The cookie settings on this website are set to 'allow all cookies' to give you the very best possible experience. If you continue without changing your settings, we will accept your consent. However, if you wish to change your browser settings at anytime go to www.aboutcookies.org for information on how to do this.

To find out more about our Cookies Policy please click here

How dry eye develops

Mucus-secreting cells create the mucin layer. Mucus coats the cornea and protects the surface.


The superficial lipid layer of the tear film is derived from the meibomian glands, embedded within the eyelids. The gland ducts open on the eyelid margin. The lipid layer serves to reduce evaporation of underlying aqueous fluid in the open eye. Abnormalities in the secreted lipids result in increased evaporation of tears.


The aqueous layer of the tear film is produced by the lacrimal gland, beneath the upper eyelid. This layer provides moisture, oxygen and electrolytes to the cornea. The concentration of the aqueous layer increases as a result of dry eye and can lead to increased tear osmolarity. In severe dry eyes the tear hypertonicity has been shown to cause ocular surface disease.


Eye surface inflammation is the key mechanism of ocular surface injury in dry eye and results in further cell damage. Inflammation may be initiated by dryness, hypertonicity of tears, microtrauma from eyelids, proinflammatory substances released by the lacrimal glands and a reduced supply of supportive factors from tears. Inflammation is enhanced by cytokines secreted by damaged surface epithelial cells and lymphocytes and leukocytes that leak out from dilated conjunctival blood vessels. Ocular surface inflammation reduces surface wettability and tear film stability. (Prog Retin Eye Res. 2004 Jul; 23(4):449-74)