Journal ArticleDOI
TFOS DEWS II pathophysiology report
Anthony J. Bron,Anthony J. Bron,Cintia S. de Paiva,Sunil K. Chauhan,Stefano Bonini,Eric E. Gabison,Sandeep Jain,Erich Knop,Maria Markoulli,Yoko Ogawa,Victor L. Perez,Yuichi Uchino,Norihiko Yokoi,Driss Zoukhri,David A. Sullivan +14 more
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TLDR
The TFOS DEWS II Pathophysiology Subcommittee reviewed the mechanisms involved in the initiation and perpetuation of dry eye disease, finding 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 to be important.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-Sjogren 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.read more
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Comparison of seven cyclosporine A formulations for dry eye disease: A systematic review and network meta-analysis
TL;DR: YangGao et al. as discussed by the authors performed randomized controlled trials of commercial cyclosporine A formulation for dry eye disease and ranked first in terms of improving tear film break-up time, while Zirun® was the most effective commercial formulation for reducing OSDI, and Clacier® was close to placebo.
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Role of stem cells in regenerative treatment of dry eye disease caused by lacrimal gland dysfunction
TL;DR: In this paper , the authors evaluate research directed at the development of clinical procedures for regeneration of the lacrimal gland using various stem cell types and their products and discuss work identifying potential therapeutic targets that may alter pathways to effect healing and ameliorate development of dry eye disease.
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Impact of Chronic Kidney Disease on Corneal Neuroimmune Features in Type 2 Diabetes
Kofi Asiedu,Maria Markoulli,Shyam Sunder Tummanapalli,Jeremy Chung Bo Chiang,Sultan A Alotaibi,Lei Wang,Roshan Dhanapalaratnam,Natalie Kwai,Ann M. Poynten,Arun V. Krishnan +9 more
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Bioelectric Responses of Conjunctival Goblet Cells to Dry Eye: Impact of Ion Channels on Exocytotic Function and Viability.
TL;DR: Four stages are identified in the bioelectric response of conjunctival goblet cells to extracellular hyperosmolarity: KATP/NSC/VGCC/P2X7 pathway, which demonstrates that the replenishment of mucin-filled granules after neural-evoked exocytosis is a multi-hour process, which VGCCs markedly accelerate.
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