Antti Vannas

Histochemical evidence of limited reinnervation of human corneal grafts

Abstract. Acetylcholinesterase (AChE) positive nerve fibers were demonstrated histochemically in the normal human cornea and in 3 corneal grafts obtained after retransplantation. In the normal cornea AChE positive nerves form stromal nerve bundles, which divide into smaller branches contributing to the basal epithelial nerve plexus. Intraepithelial terminals are branches of this plexus. In a grafted cornea obtained 29 years after surgery the epithelium was innervated by a basal epithelial plexus, but only a few stromal nerve trunks had regenerated despite the long post‐operative time. Corneal sensitivity had not returned to normal in this case. The remaining grafts, obtained less than 3 years after surgery, contained very few nerves. It seems that neither the architecture nor the density of corneal nerves fully regenerate in the graft cornea, and this probably explains why sensitivity does not return to normal.

THE ULTRASTRUCTURE OF CONTACT LENS INDUCED CHANGES

The endothelium of 15 human corneas was studied with specular and electron microscopy after exposure to a thick, low water content, soft contact lens (SCL). Five control corneas (no lens wear) were studied using the same methods. SCL wear produced obvious changes in endothelial morphology in 12 of the 15 eyes. With specular microscopy, the changes consisted of an apparent increase in separation of cells and development of areas of loss of membrane reflectivity (blebs). When viewed with electron microscopy, the changes in the same corneas consisted of oedema in the nuclear area of the cells and bulging of the posterior endothelial surface, in some cases over an area of several cells. In 4 cases, the cellular oedema was marked showing both intracellular and intercellular vacuoles. It was concluded that the transient endothelial changes seen with specular microscopy following SCL lens wear were produced by alterations in the contour of the posterior endothelial surface resulting from disturbance to the endothelial environment.

Tear plasmin activity with contact lens wear

Plasmin, a proteolytic enzyme, has been detected in the tears of patients experiencing anterior ocular disease, and during contact lens wear. Using a radial caseinolysis procedure, we examined tear plasmin levels in 66 patients who were wearing soft and rigid lenses for daily and extended wear. Compared to non-contact lens wearers, patients wearing soft and rigid lenses for extended wear were significantly more likely to exhibit tear plasmin activity. Eight hours of open-eye thick HEMA lens wear did not induce tear plasmin activity in a group of 10 subjects. However, significant increases in tear plasmin activity were recorded after short-term (1 hour) eye closure with and without lens wear, and following overnight (8 hours) eye closure without lens wear. Overnight eye closure also resulted in significantly increased numbers of epithelial cells and leucocytes in the tear fluid. Our results suggest that increased tear plasmin activity during extended contact lens wear may be attributable to the effects of eye closure rather than hypoxia or the presence of the contact lens per se.