ABSTRACT
Invasion of new vessels through Bruch’s membrane occurs as part of age-related macular degeneration (ARMD), with concurrent invasion of fibroblasts, myofibroblasts, and variety of inflammatory cells, including lymphocytes, macrophages, and foreign body giant cells. The development of choroidal neovascularization (CNV) in ARMD has been hypothesized to represent a wound-healing response to stimuli, including those elicited by oxidative damage. Destruction or suppression of neovascularization is the most commonly used approach for CNV secondary to ARMD. The antiangiogenic effect from Photodynamic therapy (PDT) with verteporfin is marked but transient, damages the underlying choriocapillaris, and induces growth factors that may lead to reproliferation of vessels. The information and data, however, suggest the possibility of enhanced therapeutic effect from a combination of treatments of CNV in ARMD, and provide information needed to design larger clinical trials. Intravitreal triamcinolone acetonide not only has the potential to combat some of these effects induced by PDT, but may also independently affect the CNV in a favorable manner.
