Dry Eye Clinic
Dr. Abdalrahman Alabsi
How Does Dry Eye Develop?
By Dr. Abdalrahman Alabsi – Ophthalmologist | Last reviewed: October 2026
The tear film is the foundation for understanding dry eye. The disease is generally classified as aqueous-deficient dry eye (a problem of quantity) or evaporative dry eye (a problem of quality) caused by dysfunction of the tear-secreting oil glands and involvement of the mucin layer.
Tear hyperosmolarity – an increased salt concentration in the tear film – is the central concept for understanding how dry eye worsens. It drives a vicious cycle of epithelial cell damage and release of inflammatory mediators, which further destabilizes the tear film and perpetuates the vicious cycle of dry eye.
Effects of increased tear salt concentration (tear hyperosmolarity) in dry eye:
Increased programmed cell death (apoptosis).
Abnormal keratinization of epithelial cells.
Increased release of inflammatory mediators.
As a result, antioxidant defenses decline and surface cells are shed, exposing immature, water-repellent cells beneath them. This further destabilizes the tear film, so that it evaporates within a few seconds – faster than normal – which in turn raises the salt concentration of the remaining tears and keeps the vicious cycle going.
Anti-inflammatory medications and eye drops play an important role in controlling the inflammation caused by dry eye. The type and duration of treatment are determined by the severity of the disease and the accompanying inflammatory stage.
Signs and symptoms of dry eye do not always match the associated inflammation:
Dry eye symptoms do not accurately predict the active underlying disease mechanism in each patient.
Inflammation-related tear proteins are higher in aqueous-deficient dry eye than in evaporative dry eye (a defect in the lipid layer and/or the mucin layer of the tears).
Normally, the tear film maintains a balance between protein-degrading enzymes (proteases) and their inhibitors. This balance is disturbed as dry eye disease becomes more severe, especially in dry eye associated with autoimmune disease such as Sjögren's disease, where plasmin activity rises about tenfold compared with normal tears and levels of protective antiproteases fall sharply as the disease worsens.
The glycocalyx barrier:
A thin layer rich in mucins – large glycoproteins that form the main component of the mucous layer covering the ocular surface epithelium. It lubricates the eye, retains water, and provides a barrier against evaporation.
The mucin layer of the tears (the inner layer in contact with the ocular surface):
It helps the tears adhere evenly to the ocular surface instead of sliding off or pooling irregularly.
Dysfunction of the tear-secreting oil glands (meibomian gland dysfunction, MGD):
Meibomian gland dysfunction (MGD) – a chronic obstruction or qualitative change in the function of the glands responsible for the protective lipid layer of the tear film – is the single most common cause of dry eye.
Meibomian gland dysfunction (evaporative dry eye) on its own often represents a low-grade, subclinical inflammatory process rather than a clearly active condition.
The effect of lipid metabolism disorders on the severity of meibomian gland dysfunction (MGD):
Patients with high total cholesterol, low-density lipoprotein (LDL), and triglycerides were found to have much greater loss of meibomian glands than healthy individuals.
Patients with long-standing dyslipidemia showed marked atrophy of the eyelid oil glands and changes in the quality of their secretions, even while being treated with cholesterol-lowering statins.
Omega-3 supplements are a beneficial factor in meibomian gland dysfunction (MGD) and one of the modifiable dietary factors supported by clinical trials, especially when the diet lacks omega-3-rich foods.
References
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2. Willcox MDP, Argüeso P, Georgiev GA, et al. TFOS DEWS II Tear Film Report. Ocul Surf. 2017;15(3):366-403. doi:10.1016/j.jtos.2017.03.006
3. Bukhari AA. Associations between the grade of meibomian gland dysfunction and dyslipidemia. Ophthalmic Plast Reconstr Surg. 2013;29(2):101-3. doi:10.1097/IOP.0b013e31827a007d
4. Stapleton F, Argüeso P, Asbell P, et al. TFOS DEWS III: Digest. Am J Ophthalmol. 2025;279:451-553. doi:10.1016/j.ajo.2025.05.040
5. Jones L, Craig JP, Markoulli M, et al. TFOS DEWS III: Management and Therapy. Am J Ophthalmol. 2025;279:289-386. doi:10.1016/j.ajo.2025.05.039
