Current and emerging therapies for corneal neovascularization

Abstract

The cornea is unique because of its complete avascularity. Corneal neovascularization (CNV) can result from a variety of etiologies including contact lens wear; corneal infections; and ocular surface diseases due to inflammation, chemical injury, and limbal stem cell deficiency. Management is focused primarily on the etiology and pathophysiology causing the CNV and involves medical and surgical options. Because inflammation is a key factor in the pathophysiology of CNV, corticosteroids and other anti-inflammatory medications remain the mainstay of treatment. Anti-VEGF therapies are gaining popularity to prevent CNV in a number of etiologies. Surgical options including vessel occlusion and ocular surface reconstruction are other options depending on etiology and response to medical therapy. Future therapies should provide more effective treatment options for the management of CNV.

Keywords: Angiogenesis; Cornea; Eye; Inflammation; Limbal stem cell deficiency; Neovascularization; Vascularization.

Figure 1.

Slit lamp photographs demonstrating CNV. Necrotic corneal ulcer and persistent epithelial defect with surrounding ring infiltrate and CNV secondary to acanthamoeba (1A, photograph courtesy of Marius Miron). Stromal CNV from acute stromal rejection of a deep anterior lamellar keratoplasty (1B). Regressing deep CNV with mild surrounding haze and lipid secondary to HSV immune stromal keratitis (1C). Deep frond of CNV with accompanying lipid deposition from long-term rigid gas permeable contact lens abuse (1D).

Figure 2.

Slit lamp photographs of CNV secondary to limbal stem cell deficiency from various etiologies are depicted: Stevens Johnson Syndrome (2A), alkaline chemical injury (2B), mucous membrane pemphigoid (2C), and long-term soft contact lens abuse (2D).