Format

Send to

Choose Destination
Ocul Surf. 2017 Jul;15(3):438-510. doi: 10.1016/j.jtos.2017.05.011. Epub 2017 Jul 20.

TFOS DEWS II pathophysiology report.

Author information

1
Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK; Vision and Eye Research Unit, Anglia Ruskin University, Cambridge, UK. Electronic address: anthony.bron@eye.ox.ac.uk.
2
Department of Ophthalmology, Baylor College of Medicine, Houston, TX, USA.
3
Schepens Eye Research Institute & Massachusetts Eye and Ear, Harvard Medical School, Boston, MA, USA.
4
Department of Ophthalmology, University Campus Biomedico, Rome, Italy.
5
Department of Ophthalmology, Fondation Ophtalmologique Rothschild & Hôpital Bichat Claude Bernard, Paris, France.
6
Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, IL, USA.
7
Departments of Cell and Neurobiology and Ocular Surface Center Berlin, Charité - Universitätsmedizin Berlin, Berlin, Germany.
8
School of Optometry and Vision Science, University of New South Wales, Sydney, Australia.
9
Department of Ophthalmology, Keio University School of Medicine, Tokyo, Japan.
10
Department of Ophthalmology, Bascom Palmer Eye Institute, University of Miami, Miami, FL, USA.
11
Department of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
12
Tufts University School of Dental Medicine, Boston, MA, USA.

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

PMID:
28736340
DOI:
10.1016/j.jtos.2017.05.011
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center