Quantified histopathology of the keratoconic cornea

• Published in: Optometry and vision science Vol. 88; no. 8; pp. 988 - 997
• Main Authors: Mathew, Jessica H, Goosey, John D, Bergmanson, Jan P G
• Format: Journal Article
• Language: English
• Published: United States 01.08.2011
• Subjects: Adolescent; Adult; Aged; Cornea - surgery; Cornea - ultrastructure; Epithelium, Corneal - ultrastructure; Humans; Keratoconus - pathology; Keratoconus - surgery; Microscopy, Electron, Transmission; Middle Aged; Severity of Illness Index; Young Adult
• ISSN: 1040-5488; 1538-9235
• DOI: 10.1097/opx.0b013e31821ffbd4

This study systematically investigated and quantified histopathological changes in a series of keratoconic (Kc) corneas using a physiologically formulated fixative to not further distort the already distorted diseased corneas. Twelve surgically removed Kc corneal buttons were immediately preserved and processed for light and transmission electron microscopy using an established corneal protocol. Measurements were taken from the central cone and peripheral regions of the host button. The sample size examined ranged in length from 390 to 2608 μm centrally and 439 to 2242 μm peripherally. The average corneal thickness was 437 μm centrally and 559 μm peripherally. Epithelial thickness varied centrally from 14 to 92 μm and peripherally from 30 to 91 μm. A marked thickening of the epithelial basement membrane was noted in 58% of corneas. Centrally, anterior limiting lamina (ALL) was thinned or lost over 60% of the area examined, whereas peripheral cornea was also affected but to a lesser extent. Histopathologically, posterior cornea remained undisturbed by the disease. Anteriorly in the stroma, an increased number of cells and tissue debris were encountered, and some of these cells were clearly not keratocytes. It is concluded that Kc pathology, at least initially, has a distinct anterior focus involving the epithelium, ALL, and anterior stroma. The epithelium had lost its cellular uniformity and was compromised by the loss or damage to the ALL. The activity of the hitherto unreported recruited stromal cells may be to break down and remove ALL and anterior stromal lamellae, leading to the overall thinning that accompanies this disease.