title: Keratocyte activation and inflammation in diffuse lamellar keratitis after formation of an epithelial defect.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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 microm), in the LASIK flap interface. A third patient examined 1 day after the onset of DLK had larger objects (approximately 13.0 microm 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.
authors.affiliation: Department of Ophthalmology, University of Helsinki, Helsinki, Finland. jukka.moilanen@hus.fi
authors.forename: Jukka A O
authors.initials: JA
authors.lastname: Moilanen
authors.forename: Juha M
authors.initials: JM
authors.lastname: Holopainen
authors.forename: Maaret
authors.initials: M
authors.lastname: Helintö
authors.forename: Minna H
authors.initials: MH
authors.lastname: Vesaluoma
authors.forename: Timo M T
authors.initials: TM
authors.lastname: Tervo
mesh_terms: D000328:Adult; D002450:Cell Communication; D002465:Cell Movement / Q000502:physiology; D003228:Conjunctiva / Q000098:blood supply; D003319:Corneal Stroma / Q000473:pathology; D004847:Epithelial Cells / Q000473:pathology*; D019573:Epithelium, Corneal / Q000473:pathology; D005260:Female; D005347:Fibroblasts / Q000473:pathology*; D006801:Humans; D007431:Intraoperative Complications; D007634:Keratitis / Q000209:etiology* / Q000473:pathology; D020731:Keratomileusis, Laser In Situ / Q000009:adverse effects*; D007962:Leukocytes / Q000502:physiology; D008297:Male; D018613:Microscopy, Confocal; D008875:Middle Aged; D011183:Postoperative Complications; D013524:Surgical Flaps / Q000473:pathology