| The ocular surface consists of the tear film, the epithelia of the cornea and conjunctiva. The diseases impairing the structure and function of ocular surface are called ocular surface diseases. Diabetes mellitus is an endocrine disease characterized of hyperglycemia, which leads to series of complications because of metabolism derangement. Diabetes mellitus can lead to many complications, such as diabetic retinopathy, cataract, ametropia and diabetic keratopathy. The investigation of ocular surface diseases in diabetic mellitus is taken into account recently.Objective: To investigate the damage of ocular surface caused by diabetic mellitus and its possible mechanism, in order to provide pathological basis for preventing and treating diabetic ocular surface disease.Methods: Animal experiment: 80 male Sprague-Daxley rats, weighted 180-200g, were randomized into diabetic and control groups respectively, each having 40. 10 rats were sacrificed at 6, 8, 10 and 12 weeks respectively after induction of diabetes mellitus by streptozotocin. The untreated rats were used as normal controls and were sacrificed at the same intervals. The histopathological changes of the lacrimal gland, the cornea and the conjunctiva of rats were observed by the light microscope. The ultrastructures of cornea were observed by transmission electronic microscopy and scanning electron microscopy. SOD activities and MDA levels in corneas were determined. Clinical observation: 35 diabetic patients (70 eyes) and 35 non-diabetic controls (70 eyes) (age and sex matched) were examined by corneal sensitivity measurement, Schirmer's test, tear film break up time measurement, fluorescein staining of the cornea, conjunctival impression cytologic analysis and fundus photography. Dry eye was investigated by questionnaire.Results: Lacrimal glandular cells were swollen 6 weeks after induction ofdiabetes by streptozotocin. Glandular cellular proliferation was observed near the blood vessel at the 10th week. Atrophy of lacrimal glandular follicles and ducts, proliferation of fibers and lymphocytic infiltrates were observed at the 12th week. The basal epithelial cells and the stroma of diabetic rats' cornea were swollen and goblet cell lost 10 weeks after induction. During the experimental period, the corneal ultrustructures of diabetic rats showed that epithelial and endothelial cells were swollen, the mitochondrions in the cytoplasm were swollen and increased. The collagen fibers appeared in disarrangement 10 weeks after induction. The corneal endothelium destructed from the periphery to the center gradually. The activities of SOD in the cornea of the diabetic rats were significantly lower than those of the controls (p<0.05) , and the levels of MDA in the cornea of diabetic rats were markedly higher than those of the controls (p<0.05) . The BUT and Schirmer test values were significantly lower in the diabetic group. The fluorescein-staining points increased in the diabetic group. Impression cytologic analysis showed goblet cells lost and conjunctiva! squamous metaplasia in the diabetic group.Conclusion: The stability of tear film decreases and the epithelia of cornea and conjunctiva destructs in diabetic patients. The damage of lacrimal gland, cornea and conjunctiva due to diabetic mellitus are the histopathological basis of diabetic ocular surface disease. Oxidative damage might be engaged in the formation of diabetic keratopathy.
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