Amardeep S Sekhon1, Bonnie He2, Alfonso Iovieno3, Sonia N Yeung3. 1. Department of Anesthesiology, Pharmacology and Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver, Canada. 2. Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada. 3. Department of Ophthalmology and Visual Sciences, University of British Columbia, Vancouver, Canada.
Abstract
Purpose: Dry eye disease (DED) and other inflammatory ocular disorders have been reported to be associated with decreased corneal endothelial cell density (CECD), however the mechanism of underlying endothelial cell loss remains unknown. Methods: We conducted a comprehensive literature search of English-written publications on dry eye disease, corneal endothelial cell loss, Sjögren's syndrome, and Graft Vs Host Disease (GVHD), to review the effects of DED and other inflammatory ocular surface conditions on CECD. Results: A total of 78 studies were included in our study. Loss of corneal neurotrophic support, cytotoxic stress, and a heightened immune response, all of which may occur secondarily to a common causative agent such as inflammation, are major contributors to reduced CECD. Conclusion: More studies are needed to determine how the interrelated pathways of altered corneal nerve function and upregulated expression of inflammatory activity influence corneal endothelial cell loss.
Purpose: Dry eye disease (DED) and other inflammatory ocular disorders have been reported to be associated with decreased corneal endothelial cell density (CECD), however the mechanism of underlying endothelial cell loss remains unknown. Methods: We conducted a comprehensive literature search of English-written publications on dry eye disease, corneal endothelial cell loss, Sjögren's syndrome, and Graft Vs Host Disease (GVHD), to review the effects of DED and other inflammatory ocular surface conditions on CECD. Results: A total of 78 studies were included in our study. Loss of corneal neurotrophic support, cytotoxic stress, and a heightened immune response, all of which may occur secondarily to a common causative agent such as inflammation, are major contributors to reduced CECD. Conclusion: More studies are needed to determine how the interrelated pathways of altered corneal nerve function and upregulated expression of inflammatory activity influence corneal endothelial cell loss.
Authors: Jiawei Ling; Ben Chung-Lap Chan; Miranda Sin-Man Tsang; Xun Gao; Ping Chung Leung; Christopher Wai-Kei Lam; Jiang-Miao Hu; Chun Kwok Wong Journal: Front Med (Lausanne) Date: 2022-01-17