I read with interest the recent work by Holopainen and Krootila and would like to ask the authors to clarify some points about their study and offer comments on their findings. The authors stated in the Methods that the central corneal thickness was recorded. However, the documented results in the Results was the corneal thickness at the thinnest point. The authors should not have neglected this disagreement because the central corneal thickness does not always represent the least value of the corneal thickness in keratoconus. I also note that the population in this study consisted of those with keratoconus and keratectasia and other patients. They might have different responses to corneal cross-linking (CXL), as evidenced by a previous study in which a significant difference in the change in pachymetry measurement between keratoconus patients and ectasia patients was found after CXL. Therefore, interdisease variability in postoperative main outcome measures, that is, corneal thickness measurements, should be considered. Also, the cornea per se in progressive keratoconus or ectasia may thin during 6 months of follow-up. This necessitates a control group in which no intervention is performed and serial corneal thickness measurements are obtained.
Corneal thinning generally is concomitant with the early CXL postoperative course. Similarly, a transient corneal thinning was observed by the authors after 1 postoperative month in their study. The physiologic features of this initial thinning are, as yet, unclear. Confocal in vivo microscopy performed after CXL treatment revealed that the subbasal nerve plexus with its branched and tortuous nerve fibers, which had been very easily identifiable before surgery, no longer could be visualized in the treated central corneal area for approximately 3 months. It is still unclear whether nerve fiber destruction occurs as a result of mechanical epithelial abrasion and of riboflavin or ultraviolet A treatment; however, the destroyed subbasal nerve plexus may reduce the corneal sensitivity with a declining function of the endothelial pump. So, I do not think that this transient corneal thinning is most likely attributable to a temporary increase in endothelial pump activity. Rather, it may involve anatomic and structural changes in corneal collagen fibrils, changes in corneal hydration, keratocyte apoptosis, and changes in glycosaminoglycans.