Corneal Endothelium - Mechanisms of Corneal Edema

Mechanisms of Corneal Edema

Corneal endothelial cells are post-mitotic and divide rarely, if at all, in the post-natal human cornea. Wounding of the corneal endothelium, as from trauma or other insults, prompts healing of the endothelial monolayer by sliding and enlargement of adjacent endothelial cells, rather than mitosis. Endothelial cell loss, if sufficiently severe, can cause endothelial cell density to fall below the threshold level needed to maintain corneal deturgescence. This threshold endothelial cell density varies considerably amongst individuals, but is typically in the range of 500 - 1000 cells/mm². Typically, loss of endothelial cell density is accompanied by increases in cell size variability (polymegathism) and cell shape variation (polymorphism). Corneal edema can also occur as the result of compromised endothelial function due to intraocular inflammation or other causes. Excess hydration of the corneal stroma disrupts the normally uniform periodic spacing of Type I collagen fibrils, creating light scatter. In addition, excessive corneal hydration can result in edema of the corneal epithelial layer, which creates irregularity at the optically critical tear film-air interface. Both stromal light scatter and surface epithelial irregularity contribute to degraded optical performance of the cornea and can compromise visual acuity.

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