As eyecare practitioners who diagnose and treat dry eye disease (DED), we understand that DED is a multifactorial process involving a loss of tear film homeostasis. Tear film instability, tissue damage, and inflammation are all connected and play self-reinforcing roles, keeping patients stuck in the DED cycle. While this cycle has multiple potential points of entry, evaporation-related tear film instability and hyperosmolarity are central, upstream mechanisms. 

The prevalence of meibomian gland dysfunction and its role in the etiology of DED prompt a reconsideration of the importance of controlling evaporation in DED management. Understanding the evaporative component in the cycle of DED and the many pathways to treatment—including treatment that directly targets tear film evaporation—is necessary to fully interrupt the vicious cycle of DED and provide long-term relief.

Download “Delving Into the Core Mechanism: Evaporation in Dry Eye Disease” by Paul Karpecki, OD, FAAO, to read about the multiple interrelated factors that contribute to the tear evaporation, tissue damage, and inflammation that characterize DED, and how that vicious cycle can be broken.

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