Purpose: To investigate whether photorefractive keratectomy (PRK) performed in infant primates can modify emmetropization and therefore could be used to study mechanisms of refractive error development.
Methods: Six healthy rhesus monkeys ranging in age from 2 to 3 months were randomly divided into two groups (n = 3 each). Anisometropia was induced in each animal by performing PRK on one eye. Hyperopic anisometropia was induced in group A monkeys by flattening the cornea of the right eye, whereas myopic anisometropia was produced in group B monkeys by steepening the cornea of the right eye. Corneal morphology and topography, refractive status, and axial growth were evaluated over a 5-month observation period.
Results: All the PRK-treated corneas were re-epithelialized and transparent within 3 days after surgery. Subsequently, all the surgically treated eyes exhibited interocular alterations in axial growth rate that were appropriate to compensate for the PRK-induced anisometropia. Specifically, vitreous chamber elongation rates were faster in the eyes with induced hyperopias than in their fellow eyes (0.63 +/- 0.05 mm vs. 0.40 +/- 0.09 mm), but slower in the eyes with induced myopia than in their fellow eyes (0.58 +/- 0.13 mm vs. 0.73 +/-0.10 mm). In some animals, the recovery from the induced anisometropia was facilitated by interocular differences in the rate of corneal flattening. However, the rates of corneal flattening in the treated eyes and their fellow eyes were not significantly different.
Conclusions: PRK-induced defocus predictably alters axial growth rate and the normal course of emmetropization in developing eyes. Thus, PRK is a useful alternative to current methods used to impose experimental refractive errors in laboratory animals. These results also indicate that refractive surgery performed in childhood may affect normal growth of the eye, resulting in decreased predictability of future refractive status.