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dc.contributor.authorFjærvoll, Ketil Andreas Olsen
dc.contributor.authorFjærvoll, Haakon Kristoffer Olsen
dc.contributor.authorMagnø, Morten Scherven
dc.contributor.authorTellefsen Nøland, Sara Julie Maria
dc.contributor.authorDartt, Darlene Ann
dc.contributor.authorVehof, Jelle
dc.contributor.authorUtheim, Tor Paaske
dc.identifier.citationFjærvoll, K., Fjærvoll, H., Magno, M., Nøland, S. T., Dartt, D. A., Vehof, J., & Utheim, T. P. (2022). Review on the possible pathophysiological mechanisms underlying visual display terminal‐associated dry eye disease. Acta ophthalmologica.en_US
dc.description.abstractBackground Visual display terminal (VDT) use is a key risk factor for dry eye disease (DED). Visual display terminal (VDT) use reduces the blink rate and increases the number of incomplete blinks. However, the exact mechanisms causing DED development from VDT use have yet to be clearly described. Purpose The purpose of the study was to conduct a review on pathophysiological mechanisms promoting VDT-associated DED. Methods A PubMed search of the literature investigating the relationship between dry eye and VDT was performed, and relevance to pathophysiology of DED was evaluated. Findings Fifty-five articles met the inclusion criteria. Several pathophysiological mechanisms were examined, and multiple hypotheses were extracted from the articles. Visual display terminal (VDT) use causes DED mainly through impaired blinking patterns. Changes in parasympathetic signalling and increased exposure to blue light, which could disrupt ocular homeostasis, were proposed in some studies but lack sufficient scientific support. Together, these changes may lead to a reduced function of the tear film, lacrimal gland, goblet cells and meibomian glands, all contributing to DED development. Conclusion Visual display terminal (VDT) use appears to induce DED through both direct and indirect routes. Decreased blink rates and increased incomplete blinks increase the exposed ocular evaporative area and inhibit lipid distribution from meibomian glands. Although not adequately investigated, changes in parasympathetic signalling may impair lacrimal gland and goblet cell function, promoting tear film instability. More studies are needed to better target and improve the treatment and prevention of VDT-associated DED.en_US
dc.rightsNavngivelse 4.0 Internasjonal*
dc.titleReview on the possible pathophysiological mechanisms underlying visual display terminal-associated dry eye diseaseen_US
dc.title.alternativeReview on the possible pathophysiological mechanisms underlying visual display terminal-associated dry eye diseaseen_US
dc.typePeer revieweden_US
dc.typeJournal articleen_US
dc.rights.holderThe authoren_US
dc.subject.nsiVDP::Medisinske Fag: 700en_US
dc.source.journalActa Ophthalmologicaen_US
dc.relation.projectNorges forskningsråd: 271555en_US

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Navngivelse 4.0 Internasjonal
Except where otherwise noted, this item's license is described as Navngivelse 4.0 Internasjonal