What Causes Dry Eye?

Dry eye is not simply a shortage of tears. Current TFOS DEWS III guidance defines it as a multifactorial, symptomatic disease involving loss of homeostasis of the tear film and/or ocular surface. Tear film instability and hyperosmolarity, ocular surface inflammation and damage, and neurosensory abnormalities are recognized as etiological factors.

In practical terms, the system that keeps the front of the eye healthy, protected and optically smooth is no longer remaining in balance. This may result from deficiencies in one or more tear components, eyelid or blinking abnormalities, ocular-surface changes, systemic disease, medications, environmental exposure or several factors occurring together.

Two people can therefore experience similar burning, watering or blurry vision while having very different underlying drivers. Identifying those drivers is important because treatment should be directed at the mechanisms affecting each individual patient.

What Is the Tear Film?

The tear film is a thin, complex layer covering the front of the eye. It provides moisture, lubrication, nutrients, immune protection and the smooth optical surface needed for clear vision.

The tear film depends on several interacting components:

• A lipid component that limits evaporation and improves tear film stability
• An aqueous component that provides moisture, nutrients and protective substances
• A mucin and glycocalyx component that helps tears spread and remain attached to the ocular surface

The eyelids, meibomian glands, lacrimal glands, conjunctival goblet cells, corneal nerves and ocular-surface tissues must work together to maintain this environment. A problem with any part of the system can contribute to dry eye, and most people with dry eye have several contributing factors at the same time.

How Does TFOS DEWS III Classify the Drivers of Dry Eye?

Dry eye was previously divided mainly into evaporative and aqueous-deficient forms. Those descriptions remain useful for explaining tear loss, but TFOS DEWS III uses a more specific etiological framework. It organizes the ocular drivers into tear component deficiencies, eyelid abnormalities and ocular-surface abnormalities.

A patient may have one dominant driver or several interacting drivers. The purpose of classification is not merely to assign a label. It is to connect the findings identified during the examination with treatments directed at those findings.

Tear Component Deficiencies

The tear film may be deficient in its lipid, aqueous or mucin and glycocalyx components. These deficiencies can occur independently, but they frequently overlap.

Lipid deficiency occurs when the tear film lacks enough healthy oil to limit evaporation. Meibomian gland dysfunction is a common driver. Obstructed, inflamed or damaged glands may release too little oil or oil that is too thick to spread effectively.

Aqueous deficiency occurs when the lacrimal glands do not produce enough of the watery portion of the tears. Potential contributors include age, medications, autoimmune disease, hormonal changes, nerve dysfunction and damage to the tear-producing glands.

Mucin and glycocalyx deficiency interferes with the ability of tears to spread across and remain attached to the ocular surface. Conjunctival disease, goblet cell loss, inflammation and epithelial damage may contribute.

Eyelid Abnormalities

The eyelids are essential for spreading tears, protecting the cornea and releasing oil from the meibomian glands. Etiological drivers in this category include abnormalities of blinking or eyelid closure and disease of the eyelid margins.

• Reduced or incomplete blinking, particularly during prolonged visual tasks
• Incomplete eyelid closure during the day or while sleeping
• Meibomian gland dysfunction and abnormal gland secretions
• Anterior blepharitis, Demodex blepharitis and ocular rosacea
• Eyelid laxity, malposition, scarring or facial nerve dysfunction

​​​​​​​Ocular Surface Abnormalities

The cornea, conjunctiva and surrounding tissues must provide a healthy surface for the tear film. TFOS DEWS III recognizes several ocular surface drivers:

• Anatomical misalignment that interferes with tear distribution, such as conjunctivochalasis
• Neural dysfunction that alters corneal sensation, blinking, tearing or the perception of discomfort
• Ocular-surface cell damage or disruption
• Primary inflammation or oxidative stress affecting the ocular surface

These abnormalities may destabilize the tear film directly. They may also intensify tear hyperosmolarity, inflammation and tissue damage, allowing the disease process to continue.

Systemic and External Contributors

Systemic disease, medications, medical procedures, contact lens wear and environmental or behavioral exposures can initiate or worsen one or more of the ocular drivers above. They are therefore evaluated alongside the tear film, eyelids and ocular surface.

Examples include autoimmune disease, diabetes, thyroid disease, hormonal changes, neurologic disease, medication effects, previous eye surgery, contact lens wear, prolonged screen use and exposure to wind, smoke or low humidity.

What Conditions Commonly Contribute to Dry Eye?

Meibomian Gland Dysfunction

Obstructed or poorly functioning meibomian glands can reduce the amount or quality of oil in the tear film. This creates a lipid deficiency, increases evaporation and may cause burning, watering, redness and fluctuating vision.

Related question: What Is Meibomian Gland Dysfunction?

Blepharitis and Demodex

Inflammation, bacterial overgrowth, accumulated debris and Demodex mites can affect the eyelid margins and eyelashes. These conditions can disrupt gland function, destabilize the tear film and contribute to chronic irritation.

Related question: What Is Anterior Blepharitis?

Ocular Rosacea

Ocular rosacea can cause inflammation of the eyelids, meibomian glands and ocular surface. Eye findings may occur even when facial rosacea is mild or absent.

Related question: Can Ocular Rosacea Cause Dry Eye?

