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XII. SUMMARY AND GENERAL CONCLUSIONS

for estimates on the cell density to be drawn. The estimated endothelial cell densities were not found to differ from a control group (Fig. 13). This finding was evidence against the view of Fuchs’ endothelial dystrophy being caused by an inadequate number of cells. It is however supported by the author’s observations on corneas with a guttate endothelium: 1) In article B and C no relation could be demonstrated between the cell density and a guttate endothelium in unoperated eyes (see also p. 20). 2) In article C the progression of guttate changes occurred independently of the cell loss. 3) In article B no postoperative guttae were found in any cornea which had not presented a guttate endothelium prior to the operation. Evidence that a guttate endothelium develops after surgery in a previous guttae-free cornea was also very small in article C in which the dystrophic changes were bilateral in 28 of 30 cases. The specular microscopic appearance of the guttate endothelium is strikingly similar to the endothelial appearance during anterior uveitis (ch. X). In contrast to the endothelial changes in Fuchs’ dystrophy, which are slowly progressive, the endothelial changes in anterior uveitis were however reversible to a large extent. As mentioned in the last section (cp. p. 37) it thus seems unlikely that the inflammatory guttae-like changes are caused by excrescences on the membrane of Descemet, as the guttate endothelium is said to be. On the other hand, the demonstration of reversible guttae-like changes raises the possibility of whether some of the changes in Fuchs’ dystrophy are reversible and not simply caused by membraneous excrescences of solid matter or conversely, whether some of the acute inflammatory changes may be precursors of more permanent lesions.