Altered corneal structures in form‐deprived highly myopic chicks

Abstract

Aims/Purpose: Myopia is a leading cause of correctable and preventable vision loss worldwide, but the relationship between myopia development and growth of the anterior segment, particularly the cornea, has not been well established. This study aims to investigate whether experimental induction of myopia influences corneal structures in animals.Methods: Ten chicks were unilaterally form deprived by covering their right eyes with translucent diffusers at post‐hatching day 6 (P6). Refractive state, corneal shape, and ocular axial dimensions were measured at 4‐day intervals until P18 using a Hartinger refractometer, a custom‐made videokeratography system, and an A‐scan ultrasonographer, respectively. Parameters in treated vs control eyes were compared at the end of treatment. Repeated one‐way ANOVA was used for statistical analysis, and all parameters were expressed as mean ± SD.Results: At the end of treatment, form‐deprived eyes were myopic (−29.48 ± 8.26D vs. ‐0.61 ± 0.32D) and axially elongated (11.15 ± 0.55 mm vs. 9.51 ± 0.20 mm). At baseline (P6), treated and fellow contralateral eyes had similar corneal power (132.22 ± 6.37D vs. 132.64 ± 5.48D, p = 0.86) and thickness (167.93 ± 6.80 μm vs. 166.43 ± 7.27 μm, p = 0.63), but at P18 form‐deprived eyes had slower corneal flattening and thickening, resulting in significantly steeper (117.73 ± 5.03D vs. 113.22 ± 3.44D, p < 0.05) and thinner corneas (176.80 ± 7.52 μm vs. 192.35 ± 5.62 μm, p < 0.001) than fellow contralateral eyes. Repeated measures correlation analysis further indicated that axial elongation from P6 to P18 was significantly associated with corneal steepening (rrm = 0.77, p < 0.001) and thinning (rrm = −0.69, p < 0.001).Conclusions: This study provides insights into the impact of form deprivation myopia on corneal structures in juvenile animals. Specifically, the corneas of form‐deprived eyes were steeper and thinner because the natural corneal flattening and thickening processes were decelerated by treatment. Further studies are warranted to reveal the mechanisms responsible for this association between development of refractive error and corneal structure.