C. Stephen Foster Introduction Prolonged inflammation of the ocular surface causes destruction of corneal stem cells that can result in corneal epithelial defects or stromal ulcers. Such surface disorders further exacerbate chronic inflammation that can lead to corneal scarring and neovascularization. Moreover, collagenases produced by keratocytes and polymorphonuclears cause progressive corneal thinning with a potential risk of corneal perforation and loss of the eye. Previous studies showed, that the basement membrane facilitates migration of epithelial cells, reinforces adhesion of basal epithelial cells, promotes epithelial differentiation, and prevents epithelial apoptosis. When persistent corneal epithelial defect develops as a consequence of severe limbal stem cell deficiency, corneal surface can be replaced by conjunctival epithelium that can acquire a corneal-type phenotype in the presence of intact basement membrane.
Amniotic membrane is composed of one epithelial cell layer, basement membrane, and avascular matrix.
It was shown that amniotic membrane comprises structures that improve healing of the epithelium defects, i.e. basement membrane and growth factors. Collagen IV, a component of corneal epithelial basement membrane, is present in the stroma of amniotic membrane. The epithelium of amniotic membrane produces basic fibroblast growth factor, hepatocyte growth factor, and transforming growth factor b . Amniotic membrane prevents inflammatory cell infiltration and reduces apoptosis in keratocytes after transplantation on the corneal surface. It is noteworthy, that matrix metalloproteinases were identified in human amniotic membrane as well.