Background: It has long been recognized that more people are emmetropic than would be expected from a random combination of the refractive and axial components of the eye. However, it has been difficult to determine whether this is the result of an active emmetropization mechanism.
Methods: This paper reviews some of the studies in animals that have been conducted during the past 20 years. Four basic paradigms have been used to determine whether the visual environment helps guide eyes to emmetropia: 1) observing the normal pattern of ocular development, 2) shifting the location of the focal plane with minus- (and plus-) power lenses, 3) removing focused images by visual form deprivation and, 4) restoring form vision after a period of visual deprivation.
Results: Data from many studies suggest that an active emmetropization mechanism guides the postnatal development of the eye, matching the axial length to the focal plane. In normal development, the axial length initially is generally short so that the photoreceptors are in front of the focal plane of the unaccommodated eye. The subsequent axial elongation eventually moves the photoreceptors to, but not past, the focal plane. When animals are raised with the focal plane shifted posteriorly with minus-power lenses, the eyes elongate to approximately match the displaced focal plane. When information about the location of the focal plane is removed by visual deprivation, the eyes elongate past the point of emmetropia and become myopic. When developing eyes that have become myopic from a brief period of form deprivation are re-exposed to patterned images, they can slow their axial elongation, gradually eliminating the myopia. Data from several species suggest that the axial length is regulated within the eye itself, involving direct, spatially local communication from the retina to the sclera. It also appears that the regulation of axial elongation involves active control of the scleral extracellular matrix.
Conclusions: If humans have a similar mechanism, then successful emmetropization in children may involve two components. One is to inherit a fully functional emmetropization mechanism. Equally important is exposure to a "normal" visual environment. Deficiencies in either, or an interaction between a compromised mechanism and a non-optimal visual environment might also prevent emmetropization.