Vitreoretinal interface abnormalities in age-related macular degeneration: Prevalence, pathophysiology, and reciprocal influence.

Age-related macular degeneration (AMD) represents a leading cause of vision loss worldwide, while vitreoretinal interface (VRI) abnormalities constitute a dynamic boundary where posterior vitreous interacts with the retinal surface. We explore the intricate relationship between VRI abnormalities and AMD, examining prevalence, underlying pathophysiological mechanisms, and their reciprocal influence on disease development, progression, and treatment outcomes. Evidence suggests a higher prevalence of vitreomacular adhesion in exudative versus nonexudative AMD, while complete posterior vitreous detachment may exert protective effects against AMD progression. Tractional forces, inflammatory mediators, and structural disruption associated with VRI abnormalities may promote AMD progression and confound assessment of anti-vascular endothelial growth factor therapy efficacy. Recent findings underscore that epiretinal membranes might act as physical barriers reducing drug penetration, while VMT/VMA can alter macular morphology, potentially mimicking or obscuring therapeutic response. Surgical management of VRI abnormalities in AMD can achieve anatomical success, though visual outcomes may be limited by underlying macular pathology. Early detection and characterization of VRI abnormalities in AMD patients could improve risk stratification, guide treatment timing, and potentially lead to novel preventive strategies, highlighting the importance of comprehensive evaluation and individualized management approaches for optimizing outcomes in this complex patient population.