Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2017 Jul;15(3):438-510.
doi: 10.1016/j.jtos.2017.05.011. Epub 2017 Jul 20.

TFOS DEWS II pathophysiology report

Anthony J Bron  1 , Cintia S de Paiva  2 , Sunil K Chauhan  3 , Stefano Bonini  4 , Eric E Gabison  5 , Sandeep Jain  6 , Erich Knop  7 , Maria Markoulli  8 , Yoko Ogawa  9 , Victor Perez  10 , Yuichi Uchino  9 , Norihiko Yokoi  11 , Driss Zoukhri  12 , David A Sullivan  3
Affiliations
Review

TFOS DEWS II pathophysiology report

Anthony J Bron et al. Ocul Surf. 2017 Jul.

Erratum in

Abstract

The TFOS DEWS II Pathophysiology Subcommittee reviewed the mechanisms involved in the initiation and perpetuation of dry eye disease. Its central mechanism is evaporative water loss leading to hyperosmolar tissue damage. Research in human disease and in animal models has shown that this, either directly or by inducing inflammation, causes a loss of both epithelial and goblet cells. The consequent decrease in surface wettability leads to early tear film breakup and amplifies hyperosmolarity via a Vicious Circle. Pain in dry eye is caused by tear hyperosmolarity, loss of lubrication, inflammatory mediators and neurosensory factors, while visual symptoms arise from tear and ocular surface irregularity. Increased friction targets damage to the lids and ocular surface, resulting in characteristic punctate epithelial keratitis, superior limbic keratoconjunctivitis, filamentary keratitis, lid parallel conjunctival folds, and lid wiper epitheliopathy. Hybrid dry eye disease, with features of both aqueous deficiency and increased evaporation, is common and efforts should be made to determine the relative contribution of each form to the total picture. To this end, practical methods are needed to measure tear evaporation in the clinic, and similarly, methods are needed to measure osmolarity at the tissue level across the ocular surface, to better determine the severity of dry eye. Areas for future research include the role of genetic mechanisms in non-Sjögren syndrome dry eye, the targeting of the terminal duct in meibomian gland disease and the influence of gaze dynamics and the closed eye state on tear stability and ocular surface inflammation.

Keywords: DEWS II; Dry eye disease; Dry eye workshop; Glycocalyx; Hyperosmolarity; Inflammation; Pathophysiology; TFOS; Vicious circle.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles