| Xerophthalmia, which is also called dry syndrome, from whatever cause is a significant cause of blindness not only because the precomeal tear film is essential for corneal transparency but also because the dry eye develops keratitis with ulceration and opacification. Henrik SjOgren first brought forward the concept of dry syndrome in 1933. The modem definition was advanced by Brewitt in 1995, which said that xerophthalmia resulted from lacrimal dysfunction and insufficiency, was one of the most popular ophthalmological disease which could progress to keratomalacia and led to blindness, was a human disease characterized by the loss of globlet cells from the conjunctival epithelium and keratinization of the corneal epithelium. Recent research found that xerophthalmia was caused by vitamin A deficiency, inflammation, immunity, apoptosis, sex hormone level and so on. But the pathogenesis of xerophthalmia is still under discussing. Especially in China, there is still a lot to be researched on the pathogenesis and therapy of xerophthalmia.Animal model is a kind of important carrier to develop clinical and basic research. Successfully establishing the animal models with xerophthalmia according to the assumed causes is the foundation to give more study on the disease. Patients with xerophthalmia are characterized by tear secretion decrease, precomeal tear film instability, thin thickness of cornea, corneal surface irregularity and so on. To diagnose the animal models as xerophthalmia can offer some proof on clinical diagnosis.The pathological changes of xerophthalmia are characterized by lymphocyte soakage in lacrimal glands, cornea ulceration, keratinization of the corneal epithelium, loss of globlet cells from the conjunctival epithelium and so on. The ultrastructural changes of xerophthalmia are endoplast breakage and mitochondria swelling in lacrimal glands, microvilli desquamation on the corneal superficial epithelial cells and so on. All these changes are due to tear deficiency and will aggravate tear deficiency. To study the pathological and ultrastructural changes of xerophthalmia will be helpful to realize the pathogenesis of it.Recent research found that apoptosis played an important role in autoimmunity disease. Views suggested that excessively strong immunoreaction was caused by the decreasement of the apoptotic lymphocyte. Apoptosis plays an important role in xerophthalmia in two sides: one is to inhibit the lacrimal glands and the conjunctival globlet cells, the other is to influence the inflammatory cells. To study the relation between apoptosis andxerophthalmia is the key to realize the pathogenesis of xerophthalmia.The traditional treatment of xerophthalmia is to take temporary solution, such as topicalapplication of tear substitute and keeping tears from evaporation. Recent research focusesin effecting a permanent cure. To treat xerophthalmia according to the causation can notonly help to realize the pathogenesis of it but also afford academic evidence for clinicaltreatment.To investigate the pathogenesis and therapy of xerophthalmia, we study the disease infour aspects.Part I The Establishment and Diagnosis of Xerophthalmia ModelsObjective: To establish and diagnose animal models with xerophthalmia.Material and Methods: 9 rabbits were given a casein-base vitamin A-deficient diet forsix months and we got xerophthalmia models. Schirmer's test, tear film break-up time(BUT), rose bangle (rb) staining and corneal thickness were performed on the eyes at 2%3> 4> 5% 6 months after and before the experiment. 9 male rabbits were castrated and after3 months we got xerophthalmia models. The aforesaid examinations were performed onthe eyes at 2 > 3 > 4 weeks, 2 and 3 months after and before the experiment.Results: Schirmer's test, tear film break-up time and corneal thickness were significantlylower in both groups after the experiment. The difference became more and moreprominent in the course of observation. Rose bangle staining was positive...
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