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.
Abstract
Journal Article
Review
eng
28736340
Bron, Anthony J., et al. "TFOS DEWS II Pathophysiology Report." The Ocular Surface, vol. 15, no. 3, 2017, pp. 438-510.
Bron AJ, de Paiva CS, Chauhan SK, et al. TFOS DEWS II pathophysiology report. Ocul Surf. 2017;15(3):438-510.
Bron, A. J., de Paiva, C. S., Chauhan, S. K., Bonini, S., Gabison, E. E., Jain, S., Knop, E., Markoulli, M., Ogawa, Y., Perez, V., Uchino, Y., Yokoi, N., Zoukhri, D., & 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 AJ, et al. TFOS DEWS II Pathophysiology Report. Ocul Surf. 2017;15(3):438-510. PubMed PMID: 28736340.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR
T1 - TFOS DEWS II pathophysiology report.
AU - Bron,Anthony J,
AU - de Paiva,Cintia S,
AU - Chauhan,Sunil K,
AU - Bonini,Stefano,
AU - Gabison,Eric E,
AU - Jain,Sandeep,
AU - Knop,Erich,
AU - Markoulli,Maria,
AU - Ogawa,Yoko,
AU - Perez,Victor,
AU - Uchino,Yuichi,
AU - Yokoi,Norihiko,
AU - Zoukhri,Driss,
AU - Sullivan,David A,
Y1 - 2017/07/20/
PY - 2017/05/26/received
PY - 2017/05/26/accepted
PY - 2017/7/25/pubmed
PY - 2018/5/15/medline
PY - 2017/7/25/entrez
KW - DEWS II
KW - Dry eye disease
KW - Dry eye workshop
KW - Glycocalyx
KW - Hyperosmolarity
KW - Inflammation
KW - Pathophysiology
KW - TFOS
KW - Vicious circle
SP - 438
EP - 510
JF - The ocular surface
JO - Ocul Surf
VL - 15
IS - 3
N2 - 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.
SN - 1937-5913
UR - https://www.unboundmedicine.com/prime/citation/28736340/TFOS_DEWS_II_pathophysiology_report_
L2 - https://linkinghub.elsevier.com/retrieve/pii/S1542-0124(17)30134-9
DB - PRIME
DP - Unbound Medicine
ER -
