title: Rethinking dry eye disease: a perspective on clinical implications.
abstract: Publication of the DEWS report in 2007 established the state of the science of dry eye disease (DED). Since that time, new evidence suggests that a rethinking of traditional concepts of dry eye disease is in order. Specifically, new evidence on the epidemiology of the disease, as well as strategies for diagnosis, have changed the understanding of DED, which is a heterogeneous disease associated with considerable variability in presentation. These advances, along with implications for clinical care, are summarized herein. The most widely used signs of DED are poorly correlated with each other and with symptoms. While symptoms are thought to be characteristic of DED, recent studies have shown that less than 60% of subjects with other objective evidence of DED are symptomatic. Thus the use of symptoms alone in diagnosis will likely result in missing a significant percentage of DED patients, particularly with early/mild disease. This could have considerable impact in patients undergoing cataract or refractive surgery as patients with DED have less than optimal visual results. The most widely used objective signs for diagnosing DED all show greater variability between eyes and in the same eye over time compared with normal subjects. This variability is thought to be a manifestation of tear film instability which results in rapid breakup of the tearfilm between blinks and is an identifier of patients with DED. This feature emphasizes the bilateral nature of the disease in most subjects not suffering from unilateral lid or other unilateral destabilizing surface disorders. Instability of the composition of the tears also occurs in dry eye disease and shows the same variance between eyes. Finally, elevated tear osmolarity has been reported to be a global marker (present in both subtypes of the disease- aqueous-deficient dry eye and evaporative dry eye). Clinically, osmolarity has been shown to be the best single metric for diagnosis of DED and is directly related to increasing severity of disease. Clinical examination and other assessments differentiate which subtype of disease is present. With effective treatment, the tear osmolarity returns to normal, and its variability between eyes and with time disappears. Other promising markers include objective measures of visual deficits, proinflammatory molecular markers and other molecular markers, specific to each disease subtype, and panels of tear proteins. As yet, however, no single protein or panel of markers has been shown to discriminate between the major forms of DED. With the advent of new tests and technology, improved endpoints for clinical trials may be established, which in turn may allow new therapeutic agents to emerge in the foreseeable future. Accurate recognition of disease is now possible and successful management of DED appears to be within our grasp, for a majority of our patients.
authors.affiliation: Professor emeritus - University of Oxford, Nuffield Laboratory of Ophthalmology, Nuffield Dept of Clinical Neurosciences, UK. Electronic address: anthony.bron@eye.ox.ac.uk.
authors.forename: Anthony J
authors.initials: AJ
authors.lastname: Bron
authors.affiliation: Professor of Vision Sciences, Glasgow Caledonian University, Scotland.
authors.forename: Alan
authors.initials: A
authors.lastname: Tomlinson
authors.affiliation: Emeritus Professor of Ophthalmology, University of Louisville; Editor-in-Chief, The Ocular Surface, USA.
authors.forename: Gary N
authors.initials: GN
authors.lastname: Foulks
authors.affiliation: Professor of Clinical Ophthalmology and Visual Sciences, Washington University School of Medicine, Director, Pepose Vision Institute, St. Louis, Missouri, USA.
authors.forename: Jay S
authors.initials: JS
authors.lastname: Pepose
authors.affiliation: Quinze-Vingts National Ophthalmology Hospital, and Vision Institute, University Paris 6, Paris, France.
authors.forename: Christophe
authors.initials: C
authors.lastname: Baudouin
authors.affiliation: Professor and Chair, Department of Ophthalmology, Heinrich-Heine-University Moorenstr. 5 40225 Düsseldorf, Germany.
authors.forename: Gerd
authors.initials: G
authors.lastname: Geerling
authors.affiliation: FERV Professor (Foundation for Education and Research in Vision), The Ocular Surface Institute, University of Houston, College of Optometry, Houston, Texas, USA.
authors.forename: Kelly K
authors.initials: KK
authors.lastname: Nichols
authors.affiliation: Clinical Professor of Ophthalmology, Georgetown University, Washington DC and George Washington University, Washington DC, USA.
authors.forename: Michael A
authors.initials: MA
authors.lastname: Lemp
mesh_terms: D001767:Blinking / Q000502:physiology*; D015352:Dry Eye Syndromes / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy; D006801:Humans; D007638:Keratoconjunctivitis Sicca / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy; D008537:Meibomian Glands / Q000502:physiology*; D009994:Osmolar Concentration; D013666:Tears / Q000502:physiology*
keywords: aqueous-deficient dry eye disease; dry eye disease; inflammation; meibomian gland dysfunction; osmolarity; point-of-care testing