A Pilot Study of Tear Dynamics
Research type
Research Study
Full title
A Pilot Study of Tear Dynamics: Tear Osmolarity and Reflex Features of the Lacrimal Functional Unit
IRAS ID
144999
Contact name
Roger Buckley
Contact email
Sponsor organisation
Anglia Ruskin University
Duration of Study in the UK
3 years, 0 months, 1 days
Research summary
Dry Eye Disease (DED) is a common, disabling, multifactorial disease of the ocular surface and tears, that causes discomfort, visual disturbance, tear film instability and tissue damage (McCarthy CA, et al.,1998; DEWS, 2007) Worldwide it affects 5-35% of the older population (Lin PY, et al., 2001). Its hallmark is tear hyperosmolarity (increased osmolarity), which causes ocular surface damage and plays a central role in initiating self-perpetuating inflammatory events.
There are two sub-groups of DED: aqueous-deficient dry eye (ADDE), where tear hyperosmolarity results from a reduction of lacrimal secretion in the presence of a normal evaporation rate and evaporative dry eye (EDE) where hyperosmolarity results from excessive evaporation with normal tear flow (MGD workshop 2011).
Homeostasis of tear osmolarity is normally achieved reflexly, through the Lacrimal Functional Unit (LFU), wherein sensory impulses from the cornea drive the secretory response of the lacrimal gland (Dartt, 2009). The LFU, together with hormonal and immunologic influences, ensure the health and integrity of the ocular surface, despite exposure to environmental stresses (Stern ME, et al., 1998; 2004).
Tear evaporation is determined by exposure of the ocular surface to the ambient environment. When the eyes are open, tear osmolarity rises, with the onset of evaporation (Nicholls JJ, Mitchell GL and King-Smith PE, 2005). This water loss is enhanced in conditions of desiccating stress, such as with reduced ambient humidity, high temperature and high airflow, which are encountered in extreme environments. These may occur with air-conditioning, desert conditions and in airplane and office environments (Wolkoff P, et al., 2005; Lindgren T, et al., 2002). In normal subjects the LFU compensates by reflexly increasing lacrimal and possibly other secretions but where this compensation is insufficient, DED may be precipitated (Pflugfelder SC, Soloman A, Stern ME, 2000).
This background and the role of the LFU in regulating tear osmolarity in normal subjects and patients with ocular surface disorders, is the focus of the planned research, with the aim of gaining a better understanding of compensatory mechanisms in normal subjects, DED and selected ocular surface disorders.REC name
London - Brighton & Sussex Research Ethics Committee
REC reference
14/LO/2175
Date of REC Opinion
22 Dec 2014
REC opinion
Further Information Favourable Opinion