Keratocyte activation and inflammation in diffuse lamellar keratitis after formation of an epithelial defect.

Abstract Purpose: To examine the inflammatory reaction in acute or late-onset post-laser in situ keratomileusis (LASIK) diffuse lamellar keratitis (DLK) associated with an epithelial defect. Setting: Department of Ophthalmology, Helsinki University Central Hospital, Helsinki, Finland. Methods: Six consecutive LASIK patients presented with stage 2 to 3 unilateral DLK 1 to 4 days after formation of an epithelial detachment (intraoperatively or up to 19 months postoperatively). Five corneas of 5 DLK patients, 1 eye twice, were examined by corneal in vivo confocal microscopy 1 to 8 days after the appearance of the epithelial defect. Confocal microscopy of conjunctival venules was performed in 2 of 6 DLK patients to quantify leukocyte rolling and extravasation. Corneas of 5 patients and conjunctival venules of 4 patients who had uneventful LASIK served as controls. Results: Two of the 4 patients examined 0 to 1 day after the onset of DLK presented with small objects, presumably inflammatory cells (diameter 6.0 to 10.0 μm), in the LASIK flap interface. A third patient examined 1 day after the onset of DLK had larger objects (approximately 13.0 μm in diameter) in the interface. Three other cases (1 to 7 days after the onset of DLK) showed changes typical of keratocyte activation and altered extracellular matrix. All cases healed completely following treatment with steroids. Control LASIK subjects showed some keratocyte activation on day 5. Conclusions: Neither uneventful LASIK nor DLK induced an inflammatory reaction displaying leukocyte rolling in conjunctival venules or extravasation into the conjunctival stroma. Diffuse lamellar keratitis related to an epithelial defect does not always lead to the appearance of inflammatory cells in the flap interface. The corneal manifestations of epithelial defect-related DLK may originate from sterile epithelial–stromal or inflammatory cell–stromal cell interactions, leading to alteration of the keratocyte phenotype.