Abstract
Correction of refractive errors by excimer laser photorefractive keratectomy (PRK) is based on remodelling of the corneal curvature by highly controlled photoablation of the anterior corneal stroma.1 Tear fluid cytokines or other modulators produced by inflammatory cells, nerve cells, corneal epithelial or stromal cells, or extracellular matrix are likely to regulate the healing of the photoablated area.2–9 As the healing of the wound determines the refractive result, it is most important to study the mechanisms that control the healing response.
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