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Aims A blind, randomised, prospective, bilateral study to investigate the efficacy of riboflavin/ultraviolet A corneal collagen cross-linkage to halt the progression of keratoconus. Methods 24 patients with early/moderate bilateral keratoconus with recent progression were recruited. One eye was randomly assigned to undergo collagen cross-linkage following epithelial removal with riboflavin 0.1% and ultraviolet A (370 nm at 3 mW/cm2M). The other remained untreated as a control. The follow-up was 18 months in 22 patients. Results At 18 months, Orbscan II 3 mm, 5 mm keratometry and simulated astigmatism and cone apex power and wave-front measurements (Keraton Scout), including root mean square, coma and pentafoil showed significant reductions from baseline in treated compared with untreated eyes (p=0.04). In treated eyes at 18 months, the best spectacle-corrected acuity improved (p=0.01), and Orbscan II-simulated keratometry (p<0.001), 3 mm keratometry (p=0.008), simulated astigmatism (p=0.007), cone apex power (p=0.002), root mean square, coma, spherical aberration, secondary astigmatism and pentafoil (p=0.05) decreased from baseline. One treated eye experienced transient recurrent corneal erosions; otherwise there were no complications attributable to the treatment. Conclusions Corneal collagen cross-linkage appears to be an effective and safe modality to halt the progression of keratoconus. Improvements in visual and topographic parameters are seen in some eyes. [ABSTRACT FROM AUTHOR]

Corneal neovascularization, the growth of new blood vessels in the cornea, is a leading cause of vision impairment after corneal injury. Neovascularization typically occurs in response to corneal injury such as that caused by infection, physical trauma, chemical burns or in the setting of corneal transplant rejection. The NADPH oxidase enzyme complex is involved in cell signalling for wound-healing angiogenesis, but its role in corneal neovascularization has not been studied. We have now analysed the role of the Nox2 isoform of NADPH oxidase in corneal neovascularization in mice following chemical injury. C57BL/6 mice aged 8-14 weeks were cauterized with an applicator coated with 75% silver nitrate and 25% potassium nitrate for 8 s. Neovascularization extending radially from limbal vessels was observed in corneal whole-mounts from cauterized wild type mice and CD31+ vessels were identified in cauterized corneal sections at day 7. In contrast, in Nox2 knockout (Nox2 KO) mice vascular endothelial growth factor-A (Vegf-A), Flt1 mRNA expression, and the extent of corneal neovascularization were all markedly reduced compared with their wild type controls. The accumulation of Iba-1+ microglia and macrophages in the cornea was significantly less in Nox2 KO than in wild type mice. In conclusion, we have demonstrated that Nox2 is implicated in the inflammatory and neovascular response to corneal chemical injury in mice and clearly VEGF is a mediator of this effect. This work raises the possibility that therapies targeting Nox2 may have potential for suppressing corneal neovascularization and inflammation in humans. [ABSTRACT FROM AUTHOR]