Keratoconus and other corneal conditions associated with progressive stromal thinning including keratectasia after laser-assisted in situ kerato-mileusis (LASIK) and pellucid marginal degeneration represent therapeutic challenges. Until recently, available therapies including contact lenses, epikeratoplasty, intrastromal corneal rings, and corneal transplantation targeted, in principle, the abnormal shape of the cornea by mechanical means. The underlying molecular pathogenic mechanisms of corneal ectasia were not addressed with any of these therapies until the introduction of corneal collagen cross-linking to clinical practice in 1999.l This breakthrough clinical application was the result of multiple laboratory observations and discoveries made over preceding decades.
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