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The role of ultraviolet-B in corneal healing following excimer Laser in situ Keratomileusis

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Pathology Oncology Research

Abstract

Corneal photoablation with the 193 nm argon fluorid excimer laser during photorefractive keratectomy (PRK) in high diopter range is frequently associated with subepithelial haze and consequent refractive regression due to avascular corneal wound healing. The wound healing response can be augmented by Ultraviolet-B (UV-B) exposure originating from sun or solarium. Clinically Laser in situ Keratomileusis (LASIK) even in high diopter range is associated with less subepithelial haze and regression than PRK. In an animal model, the morphologic changes of the rabbit cornea were evaluated following LASIK and secondary UV-B exposure. Light microsopic changes were found to be insignificant. Transmission electron microscopy (TEM) normal epithelium, epithelial adhesion structures and normal anterior stroma showed in the LASIK treated UV-B irradiated rabbit eyes. Around the peripheral LASIK cut, migrating keratocytes with pseudopodia were observed. Under the flap (160 μm depth) the overall stromal collagen structure was normal, some activated keratocytes and mild extracellular matrix formation within and around keratocytes were noted. Within activated keratocytes TEM showed prominent rough endoplasmic reticulum, Golgi apparatus, mitochondria and extracellular vacuoles, which showed resolution with time. These changes were much milder than in PRK treated-UV-B irradiated eyes. Secondary UV-B caused no long-term disturbance in corneal transparency in LASIK and UV-B treated rabbit eyes.

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Authors and Affiliations

  1. 1st Department of Ophthalmology, Semmelweis University, Tömô u. 25-29, 1083, Budapest, Hungary

    Zoltán Zsolt Nagy, Jeannette Tóth, Attila Nagymihály & Ildikó Süveges

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  1. Zoltán Zsolt Nagy
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  2. Jeannette Tóth
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  3. Attila Nagymihály
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  4. Ildikó Süveges
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Nagy, Z.Z., Tóth, J., Nagymihály, A. et al. The role of ultraviolet-B in corneal healing following excimer Laser in situ Keratomileusis. Pathol. Oncol. Res. 8, 41–46 (2002). https://doi.org/10.1007/BF03033700

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  • DOI: https://doi.org/10.1007/BF03033700

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