What ocular interface may significantly modify the response to therapy with anti-VEGF agents?

The vitreoretinal interface plays a crucial role in modifying the response to therapy with anti-VEGF agents for several reasons. First, the vitreous body is filled with hyaluronic acid and collagen, which can influence the distribution and efficacy of anti-VEGF agents once they are injected into the eye. If the vitreous has abnormal attachments or if there is a posterior vitreous detachment, it can affect how well the drug penetrates to reach the retinal tissue.

Additionally, the presence of any abnormalities at the vitreoretinal interface, such as epiretinal membranes or tractional changes, can further impact the delivery and action of the anti-VEGF agents. For effective treatment of conditions like age-related macular degeneration (AMD) or other causes of choroidal neovascularization (CNV), the interaction of the medication with the retinal layers is critical. If the integrity of this interface is disrupted or altered, it may lead to a reduced response to treatment, affecting the overall visual outcomes.

In contrast, while the retinal, corneal, and pupillary interfaces do play roles in vision and ocular health, they do not have the same direct impact on the pharmacodynamics of anti-VEGF therapy as the vitreoretinal interface does.