“Dry eye is a multifactorial disease of the ocular surface characterized by a loss of homeostasis of the tear film, and accompanied by ocular symptoms, in which tear film instability and hyperosmolarity, ocular surface inflammation and damage, and neurosensory abnormalities play etiological roles.” 

Tear Film and Ocular Surface Dry Eye Workshop, 2017  

The tear film is incredibly complex, made up of >1500 proteins, electrolytes, mucins, (O)-Acylated ω-hydroxy fatty acids (OAHFAs), cholestryl esters and wax esters. It has two dynamic layers; the surface lipid layer which prevents evaporation of your tears and stabilises the tear film; and the inner mucoaqueous layer which lubricates and provides nutrients to the ocular surface, and defends against infection. Normally, tear production and evaporation and drainage are in equilibrium. If something disrupts this balance, it leads to increased tear saltiness, inflammation, potential damage to the ocular surface and dry eye symptoms. 

If the lipid layer is deficient, it thins and breaks in between blinks, and mucoaqueous tears start to evaporate. In response the lacrimal glands are stimulated by a neural reflex arc to produce more mucoaqueous tears to protect the integrity of the ocular surface, often leading to wateriness, but not relief of symptoms. This lipid layer is produced by meibomian glands in the upper and lower eyelids. Problems with the quality or quantity of oils produced by these glands may lead to obstruction and inflammation, and is a condition termed Meibomian Gland Dysfunction (MGD) or posterior blepharitis. 

If the mucoaqueous layer is deficient, there is not enough volume to sufficiently lubricate the eye on blinking, leading to discomfort due to friction and potentially ocular surface damage from desiccation. The mucoaqueous layer is produced by the lacrimal gland and accessory glands Krause and Wolfring.