May 2007
Volume 48, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2007
Pathological and Morphometrical Alterations in the Keratoconic Cornea
Author Affiliations & Notes
  • J. R. Horne
    College of Optometry, University of Houston-Main, Houston, Texas
    Texas Eye Research and Technology Center, Houston, Texas
  • J. Goosey
    College of Optometry, University of Houston-Main, Houston, Texas
  • J. P. Bergmanson
    College of Optometry, University of Houston-Main, Houston, Texas
    Texas Eye Research and Technology Center, Houston, Texas
  • Footnotes
    Commercial Relationships J.R. Horne, None; J. Goosey, None; J.P. Bergmanson, None.
  • Footnotes
    Support Eye Birth Defects Foundation
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 1863. doi:https://doi.org/
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      J. R. Horne, J. Goosey, J. P. Bergmanson; Pathological and Morphometrical Alterations in the Keratoconic Cornea. Invest. Ophthalmol. Vis. Sci. 2007;48(13):1863. doi: https://doi.org/.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose:: Literature is largely limited to descriptive, pathological accounts of keratoconus (Kc). This study quantitatively analyzed Kc corneas, apically and peripherally, for structural changes occurring secondary to the disease process.

Methods:: An established protocol was used to preserve and prepare surgically removed corneas (2LKP, 7PKP) for light microscopy (LM). Images were taken from the cone apex and the periphery of the corneal button at 100x magnification using an Olympus BX51 digital microscope. Two transverse LM sections, approximately 200um apart, from both regions, were obtained and measurements from epithelium, anterior limiting lamina (ALL), and stroma were taken using NIH Image 1.63 software. Each measurement was repeated three times and averaged.

Results:: ALL in the apical cone was extensively affected by the disease. 56% of the area surveyed showed thinning of ALL, which, in 27% of this area, was completely absent. In the periphery, ALL was of reduced thickness over 11% of the tissue length and, of this area, 22% was completely eliminated. Apically in 8 corneas, there was a 30 % loss of peripheral stromal thickness. No histopathological manifestation of the disease was noted in the posterior cornea in any of the specimens.

Conclusions:: Kc is histopathologically apparent in the anterior cornea before it is manifested posteriorly. Epithelial cells may be involved in the pathophysiology of Kc, but the thickness variations of this layer may be more related to the consistently compromised ALL. In Kc, activated stromal cells appear to be involved in the phagocytosis of the ALL and stroma causing corneal thinning. These cells may also contribute to anterior scar formation. Peripheral to the cone, the cornea exhibited similar manifestations to those noted in the ectactic portion but changes were less pronounced. It is concluded that the loss of ALL and stromal tissue in the cone, perhaps in the presence of an inherent tissue weakening factor, leads to ectasia in Kc.

Keywords: cornea: basic science 
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