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DOI: 10.1055/a-0898-3857
Dry Eye Etiology: Focus on Friction
Ätiologie des trockenen Auges: Reibung im FokusThe “dry eye” continues to gain importance in everyday clinical practice. Not only is it often a challenge from a medical point of view of differential diagnosis, but also therapeutically, the way to success is neither short nor well predictable. The time required for these patients should not be underestimated as well as the often-enormous suffering that is sometimes in no relation to the anatomical or physiological findings. Therefore, the models for dry eye and its pathogenesis are so important, as they often offer the most important guidance in the search for appropriate diagnosis and therapy for the ophthalmologist, especially if there is a lack of measurable findings. Trust in these models carries an obligation. Being a field of great dynamics, subject to newer and deeper insights into the dynamics of events, a constant reassessment and transformation of each model is therefore a compulsory necessity. In comparison to the previous, more static models, we are currently on the threshold of new thinking, appreciating more the dynamics and the physiological variability of the ocular surface and its lubrication dynamics. Most recently, the Tear Film and Ocular Surface Society (TFOS) published in its Dry Eye Work Shop II (DEWS II) report of the current expert consensus on the definition and classification of dry eye as a disease characterized by a loss of homeostasis of the tear film [1]. The definition of tear film homeostasis remained vague, acknowledging the possibility of many different changes that can occur in the tear film and ocular surface. The current classification of dry eye distinguishes two underlying but often overlapping etiologies: aqueous deficient and evaporative tear film. The report concludes that Meibomian Gland Disease is considered the leading cause of dry eye in clinic and population-based studies. The TFOS DEWS II tear film report states that it is purported that the tear film lipid layer is responsible for the resistance of healthy tears against evaporation [2]. On the other hand, King-Smith and colleagues suggested a lack of correspondence between dry eye and both the lipid layer thickness and thinning rate [3]. The thinning rate of the tear film was not affected by apparent thickening of the lipid layer with lipid emulsion-based eye drops, suggesting that lipid was a poor barrier to evaporation [4]. Therefore, the DEWS II report concluded that the thickness of the lipid layer may not affect the evaporation rate unless it is very thin or completely absent. The TFOS pathophysiology report points to the enormous water-binding capacity of gel-forming mucins, like MUC5AC, secreted by the goblet cells of the conjunctiva as well as their moistening effect and lubricative function at the ocular surface [5], [6], [7].
Publication History
Received: 02 February 2019
Accepted: 26 February 2019
Article published online:
30 July 2019
© 2020. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commecial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/)
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