The cleavage plane of corneal epithelial adhesion complex in traumatic recurrent corneal erosion.

PURPOSE To determine the anatomic cleavage plane of the corneal epithelial adhesion complex in eyes with traumatic recurrent corneal erosion (RCE). METHODS A loosened sheet of corneal epithelium was obtained from corneal epithelial wounds in eight patients with traumatic RCE, before each patient underwent phototherapeutic keratectomy. Three control groups were employed in the study, including normal corneal epithelial sheets obtained by mechanical separation, normal corneal tissues obtained by partial lamellar keratectomy during pterygial surgery, and corneal tissues from three residual corneoscleral rims of corneas donated for transplantation. Immunofluorescence staining was performed using monoclonal antibodies against integrins beta1 and beta4, laminin 5, and collagen VII to identify abnormalities in specific layers of the adhesion complex. RESULTS In both experimental and control specimens, the suprabasal and basal cells stained positive for integrin beta1, and basal cells stained positive for integrin beta4. Similarly, a continuous line along the base of each epithelial sheet and each control specimen stained positive for laminin 5, a major basement membrane component. In contrast, in all controls there was a continuous linear staining pattern along the basement membrane of stain positive for collagen VII, a marker for the presence of fibrils that anchor corneal basement membrane to Bowman's layer, but epithelial sheets from eyes with RCE showed either a discontinuous line stained positive for collagen VII (three out of eight specimens) or no positively stained areas (five out of eight specimens). The results indicated the cleavage plane of RCE was located at collagen VII layer, between basement membrane and Bowman's layer. CONCLUSIONS This study identified a defect in collagen fibrils that anchor the corneal epithelium basement membrane to Bowman's layer as the cause of corneal epithelial loss in cases of traumatic RCE. As hemidesmosomes do not seem to be impaired, a treatment specific to restore anchoring fibril function might prove helpful.