Abstract

The purpose of this study was to develop and test a nonlinear optical device to photoactivate riboflavin to produce spatially controlled collagen crosslinking and mechanical stiffening within the cornea. A nonlinear optical device using a variable numerical aperture objective was built and coupled to a Chameleon femtosecond laser. Ex vivo rabbit eyes were then saturated with riboflavin and scanned with various scanning parameters over a 4 mm area in the central cornea. Effectiveness of NLO CXL was assessed by evaluating corneal collagen auto fluorescence (CAF). To determine mechanical stiffening effects, corneas were removed from the eye and subjected to indentation testing using a 1 mm diameter probe and force transducer. NLO CXL was also compared to standard UVA CXL. The NLO CXL delivery device was able to induce a significant increase in corneal stiffness, comparable to the increase produced by standard UVA CXL.

Highlights

  • UVA-riboflavin crosslinking (UVA CXL), developed by Spoerl and Wollensak [1,2,3], is commonly used to induce crosslinking and stiffening of the corneal stroma as a therapeutic treatment for keratoconus and post LASIK ectasia that cause progressive, severe astigmatism

  • 3.1 Control of NLO CXL focal volume and depth Two-photon excited fluorescent images of riboflavin taken with the SPOT RT3 camera are shown in Fig. 3, and demonstrate control of fluorescent focal volume (Fig. 3(A)) and depth (Fig. 3(B))

  • As the beam expander setting increased from 1 to 5 the axial Full width half max (FWHM) length decreased from 79.5 μm to 28.6 μm

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Summary

Introduction

UVA-riboflavin crosslinking (UVA CXL), developed by Spoerl and Wollensak [1,2,3], is commonly used to induce crosslinking and stiffening of the corneal stroma as a therapeutic treatment for keratoconus and post LASIK ectasia that cause progressive, severe astigmatism. The parameters of standard UVA CXL were carefully chosen to reduce these risks, and the risk of corneal endothelial damage is only reached in corneas thinner than 400 μm [14]. This means that patients who have progressed further, and whose corneas are thinner than 400 μm, are not eligible for standard treatment. It is difficult to control the lateral position of crosslinking and the volume of crosslinking begins at the corneal surface, going only as deep as UVA light can penetrate into the tissue, diminishing in effectiveness with depth [3]

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