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Study finds that Dry Eye Disease (DED) progression may be delayed by breaking the chronic cycle of ocular surface inflammation

Study: The Core Mechanism of Dry Eye Disease (DED) Is Inflammation
Publication: Eye Contact Lens. 2014 Jul; 40(4): 248–256. doi: 10.1097/ICL.0000000000000042
Date published: July 24, 2014
Authors: Yi Wei, PhD and Penny A. Asbell, MD, FACS, MBA
Summary: 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. The literature review study clearly demonstrate that inflammation is the core mechanism and plays a key role in the pathogenesis of DED as evidenced by research utilizing tissue culture, animal models and subjects with DED. 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. Therefore, developing biomarkers to monitor the ocular surface inflammatory status will not only improve our knowledge to fully understand the mechanisms leading to DED, to better classify the severity of DED, to measure the objective metrics for outcome of treatment, but also provide directions to develop effective and safe anti-inflammatory treatments that will be beneficial for patients with DED. Inflammation is part of the complex biological response of vascular tissues to harmful stimuli, such as pathogens, damaged cells, or irritants.5 As such, it is a protective attempt by the organism to remove the injurious stimuli and to initiate the healing process. Several reports reveal improvement of DED symptoms and/or signs in patients treated with topical or systematic anti-inflammatory drugs. Oxidative stress is caused by an imbalance between the production of reactive oxygen species and the ability of a biological system’s defense mechanisms to eliminate the stress. Based on this new hypothesis of DED pathogenesis, a cure or delay in DED progression may be achieved by any means that breaks the chronic cycle of ocular surface inflammation.

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