With great anticipation, the updated report of the TFOS Dry Eye WorkShop (DEWS II) was released last week. The first DEWS report was released in 2007.
Here are five things you need to know about TFOS DEWS II.1
1. There is a revised definition of dry eye disease (DED).
“Dry eye is a multifactorial disease of the ocular surface characterized by a loss of homeostasis of the tear film, and accompanied by ocular symptoms, in which tear film instability and hyperosmolarity, ocular surface inflammation and damage, and neurosensory abnormalities play etiological roles.”
Key points to note in this definition are the addition of the phrase “loss of homeostasis” and neurosensory abnormalities, which contribute to the common mismatch between signs and symptoms.
2. Meibomian gland dysfunction (MGD) and Sjögren and non-Sjögren lacrimal disease remain leading causes of evaporative and aqueous-deficient DED; however, many hybrid forms of DED exist.
The core mechanism of DED is tear hyperosmolarity—the hallmark of the disease. Hyperosmolarity damages the ocular surface both directly and by initiating inflammation. These sequelae lead to a cycle of events termed the “vicious circle.” The vicious circle explains how ocular surface damage is initiated and self-perpetuated in DED.
Tear hyperosmolarity, with inflammatory mediators, may induce DED symptoms and cause damage to epithelial cells, surface microvilli, barrier function, the glycocalyx, and goblet cells. Epithelial cell damage, lipid layer and blinking abnormalities, defective glycocalyx, loss of gel mucin, and reduction in tear volume may result in loss of lubrication between the globe and eyelids, resulting in increased friction and dry eye symptoms.