Summary: Corneal angiogenesis is associated with the most common forms of corneal blindness both worldwide as well as inindustrialized countries. Corneal angiogenesis is primarily caused by inflammatorydiseases of the cornea (most commonly keratitis), corneal hypoxia (contact lens wear) and limbal antiangiogenic barrier defects (mostcommonly aniridia, chemical burns).Currently, it’s evident that angiogenesis is tightly controlled by twocounterbalancing systems: angiogenic stimulating factors and angiogenicinhibiting factors, both secrete physiologically and keep balance innormal cornea. Corneal NV starts when the balance is shifted towardsangiogenic growth factors such as: (VEGF), (PDGF), (FGF), etc.In corneal inflammation, (hem) angiogenesis (i.e. outgrowth ofpathologic blood vessels into the cornea) is usually accompanied bylymphangiogenesis (outgrowth of lymphatic vessels).Complications of corneal angiogenesis leading to reduced visualacuity include: lipid keratopathy , intrastromal hemorrhage, secondarystromal edema due to leakage from immature blood vessels, in additioncorneal angiogenesis makes such a cornea a high-risk recipient bed in thecase of subsequent keratoplastyAntiangiogenic treatments fall into three categories: Angiostatice.g., steroids and ionidizing radiation, angioregressive e.g. anti-VEGF,endostatin, cyclosporine and angio-occlusive e.g. corneal photodynamictherapy, fineneedle diathermy.These antiangiogenic and antilymphangiogenic therapies appear toinhibit corneal NV and improve graft survival after both low-risk andhigh-risk keratoplasty by reducing the incidence of immune rejections.Result: Corneal hem- and lymphangiogenesis can cause asignificant reduction in visual acuity and blindness as well as render thesecorneas high risk in the case of a subsequent penetrating keratoplasty.Antiangiogenic treatment e.g., steroids, anti-VEGF and cornealphotodynamic therapy will dramatically improve the potential to inhibitcorneal angiogenesis effectively.