The normal cornea is transparent and maintains itself as an immune privileged site, in part because it is avascular. Ocular insult and ocular hypoxia due to infectious keratitis, immunological conditions, corneal trauma, alkali injury, and contact lens (CL) wear [1, 2, 3] can encourage new blood vessels to grow from the limbus and, hence, neovascularization (NV). NV is generally accompanied with an inflammatory response and always represents a state of disease.
With CL wear, superficial NV is more common than deep stromal vessels. It is speculated that deep stromal NV may reflect a more profound insult (hypoxia) compared to that which generates only superficial NV. Both superficial and deep stromal NV are reported with the use of hydrogel, hard (polymethyl methacrylate [PMMA]), rigid gas permeable CLs, and scleral lenses, especially with a history of aphakia, extended wear, poor compliance, low oxygen permeable CLs, long-term CL wear (many years), and poor follow-up care.  Deep stromal NV is serious, possibly leading to loss of optical transparency of the tissue through stromal hemorrhage, scarring, and lipid deposition.
NV is believed to result from an inflammatory or hypoxic disruption of an exquisitely balanced corneal immune system. [5, 6, 7] Hydrogel, hard, rigid gas-permeable CLs and scleral lenses stimulate NV by either mechanically irritating the limbal sulcus or by creating corneal hypoxia, which leads to limbal inflammation, epithelial erosion, or hypertrophy, and, hence, angiogenic mediator release. 
Epithelial trauma  and/or hypoxia  may stimulate production of angiogenic factors by local epithelial cells, keratocytes, and infiltrating leukocytes [11, 12] (eg, macrophages, neutrophils). Some of these factors (ie, acidic and basic fibroblast growth factors, interleukin 1 [IL-1], and vascular endothelial growth factor [VEGF]) have been identified and isolated from cornea and tears. Angiogenic factors  stimulate a localized enzymatic degradation of the basement membrane of perilimbal vessels at the apex of a vascular loop. Vascular endothelial cells migrate and proliferate to form new blood vessels. 
Prevalence among CL wearers ranges from 0.1%-37%. [15, 16] Prevalence is lower in those who wear (rigid) gas permeable lenses than in soft CL wearers because the diameter of soft CLs are larger and cover the entire cornea, limbus, and surrounding perilimbal conjunctiva, decreasing oxygen from the atmosphere. [17, 18, 3] There is an increased risk for patients who have high myopia, dry eyes, or ocular surface disease (eg, idiopathic or associated with other diseases, such as acne rosacea, Sjögren syndrome, and immune dysfunction). There is also an increased risk in those who use extended wear hydrogel CLs and in those who use aphakic or therapeutic CLs.
Silicone hydrogel CLs with oxygen permeabilities approaching 100-200 Fatt Dk units have decreased the incidence of corneal NV among CL users. 
This condition is not associated with mortality. Symptoms can range from asymptomatic and mild to severe with loss of vision. NV in the cornea's visual axis can threaten visual function directly or through secondary hemorrhage,  scarring, or lipid deposition.
Incidence of subsequent corneal graft rejection is estimated by one study to be 1.7 times higher in a setting of vascularized rather than nonvascularized host corneas. Risk and severity of a graft rejection is believed to depend on the depth and extent of NV; hence, deep stromal vessels incur more risk than superficial pannus, and the more quadrants involved, the higher the risk of rejection. 
No ethnic predilection exists.
No gender predilection exists.
NV can occur and progress at any age.
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