The process of emmetropization is the adjustment of the length of the optical axis to the given optical properties of the cornea and lens after the end of the second year of life. Since its underlying mechanisms have not been fully explored yet, we reviewed findings available in the literature to discuss its potential etiology and the mechanism of myopization as an overshooting of emmetropization.
The process of emmetropization occurs by axial elongation. Up to the end of the second year of life, the eye grows spherically by active increase in scleral volume. Axial elongation in the process of emmetropization is associated with thinning of the retina and reduced density of retinal pigment epithelium cells (RPE) in the retro-equatorial region, and with thinning more of the choroid than of the sclera, starting at the equator and being most marked at the posterior pole. In contrast, retinal thickness and RPE density in the macular region and thickness of Bruch's membrane (BM) in any region are independent of axial length.
It led to the hypothesis that axial elongation occurs by production of BM in the retro-equatorial region leading to a decreased RPE density and retinal thinning in that region and a more tube-like than spherical enlargement of the globe, without compromise in the density of the macular RPE cells and in macular retinal thickness. The increased disc-fovea distance in axially myopic eyes is caused by the development and enlargement of parapapillary, BM free, gamma zone while the length of macular BM, and indirectly macular RPE cell density and macular retinal thickness, remain constant. The target tissue for medical modification of emmetropization/myopization may be the RPE, producing and elongating BM in the retro-equatorial region.
Axial elongation in the process of emmetropization may occur by production and sagittal expansion of the Bruch membrane in the retroequatorial region leading to decreased retinal pigment epithelium cell density and retinal thinning in that region, and unchanged retinal pigment epithelium cell density and unchanged retinal thickness in the macula, with parapapillary gamma zone compensating for the increased disk–fovea distance, compression of the posterior choroid, and secondary scleral thinning.
*Beijing Institute of Ophthalmology, Beijing Ophthalmology and Visual Science Key Lab, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China;
†Department of Ophthalmology, Medical Faculty Mannheim of the Ruprecht-Karls-University of Heidelberg, Mannheim, Germany;
‡Department of Ophthalmology and Visual Science, Tokyo Medical and Dental University, Tokyo, Japan; and
§Eye Institute of Shandong University of Traditional Chinese Medicine, Jinan, Shandong, China.
Reprint requests: Jost B. Jonas, MD, Universitäts-Augenklinik, Theodor-Kutzer-Ufer 1-3, Mannheim 68167, Germany; e-mail: firstname.lastname@example.org
J. B. Jonas: Consultant for Mundipharma Co, (Cambridge, United Kingdom); Patent holder with Biocompatibles UK Ltd (Franham, Surrey, United Kingdom) (Title: Treatment of eye diseases using encapsulated cells encoding and secreting neuroprotective factor and/or anti-angiogenic factor; Patent number: 20120263794), and Patent application with the University of Heidelberg (Heidelberg, Germany) (Title: Agents for use in the therapeutic or prophylactic treatment of myopia or hyperopia; Europäische Patentanmeldung 15 000 771.4). S. Panda-Jonas: Patent holder with Biocompatible UK Ltd (Title: Treatment of eye diseases using encapsulated cells encoding and secreting neuroprotective factor and/or anti-angiogenic factor; Patent number: 20120263794), and patent application with the University of Heidelberg (Title: Agents for use in the therapeutic or prophylactic treatment of myopia or hyperopia; Europäische Patentanmeldung 15 000 771.4). The remaining authors have no financial/conflicting interests to disclose.