What is dry eye?

Dry eye, also known as dry eye syndrome or keratoconjunctivitis sicca, is a common condition characterized by insufficient tear production or poor quality of tears, leading to discomfort, irritation, and inflammation of the eyes. Tears play a crucial role in maintaining the health and lubrication of the ocular surface, providing moisture, nutrients, and protection against infections. When the quantity or quality of tears is inadequate, it can result in a range of symptoms and complications associated with dry eye.


What is the relationship between dry eye and oxidative stress?

The relationship between dry eye and oxidative stress is intricate, as oxidative stress plays a significant role in the pathogenesis and progression of dry eye syndrome. Here’s how oxidative stress influences dry eye:


  • Tear Film Stability: Oxidative stress can disrupt the composition and stability of the tear film, which consists of three layers: lipid, aqueous, and mucin. The lipid layer helps prevent tear evaporation, the aqueous layer provides moisture and nutrients to the ocular surface, and the mucin layer helps maintain tear film adhesion to the cornea. Oxidative damage to lipids, proteins, and mucins in the tear film can impair tear film stability, leading to increased tear evaporation and reduced tear retention on the ocular surface, characteristic features of dry eye.


  • Inflammation: Oxidative stress can promote inflammation on the ocular surface, contributing to the pathogenesis of dry eye. Reactive oxygen species (ROS) generated during oxidative stress can activate inflammatory pathways and stimulate the production of pro-inflammatory cytokines, chemokines, and inflammatory mediators in the conjunctiva, cornea, and lacrimal glands. Chronic inflammation in the tear film and ocular surface tissues can disrupt tear production, exacerbate ocular surface damage, and worsen dry eye symptoms.


  • Ocular Surface Damage: Oxidative stress-induced damage to ocular surface tissues, including the cornea, conjunctiva, and meibomian glands, can compromise the integrity and function of the tear film and exacerbate dry eye symptoms. ROS can induce oxidative damage to epithelial cells, basement membranes, and extracellular matrix proteins in the ocular surface tissues, leading to epithelial barrier dysfunction, increased permeability, and loss of goblet cells that produce mucin. Additionally, oxidative stress can impair meibomian gland function and alter the composition of meibum, the oily secretion that helps stabilize the tear film and prevent tear evaporation.


  • Antioxidant Defenses: The ocular surface is equipped with antioxidant defense mechanisms to neutralize ROS and protect against oxidative damage. Antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase, as well as non-enzymatic antioxidants such as vitamins C and E, play a crucial role in scavenging ROS and maintaining redox balance in the tear film and ocular surface tissues. However, oxidative stress can overwhelm antioxidant defenses, leading to oxidative damage and exacerbation of dry eye symptoms.


  • Complications of Dry Eye: Oxidative stress is implicated in the development and progression of complications associated with dry eye, such as corneal epithelial defects, corneal erosions, and corneal ulcers. Oxidative damage to corneal epithelial cells and basement membranes can impair wound healing and increase the risk of corneal complications in individuals with dry eye. Additionally, oxidative stress-induced inflammation and fibrosis in the lacrimal glands can impair tear production and exacerbate tear film instability in severe cases of dry eye.


Overall, oxidative stress plays a significant role in the pathogenesis and progression of dry eye by disrupting tear film stability, promoting inflammation, inducing ocular surface damage, impairing antioxidant defenses, and contributing to the development of complications associated with the condition.