with different clinical pathologies. A detailed analysis of vitreous pathophysiology that leads to APVD and VS will enable a better understanding of vitreoretinal disease pathogenesis, improve diagnostic acumen, and provide new directions for therapeutic approaches that will ultimately lead to effective preventative strategies.

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