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The initial description of Fuchs’ endothelial corneal dystrophy (FECD) in 19101 was made without a slit-lamp biomicroscope and, thus, did not include ‘drop-like’ excrescences beneath the endothelium observed by Vogt in 1921 who is credited with coining the term ‘guttae’ (Latin for drops).2 The origin of gutta has remained obscure. Possible explanations could be that they arise as cellular secretions3 or as extrusions from weak areas in Descemet membrane (DM).4
Limited reports describe morphologies of guttae in FECD. Laing et al described five stages distinguished by size, abnormalities of cells, coalescence of multiple guttae, and contour. They observed several stages in the same cornea.3 Gottsch et al suggest distinct guttae morphologies arise from specific genetic causes of FECD.4
Our studies of a transgenic mouse model of early onset FECD5 suggest novel insights into the origin of guttae.
Transgenic mice harbouring the Q455 K mutation in the α 2 collagen VIII gene, confocal microscopy, periodic acid Schiff staining, and transmission electron microscopy (TEM) were described previously.5
Confocal microscopy of a homozygous Q455 K mouse shows endothelial polymegathism and pleomorphism (figure 1A). Laing et al’s stage 1 and stage 2 guttae are present. Also seen is a distinct, sharply raised gutta occurring at a cell border, a morphology ascribed by …