Abstract
Keratoconjunctivitis sicca (KCS), or dry eye, is a major cause of ocular morbidity in humans and dogs.1,2 Although the cause of KCS in dogs often cannot be determined, as in non-Sjögren’s dry eyes, histopathologic and serologic studies suggest that canine KCS frequently results from immune-mediated lacrimal gland destruction or dysfunction. Tear film deficiencies cause changes in the conjunctival epithelium that may account for many of the clinical symptoms and the corneal morbidity in these cases. The normal conjunctival surface is composed of nonkeratinized, stratified, squamous epithelium with goblet cells. These cells and the products from them, including mucin, are critical for ocular surface integrity. Squamous metaplasia from cuboidal epithelium to increasing keratinization and goblet cell loss is associated with KCS in patients with Sjögren’s syndrome and with ocular problems in postmenopausal women.2–4 Methods for staging squamous metaplasia by impression cytology have been established for use in humans.2,5–7Although KCS in dogs and response to treatment with cyclosporine have been characterized histologically by biopsy of lacrimal glands, there are no reports on conjunctival cytology from dogs with KCS.1,8 Clinical trials in dogs and humans have supported the validity of treating KCS with cyclosporine. In this project we characterized conjunctival cytology from dogs with KCS before and after treatment with cyclosporine in order to determine the effect of topical cyclosporine treatment on the conjunctival epithelium.
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