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Research into the etiology of dry eye syndrome has painted a picture of a highly complex disease that has evolved over the decades. Exhaustive efforts have been expended on shedding light on the mechanisms of dry eye disease. Nevertheless, as more is learned, more questions arise.
Debate about the causes of dry eye began in the 1940s with Dr. Henrik Sjögren suggesting a force was pulling water across the ocular surface. The importance of tear film osmolarity later leapt to the forefront as a factor in the rates of tear production and tear film evaporation, which was supported by subsequent observations that upheld the role of tear film osmolarity in dry eye. The theory that inflammation caused dry eye entered the debate, but was negated early on and did not resurface for decades. In the 1980s, Jeffrey Gilbard, MD, R. Linsy Farris, MD, and colleagues reported that dry eye disease is dependent on and proportional to the increase in tear film osmolarity. They said that tear film osmolarity increases as the result of any condition that decreases tear production, including lacrimal gland disease, any condition that decreases corneal sensation, or any condition that increases tear film evaporation, including enlarged palpebral fissure widths or meibomian gland dysfunction.
Creation of the Dysfunctional Tear Syndrome Study Group was an early effort by dry eye clinicians to develop a plan to diagnose and treat patients with dry eye. The consensus panel comprised 17 international authorities who met in the fall of 2003 at the Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore.