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Related Experiment Videos

Keratoconus morphology and cell dystrophy: a SEM study.

W L Jongebloed1, F Dijk, J G Worst

  • 1Lab. Histologie & Cell Biology, University of Groningen, The Netherlands.

Documenta Ophthalmologica. Advances in Ophthalmology
|August 1, 1989
PubMed
Summary
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This study visualizes keratoconus with Descemet rupture, revealing endothelial cell failure and epithelial changes. The findings highlight the topographical correlation between endothelial and epithelial pathologies in this condition.

Area of Science:

  • Ophthalmology
  • Cell Biology
  • Pathology

Background:

  • Keratoconus is a progressive thinning of the cornea.
  • Descemet membrane rupture can occur in advanced keratoconus, leading to corneal edema.
  • Endothelial dysfunction is a critical factor in corneal pathology.

Purpose of the Study:

  • To illustrate the ultrastructural changes in keratoconus with Descemet rupture using Scanning Electron Microscopy (SEM).
  • To investigate the pathological manifestations in both the endothelial and epithelial layers of the cornea.
  • To emphasize the topographical relationship between endothelial and epithelial damage.

Main Methods:

  • Scanning Electron Microscopy (SEM) imaging of corneal tissue from a patient with keratoconus and Descemet rupture.

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  • Detailed morphological analysis of endothelial cells and epithelial cells.

    • Main Results:

    • SEM revealed a Descemet membrane rupture with observable stromal pathology.
    • Severe endothelial cell degradation, including membrane perforation and cell lysis, was noted outside the rupture area.
    • Epithelial pathology included cell membrane degradation and irregularly shaped cells, particularly over surface depressions, correlating topographically with endothelial damage.

    Conclusions:

    • Descemet membrane rupture in keratoconus leads to significant endothelial cell failure.
    • Corneal epithelial changes mirror the underlying endothelial pathology.
    • SEM is a valuable tool for visualizing the complex interplay of cellular damage in keratoconus.