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Updated: Jul 2, 2026

Development of a Noninvasive, Laser-Assisted Experimental Model of Corneal Endothelial Cell Loss
Published on: April 24, 2020
[Pathogenesis of Fuchs endothelial corneal dystrophy, the fibrillar layer and individualized treatment]
Antonia Howaldt1, Thomas Clahsen2,3, Mert Mestanoglu2
1Department of Ophthalmology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Kerpener Str. 62, 50937, Köln, Deutschland. antonia.howaldt@uk-koeln.de.
Abstract:
Fuchs endothelial corneal dystrophy (FECD) is a genetic and age-associated corneal disease characterized by an accelerated loss of corneal endothelial cells and an increased subendothelial deposition of extracellular matrix (ECM). Clinically, advanced disease leads to corneal edema with subsequent reduction in visual acuity. In the majority of patients with advanced FECD, a fibrillar layer (FL) appears on the posterior corneal surface. This FL is mostly localized in the inferotemporal corneal quadrant, marks areas with significantly reduced endothelial cell density and increased corneal thickness in the sense of edema and can be visualized and measured using Scheimpflug backscatter analysis due to increased backscatter. FECD is currently the most common indication for corneal transplantation worldwide, usually in the form of Descemet membrane endothelial keratoplasty (DMEK). New treatment approaches include variations of DMEK surgery such as hemi- or quarter DMEK with individualized and smaller grafts or Descemet membrane stripping only (DSO). In the future, clinical imaging of the FL as a particularly affected endothelial area could be important for FECD progression assessment and planning of surgical interventions. This article provides an overview of the current state of research on the clinical aspects, pathogenesis, fibrillar layer and individualized treatment of FECD.
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