Repair of the corneal epithelial adhesion structures following keratectomy wounds in diabetic rabbits.

In corneal tissue from a diabetic patient 15 months after delayed epithelial healing following vitrectomy surgery, electron microscopy revealed a discontinuous basement membrane; immunohistochemically, fibronectin was present in the basement membrane zone. To determine whether alterations in repair of the basement membrane, anchoring fibrils and hemidesmosomes occur in wounds in diabetics, we studied the pattern of histochemical localization of bullous pemphigoid antigen (the intracellular hemidesmosome plaque component), laminin and type VII collagen (the anchoring fibril collagen) in alloxan-induced diabetic rabbits following superficial keratectomy. Ultrastructural studies of basal laminae and hemidesmosomes also were performed. Epithelial wound closure was complete by 66-72 h after 7-mm superficial keratectomies. Type VII collagen localized at the base of the epithelium at the wound periphery by 66 h, appearing as a beaded line underlying the epithelium; at 1 week, as in control rabbits, the localization zone extended across the wound bed. Polyclonal antibodies to laminin and bullous pemphigoid antigen showed similar localization. Small segments of basal laminae were noted by electron microscopy of the wound periphery as early as 66 h post-keratectomy. By 2 weeks, an increase in hemidesmonsomes associated with segments of discontinuous basal lamina was apparent. No obvious differences in the time or pattern of re-appearance of the adhesion complex in keratectomy wounds could be discerned between normoglycemic and hyperglycemic rabbits. Thus, healing defects in diabetics may be due to factors other than reassembly of adhesion structures.