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TFOS DEWS II pathophysiology report.

Publication ,  Journal Article
Bron, AJ; de Paiva, CS; Chauhan, SK; Bonini, S; Gabison, EE; Jain, S; Knop, E; Markoulli, M; Ogawa, Y; Perez, V; Uchino, Y; Yokoi, N ...
Published in: The ocular surface
July 2017

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.

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Published In

The ocular surface

DOI

EISSN

1937-5913

ISSN

1542-0124

Publication Date

July 2017

Volume

15

Issue

3

Start / End Page

438 / 510

Related Subject Headings

  • Tears
  • Ophthalmology & Optometry
  • Meibomian Glands
  • Keratoconjunctivitis Sicca
  • Humans
  • Dry Eye Syndromes
  • Conjunctiva
  • 3212 Ophthalmology and optometry
  • 1113 Opthalmology and Optometry
 

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Bron, A. J., de Paiva, C. S., Chauhan, S. K., Bonini, S., Gabison, E. E., Jain, S., … Sullivan, D. A. (2017). TFOS DEWS II pathophysiology report. The Ocular Surface, 15(3), 438–510. https://doi.org/10.1016/j.jtos.2017.05.011
Bron, Anthony J., Cintia S. de Paiva, Sunil K. Chauhan, Stefano Bonini, Eric E. Gabison, Sandeep Jain, Erich Knop, et al. “TFOS DEWS II pathophysiology report.The Ocular Surface 15, no. 3 (July 2017): 438–510. https://doi.org/10.1016/j.jtos.2017.05.011.
Bron AJ, de Paiva CS, Chauhan SK, Bonini S, Gabison EE, Jain S, et al. TFOS DEWS II pathophysiology report. The ocular surface. 2017 Jul;15(3):438–510.
Bron, Anthony J., et al. “TFOS DEWS II pathophysiology report.The Ocular Surface, vol. 15, no. 3, July 2017, pp. 438–510. Epmc, doi:10.1016/j.jtos.2017.05.011.
Bron AJ, de Paiva CS, Chauhan SK, Bonini S, Gabison EE, Jain S, Knop E, Markoulli M, Ogawa Y, Perez V, Uchino Y, Yokoi N, Zoukhri D, Sullivan DA. TFOS DEWS II pathophysiology report. The ocular surface. 2017 Jul;15(3):438–510.
Journal cover image

Published In

The ocular surface

DOI

EISSN

1937-5913

ISSN

1542-0124

Publication Date

July 2017

Volume

15

Issue

3

Start / End Page

438 / 510

Related Subject Headings

  • Tears
  • Ophthalmology & Optometry
  • Meibomian Glands
  • Keratoconjunctivitis Sicca
  • Humans
  • Dry Eye Syndromes
  • Conjunctiva
  • 3212 Ophthalmology and optometry
  • 1113 Opthalmology and Optometry