Abstract

* * Dry eye disease is a devastating and multifactorial disorder of the tear-film layer and ocular surface. Multiple symptoms include multiple eye irritation, and visual disturbances, and signs have tear-film instability, along with the potential for injuring the ocular surface. Accumulating evidence indicates that dry eye disease is accompanied by hyperosmolarity of the tear film and inflammation of the ocular surface microenvironment. Most cases of dry eye disease are secondary to any of a vast array of inflammatory conditions and disorders, including auto- and alloimmune diseases, infection, aging, neuroinflammation, and sterile Inflammation. Sterile inflammation is induced by several different kinds of non-infectious triggers, including altered cellular and tissue states. New results have implicated damage-associated molecular patterns, microorganisms, and neurotransmitters in primary dry eye disease. Furthermore, in conjunction with inflammatory and fibrotic changes, the renin angiotensin system and epithelial mesenchymal transition may be involved in disease-associated and immune-mediated dry eye disease, such as chronic GVHD-related dry eye. Collectively, studies show that at least some and possibly many factors influence the condition of the ocular surface, leading to chronic inflammation that exacerbates dry eye symptoms in a vicious cycle. Since the pathway for each type of dry eye disease may differ, and specific pathways may be responsible for the disease in individual patients, patient-tailored therapies should be developed in the future. In this review article, we focus on emerging concepts on the role of the inflammatory process in dry eye disease.

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