Incomplete Blinking or Eyelid Closure

A complete blink spreads tears across the cornea and helps release oil from the meibomian glands. Incomplete blinking, eyelid position abnormalities or sleeping with the eyes partially open can leave areas of the ocular surface exposed.

Related question: Why Are My Eyes Dry When I Wake Up?

Conjunctivochalasis

Loose folds of conjunctival tissue may interfere with the normal distribution and drainage of tears. This anatomical misalignment can contribute to irritation, fluctuating vision or excessive watering.

Ocular Surface Inflammation or Damage

Inflammation and corneal or conjunctival damage can reduce tear film stability. Tear film instability and hyperosmolarity can then promote additional inflammation and tissue damage, creating a self perpetuating cycle.

Neurosensory Abnormalities

Corneal nerves help regulate tearing, blinking and ocular sensation. Abnormal nerve function may reduce protective responses, contribute to surface damage or produce symptoms that are greater or less severe than the visible clinical findings.

Can Medical Conditions Cause Dry Eye?

Yes. Systemic conditions can affect tear production, gland function, inflammation, neural regulation, eyelid closure and ocular surface healing. Dry eye may be associated with:

• Sjögren's disease
• Rheumatoid arthritis
• Lupus
• Thyroid disease
• Diabetes
• Rosacea
• Hormonal changes associated with menopause
• Certain neurologic conditions
• Conditions affecting the eyelids or facial nerves

Dry eye alone does not prove that a person has a systemic disease. However, the pattern and severity of the findings may indicate that additional medical evaluation or coordinated care is appropriate.

Related question: Can Menopause Cause Dry Eye?

Related question: Can Sjögren’s Disease Cause Dry Eye?

Can Medications Contribute?

Some prescription and over the counter medications can reduce tear production, alter gland function or affect blinking and corneal sensation.

Potential contributors include certain antihistamines, decongestants, antidepressants, blood-pressure medications, acne medications, hormonal therapies and medicines with anticholinergic effects.

Medicated eye drops can also affect the ocular surface, particularly when they contain preservatives and are used frequently.

Never discontinue a medication without consulting the clinician who prescribed it.

Related question: Can Medications Cause Dry Eye?

Can Lifestyle and Environmental Factors Cause Dry Eye?

Environmental and behavioral factors can create or amplify tear film, eyelid and ocular surface abnormalities. These include:

• Prolonged computer or digital device use
• Reduced or incomplete blinking
• Contact lens wear
• Wind, smoke and low humidity
• Air conditioning, heating vents and fans
• Inadequate sleep
• Previous eye surgery
• Occupational exposure to dust, chemicals or moving air

These factors may be dominant drivers for some patients. For others, they reveal or worsen an underlying condition that was already present.

Related question: Does Screen Time Cause Dry Eye?

Related question: Can Contact Lenses Cause Dry Eye?

Why Does Determining the Etiological Drivers Matter?

Artificial tears may temporarily improve symptoms, but they cannot correct every tear film, eyelid, ocular surface or neurosensory abnormality.

For example:

• Water based drops do not reopen obstructed meibomian glands.
• Lubrication does not eliminate Demodex.
• Warm compresses do not correct every form of aqueous or mucin deficiency.
• Tear conservation does not necessarily address active eyelid or ocular surface inflammation.
• Screen breaks cannot repair damaged or atrophied glands.
• Increasing lubrication alone may not address abnormal corneal sensation or incomplete eyelid closure.

TFOS DEWS III emphasizes matching treatment to the etiological drivers identified in each patient. Because several drivers often occur together, treatment may need to address multiple mechanisms at the same time.

Related question: How Does a Dry Eye Doctor Choose the Right Treatment?

How Are the Causes of Dry Eye Identified?

At EnVision Dry Eye Center, a comprehensive evaluation may include:

• Meibography to examine meibomian gland structure
• Noninvasive tear breakup time to measure tear-film stability
• Tear osmolarity to evaluate tear-film concentration and homeostasis
• Fluorescein staining to identify corneal and conjunctival damage
• High-resolution slit-lamp imaging
• Evaluation of eyelid margins, gland secretions, blink completeness and eyelid closure
• Assessment of corneal sensation when clinically indicated
• Review of symptoms, systemic conditions, medications, environmental exposures and prior treatments

​​​​​​​No single test explains every case. The findings must be interpreted together to identify the clinically important drivers and determine how they interact.

Related question: What Happens During a Comprehensive Dry Eye Evaluation?

Schedule a Comprehensive Dry-Eye Evaluation

Because dry eye is multifactorial, identifying the underlying etiological drivers is an important step toward developing an effective treatment plan.

At EnVision Dry Eye Center, Dr. Jason Besecker uses advanced diagnostic testing to evaluate the tear film, meibomian glands, eyelids, corneal nerves and ocular surface. He then develops a personalized treatment plan based on each patient's specific findings.

EnVision Dry Eye Center
3752 E Amity Avenue, Suite 103
Nampa, Idaho 83687
(208) 490-8823

Request a Comprehensive Dry-Eye Evaluation

Medically reviewed by Jason Besecker, OD, MS
Last updated: October 2026

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Clinical References

• TFOS DEWS III: Executive Summary (2025)
• TFOS DEWS III: Diagnostic Methodology (2025)
• TFOS DEWS III: Management and Therapy (2025)