The article by Caporossi et al.1 about corneal crosslinking with riboflavin and ultraviolet-A (UVA) for the treatment of keratoconus in combination with the findings of other recent studies offers the scientific community an innovative and probably promising solution for this ectatic dystrophy of the cornea. Because the technique is extremely new and currently under study, we believe that future authors of similar articles should be very careful with the experimental design and the interpretation of findings. A rather significant issue is that although the authors describe noticeable changes in the UVA, best corrected visual acuity, and K-readings of these patients, they do not give an adequate explanation of why this occurs. It is known that the physicochemical properties of collagen change after corneal crosslinking and the stiffening effect stabilizes keratoconus,2 but in what way? One possible explanation is that the increase in the rigidity of the collagen causes flattening of the corneal apex. Another important aspect of the corneal crosslinking technique that should be considered is that crosslinking of collagen is a natural effect of aging.3 We are actually increasing rigidity by aging the cornea, and the long-term results of that might not be beneficial. Apart from this, we cannot exclude with certainty that the induced rigidity of the cornea will not promote premature ocular rigidity in general, creating future severe ocular problems (for example, age-related macular degeneration4). Finally, other ocular parameters such as tear function, corneal sensitivity, and alterations in conjunctival epithelium and goblet cells should be included in future studies. Understanding the true nature of the corneal crosslinking mechanism will guide us to finding a convenient solution for these patients and maybe improve their quality of life.
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Kymionis et al. (2007) studied this question.
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