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The Core Mechanism of Dry Eye Disease Is Inflammation

Wei, Yi Ph.D.; Asbell, Penny A. M.D., M.B.A.


In the article appearing on page 248, of volume 40, issue 4, there is an error in the text. In the second paragraph on page 248, the third sentence “The search revealed a total of 458 articles, include 354 original studies (77.29%) and 104 reviews (22.71%).” should be replaced with the following text: The search revealed a total of 4059 articles by key words “dry eye” and 458 articles by key words “dry eye + inflammation.” Almost 11.3% of DED articles are related to inflammation. These 458 inflammation-related DED articles include 354 original studies (77.29%) and 104 reviews (22.71 %).

Eye & Contact Lens. 40(5):311, September 2014.

Eye & Contact Lens: Science & Clinical Practice: July 2014 - Volume 40 - Issue 4 - p 248–256
doi: 10.1097/ICL.0000000000000042
Review Article

Purpose: The purpose of this article is to review the evidence for the hypothesis that the core mechanism of dry eye disease (DED) is inflammation, including evidence from recent basic, clinical, and translational research involving human patients, animal models, and cell cultures.

Methods: Using the key words “dry eye + inflammation,” the authors conducted a comprehensive search of the PubMed and Web of Science databases for scientific articles published in English between January 1, 1900 and August 30, 2013 on the role of inflammation in DED in cell cultures, animal models, and humans. The resulting articles were then categorized and reviewed.

Results: The literature search revealed a total of 458 publications, almost all published after 1992. The percentages of original studies and review articles are 77.29% (354) and 22.71% (104), respectively. Among the original studies, the number of reports on human DED is 200 (43.7%), on animal models is 115 (25.1%), and cell cultures is 39 (8.5%). A yearly distributing plot revealed that 76% were published from 2003 to 2011, 53% from 2008 to 2012, and 11% during the first 9 months of 2013. This distribution signifies a rapidly growing awareness of the importance of inflammation in DED pathogenesis.

Conclusions: Inflammation plays a key role in the pathogenesis of DED as evidenced by research using tissue culture, animal models, and subjects with DED. Developing biomarkers for inflammation of the ocular surface will provide improved understanding of the mechanisms leading to DED, classification of the severity of DED, and objective metrics for outcome measures of treatment. The chronicity of the disease suggests that dysregulation of immune mechanisms leads to a cycle of continued inflammation, accompanied by alterations in both innate and adaptive immune responses. Given the underlying mechanism for DED, developing effective and safe anti-inflammatory treatments is likely to be beneficial for patients with DED.

Icahn School of Medicine at Mount Sinai (Y.W., P.A.A.), New York, NY.

Address correspondence to Penny A. Asbell, M.D., M.B.A., Icahn School of Medicine at Mount Sinai, New York, NY; e-mail:

Supported by the National Eye Institute of the National Institutes of Health grant to P. A. Asbell (1U10EY022881-01).

The authors have no conflicts of interest to disclose.

Accepted April 25, 2014

© 2014 Contact Lens Association of Ophthalmologists, Inc.