Clinicians have long known that multiple factors influence tear film homeostasis. These factors were laid out very clearly in the “TFOS DEWS II pathophysiology report,” released by the Tear Film and Ocular Surface Society in July 2017.1
According to the report, hyperosmolarity is a core mechanism of dry eye disease. Its causes and effects, combined with those of inflammation, make up the vicious cycle that underpins the chronic, progressive nature of dry eye.
Moving forward, our goal is to utilize this information to shape diagnostic testing for dry eye disease toward accurate, objective, early identification.
No matter the cause of a patient’s dry eye disease, whether excessive evaporation or low production of aqueous, one result is a decrease in the relative volume of the aqueous component of the tear film, or hyperosmolarity.1
Surface epithelial cells sense the hyperosmolar environment and release inflammatory mediators, which cause cellular damage to the ocular surface, triggering heightened immune system activity. Inflammation and hyperosmolarity continue, perpetuating the vicious cycle of dry eye disease. Both mechanisms contribute to destabilization of the ocular surface and are exacerbated by the effects, continuing the cycle.