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Macular interface pathophysiology
Author(s) -
BASTAKIS GEORGE
Publication year - 2019
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2019.8223
Subject(s) - posterior vitreous detachment , epiretinal membrane , retina , ophthalmology , pathophysiology , medicine , vitreous membrane , vitrectomy , pathology , visual acuity , biology , neuroscience
The vitreous body occupies nearly 80% of the total ocular volume. It constitutes a dynamic structure that normally changes composition and formation through time. Vitreous characteristics can also change owing trauma, metabolic or oxidative factors. Physiologically, the process of gradual vitreous liquefaction (synchysis) comes along with the progressive vitreous collagen fibrils packing and aggregation (syneresis). Both synchysis and syneresis can lead to posterior vitreous detachment (PVD) after normal cortex dehiscence from the underlying retina tissue (vitreoretinal interface). In contrast, when the dehiscence process is abnormal (anomalous, incomplete or partial), various pathological conditions can be created on the retina. The pathologies formed specifically on the macular region from the above conditions are named vitreomacular interface diseases (VMID). In this presentation, we will analyse the pathophysiological mechanisms of different VMID like a macular hole (MH), vitreomacular traction syndrome (VTS) and epiretinal membrane (ERM). Moreover, we will present different molecular and cellular components mentioned in the literature and implicated in VMID formation, and we will try to highlight potential future treatment options for the diseases.