The concept of keratoconus as a true corneal ectasia is being increasingly challenged in recent studies. Indeed, ectasia implies stromal stretching; an anisometric process which should result in an increase of the surface area. However, studies on this subject are conflicting. Using raw data from Placido specular corneal topography, Smolek and Klyce analysed anterior corneal surface area in normal corneas and keratoconus. They concluded that corneal surface area was similar in both groups, which strongly suggested keratoconus as a form of warpage rather than a true ectasia. They also followed a case showing no area increase at all with keratoconus progression. More recently, Kitazawa et al., as well as Cavas-Martinez et al., found greater central corneal surface area in keratoconus[13,14] using data from anterior and posterior corneal surface areas obtained with an anterior segment OCT and a Sirius system corneal topographer respectively. However, it is important to note that those studies used particular geometrical assumptions and algorithms, rather than direct elevation based discrete surface element summing  for calculating the corneal surface area, and did not take the total diameter of the cornea into account.
In the present study, we challenged our previous findings excluding potential inter-individual biases. To calculate corneal surface area, we used a previously described method inspired from landscape measurements using raw elevation data with no assumption on the corneal shape or local curvature. We obtained elevation data from topographic measurements of Orbscan II which has been shown to be repeatable  and we extrapolated surface areas up to measured corneal diameter.
We found that although anterior and posterior corneal surface area was slightly greater in affected eyes, it is unlikely that this difference reflects a true ectatic process (difference between the means of 1.6 mm² which represents an increase of about 1.17% and 1.09% of the anterior and posterior corneal surfaces, respectively). Moreover, corneal surface area remained strongly correlated, and Bland-Altman analysis also showed a strong inter-ocular agreement. Our results show, that in the same individual suffering from a UHAKC, there was a statistically significant, although clinically irrelevant difference between the affected and less or unaffected eye. If it was assumed that both corneas exhibited a high degree of enantiomorphism before the onset of unilateral keratoconus, then the small difference measured after the onset of keratoconus reflects a different process from true ectasia. Epithelial remodelling could probably influence the anterior area of the cornea  and contribute to corneal surface modifications.
In addition, surface area showed greater correlation with corneal diameter and anterior chamber depth than with maximal keratometry and minimal pachymetry. In our opinion these results demonstrate that it is unlikely that increased corneal surface area is a sign of keratoconus progression or keratoconus severity, and is not consistent with increasing surface area from a stromal stretching effect in progressive keratoconus
Rather, the data strongly suggests that a progressive surface areas increase resulting from stromal stretching as keratoconus progresses seems inconsistent. Corneal surface area and corneal diameter differences observed in patients with highly asymmetric keratoconus are consistent with our previous results between normal eyes and keratoconus. These observations suggest that keratoconus corresponds to a corneal surface area redistribution rather than a significant corneal stretching. It more likely represents a permanent corneal deformation with a relatively stable total surface area, and therefore may be considered as an extreme form of corneal warpage caused by structural damage secondary to stromal degeneration and external forces . We have previously shown that unilateral eye-rubbing and nocturnal compression on the same side can lead to UHAKC. In this case-control study, we found that patients with unilateral or highly asymmetric keratoconus reported significantly more eye rubbing and more rubbing in the affected eye. Sleeping on the side or stomach was also found to be a risk factor for developing keratoconus. Surprisingly, we did not find an increased risk in the presence of a family history of keratoconus.
We measured a slight increase in the depth of the anterior chamber on the affected side. In the context of a generally isometric deformation, the average curvature of the corneal surfaces is largely unaffected, which implies that an increase in the paracentral curvature is necessarily accompanied by a decrease in the peripheral curvature, and an increase in the negative asphericity of the corneal profile. A central sagittal curvature steepening with a concomitant peripheral flattening could explain a slight central deepening of anterior chamber. The entire anterior chamber volume could be studied to clarify this finding.
In light of our previous study which showed greater corneal diameter in keratoconus than normal eyes, we aimed to establish the role of horizontal corneal diameter in the surface area differences we observed. We found in UHAKC that corneal diameter was slightly greater in the affected eye, however this difference was small and at the limit of statistical significance. Moreover, Bland-Altman analysis showed strong agreement between the keratoconus eye and the fellow eye. We thus hypothesised that it seems unlikely that corneal diameter is a marker or a consequence of severity and progression of keratoconus. To explain the presence of a larger corneal diameter in patients with keratoconus, we can hypothesize that a larger corneal diameter offers less mechanical resistance due to reduced scleral support. More studies are needed to clarify the possible role of corneal diameter in keratoconus pathogenesis.