Diabetic retinopathy (DR) is the major diabetic complication in the eye.
1 The most severe proliferative stage cannot be reproduced in animals. Vision loss from diabetes is mainly due to the retinal changes. However, other parts of the eye are also affected in up to 30% of cases: iris, with neovascularization and neovascular glaucoma; lens, with diabetic cataract; optic nerve, with glaucomatous neuropathy.
2–5 Also, 50% to 70% of patients have corneal abnormalities including recurrent erosions, delayed and incomplete wound healing, ulcers and edema, complications after vitrectomy, laser photocoagulation, and corneal surgery, as well as limbal epithelial stem cell (LESC) alterations.
6–14 Corneal neuropathy, manifested by loss of corneal sensation, and progressively reduced density of corneal stromal and subbasal nerves is also widespread in diabetic patients.
12,14–20 It has been suggested that diabetic neuropathy contributes to epithelial degenerative changes seen in diabetic keratopathy.
21–23 Diminished sensation in animal models and corneal nerve changes appear within the first 1 to 2 months of diabetes,
24,25 which supports the role of neuropathy in causing keratopathy.
26 However, corneal epithelial cells in culture exposed to high glucose to mimic the diabetic insult show altered signaling through epidermal growth factor receptor (EGFR) and slow wound healing,
27 similar to the in vivo situation.
24,28 Genetic or acquired limbal stem cell deficiency is also accompanied by nerve changes similar to those found in diabetics,
29–31 which suggests that epithelial alterations may in turn lead to the development of corneal neuropathy.