Mucin-synthesizing genes representing both transmembrane mucins and goblet cell–secreted soluble mucins have been isolated and their roles in hydration and stabilization of the tear film are being investigated in patients with KCS, according to Chiang and colleagues. A defect in these and other mucin genes may be a factor in the development of DED.
Besides DED, other conditions may eventually lead to loss of goblet cells, including ocular cicatricial pemphigoid (also called mucous membrane pemphigoid), Stevens-Johnson syndrome, and vitamin A deficiency. These conditions may lead to drying and eventual keratinization of the ocular epithelium. Both classes of mucins are decreased in these diseases, and, on a molecular level, mucin gene expression, translation, and posttranslational processing are altered.
Mucin deficiency leads to poor wetting of the corneal surface with subsequent desiccation and epithelial damage, even in the presence of adequate aqueous tear production.
Learn more about mucin deficiency in DED.
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Cite this: Christina R. Prescott. Fast Five Quiz: Dry Eye Disease (Keratoconjunctivitis Sicca) Etiology and Pathophysiology - Medscape - Nov 10, 2022.