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Ellison Bentley, Sean Campbell, Heung M. Woo, Christopher J. Murphy; The Effect of Chronic Corneal Epithelial Debridement on Epithelial and Stromal Morphology in Dogs. Invest. Ophthalmol. Vis. Sci. 2002;43(7):2136-2142. doi: https://doi.org/.
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purpose. To determine the effect of chronic corneal epithelial debridement on epithelial and stromal morphology and extracellular matrix components, and to compare those changes to those in spontaneous chronic corneal epithelial defects (SCCED) in dogs.
methods. Axial corneal epithelial wounds, 10 mm in diameter, were created weekly for 8 weeks in five normal adult laboratory beagles. Slit lamp biomicroscopy and corneal pachymetry were performed weekly before wounding. Three days after the last debridement the dogs were killed humanely, and corneas were processed for light and electron microscopy and immunohistochemistry for collagen IV, collagen VII, fibronectin, and laminin.
results. No significant changes in corneal thickness were found. All samples demonstrated epithelial dysmaturation adjacent to the wound edge, and, in four of five, a narrow zone of nonadherent epithelium formed adjacent to the exposed stroma. All samples had a stromal acellular zone in the area of the defect and continuing for a short distance under the adjacent attached epithelium. Experimentally wounded dogs did not form the superficial hyaline acellular lamina found in 92% of dogs with SCCED. Laminin, collagen IV, and fibronectin were present on the stromal surface in all samples, and collagen VII was present in four of five samples. Transmission electron microscopy (TEM) demonstrated the presence of basement membrane on the surface of the exposed stroma.
conclusions. Epithelial changes are similar between experimentally wounded dogs and dogs with SCCED. The stromal acellular zone that forms in experimentally wounded dogs is distinct from the hyaline lamina observed in dogs with SCCED. The difference in the acellular stromal layers between chronically wounded dogs and dogs with SCCED may be of relevance to our understanding of the pathophysiology of persistent epithelial defects.
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