Dry eye in Sjögren’s syndrome is a condition where the eyes become very dry, uncomfortable, and sometimes damaged because a person’s immune system attacks the glands that make tears. Sjögren’s syndrome is an autoimmune disease. That means the body’s defense system mistakenly attacks its own tissues—in this case, the tear and saliva glands. The result in the eye is called keratoconjunctivitis sicca, which simply means dryness and inflammation of the surface of the eye. This dryness is usually aqueous-deficient (too little watery tear), but over time other factors like oil-layer problems can also make it worse. The disease causes a loss of balance (homeostasis) in the tear film, leading to unstable tears, higher saltiness (osmolarity), inflammation, and damage to the surface of the eye. Neurological changes can also make symptoms worse or inconsistent, meaning sometimes patients feel pain even when signs are mild. PubMedPubMedReview of Optometry

Dry eye in Sjögren’s syndrome is a persistent lack of enough good-quality tears because the immune system attacks the tear-producing glands. Sjögren’s syndrome is an autoimmune disease where white blood cells infiltrate and damage the lacrimal (tear) and salivary glands, causing dryness of the eyes and mouth. The dry eye that results is often called aqueous-deficient dry eye, meaning the eye cannot make enough of the watery (aqueous) layer of the tear film. This leads to irritation, burning, blurriness, redness, and in severe cases, damage to the surface of the eye. The condition is chronic and can be painful, but a layered approach—combining behavioral changes, targeted therapies, supplements, and in some cases advanced treatments—can control symptoms and protect vision. PMC Sjögren’s Foundation ScienceDirect

Because it affects tear production and the eye surface in several ways, dry eye in Sjögren’s syndrome is considered multifactorial—more than one thing causes the problem, and they feed into each other: less tears → surface damage → inflammation → more tear instability, and so on. This article explains the types, the main causes, the symptoms people feel, and the tests doctors use to diagnose it. All explanations are in plain English to help understanding. TFOS ReportPMC


Types

1. Types of Sjögren’s Syndrome (that cause dry eye):
There are two main forms of Sjögren’s syndrome.

  • Primary Sjögren’s syndrome happens alone, without another autoimmune disease. It mainly affects tear and saliva glands, causing dry eyes and dry mouth. NCBIPMC

  • Secondary Sjögren’s syndrome happens together with another autoimmune disease, like rheumatoid arthritis or lupus. In these cases, the same immune attack that affects other organs also involves the tear glands, producing dry eye. Review of OptometryMedscape

2. Types of Dry Eye Mechanism in Sjögren’s:

  • Aqueous-deficient dry eye: This is the main type in Sjögren’s. The immune system damages the lacrimal glands that make the watery part of tears. So the eye simply doesn’t get enough of that layer. PubMedTFOS Report

  • Evaporative dry eye (mixed component): Even though Sjögren’s begins with low tear volume, over time the oil layer (made by meibomian glands) may fail or become abnormal. This makes tears evaporate faster, adding a second problem and making symptoms worse. PMC

  • Mixed dry eye: Many people with Sjögren’s have both watery deficiency and increased evaporation together. The two problems combine and amplify each other. PubMedPubMed

  • Neurosensory or neuropathic component: Damage or changes in corneal nerves can cause abnormal sensation—sometimes people feel pain or dryness even when the surface looks less damaged, or they feel less sensation despite significant disease. This is part of modern understanding of dry eye and is included in the current definition. Review of OptometryPMCPMC

3. Severity Types (common clinical framing):
Although there is not a single universal scale, clinicians often describe dry eye in Sjögren’s as mild, moderate, or severe depending on symptoms, physical findings, and test results. Severe cases show surface damage, very low tear production, and measurable inflammation. ACS Publications


Causes of Dry Eye in Sjögren’s Syndrome

  1. Autoimmune attack on lacrimal glands: The immune system sends white blood cells (especially T and B lymphocytes) into the tear glands and damages them, reducing tear production. This is the central cause. PMC

  2. Lymphocytic infiltration and inflammation: Clusters of immune cells grow inside the glands, causing swelling, fibrosis (scar), and loss of normal gland tissue. PMC

  3. Autoantibodies (anti-SSA/Ro, anti-SSB/La): These antibodies reflect the immune misdirection and are part of the disease process; their presence correlates with gland dysfunction and contributes to the chronic inflammatory state. ScienceDirect

  4. Cytokine-mediated cell death (e.g., IFN-γ effects): Inflammatory signaling molecules like interferon-gamma increase cell death in glandular cells, worsening tear production. PMC

  5. Altered signaling pathways (e.g., NFκB activity): Changes in intracellular signals can promote gland cell damage before immune cells even arrive, helping start and keep inflammation going. PMC

  6. Goblet cell loss on the conjunctiva: The mucin layer (a component of tears) is reduced because the goblet cells that produce it are destroyed or reduced, destabilizing the tear film. PubMed

  7. Tear film instability: Even small changes in any tear component (water, mucin, or oil) cause the tear to break up quickly, exposing the surface to drying and damage. PubMedTFOS Report

  8. Hyperosmolarity: When the tear film loses water, its salt concentration goes up. High saltiness irritates surface cells and drives more inflammation, creating a vicious cycle. PubMedPubMed

  9. Meibomian gland dysfunction (secondary evaporative loss): The oil layer becomes poor or missing, increasing tear evaporation and worsening dryness. Sjögren’s patients often develop or coexist with MGD. PMCPubMed

  10. Age and hormone changes: Older age and hormonal shifts (especially in women around menopause) reduce gland function and make the ocular surface more vulnerable. AAO

  11. Neurosensory abnormalities: Changes in corneal nerve signaling cause abnormal sensations (like pain without a clear sign) or can reduce reflex tear production. Review of OptometryPMC

  12. Environmental factors (dry air, wind, screen use): They increase tear evaporation and stress the already fragile tear film, making symptoms worse. TFOS Report

  13. Blink reduction (e.g., from screen time): Fewer or incomplete blinks decrease tear spreading and renewal, contributing to localized drying. TFOS Report

  14. Use of contributing medications: Drugs like antihistamines, antidepressants, beta-blockers, and diuretics can reduce tear production or alter tear quality, worsening the underlying Sjögren’s dry eye. reviewofcontactlenses.com

  15. Secondary infection and surface damage: A damaged ocular surface is more prone to low-grade infections or colonization that maintain inflammation. TFOS Report

  16. Eyelid abnormalities (e.g., malposition, incomplete closure): If eyelids do not close well, the eye dries out faster and surface healing is impaired. TFOS Report

  17. Inadequate reflex tearing: Nerve dysfunction can reduce the natural reflex that produces tears in response to dryness or irritation. Review of OptometryPMC

  18. Systemic inflammation from other autoimmune overlap (e.g., rheumatoid arthritis): Coexisting inflammatory diseases can amplify systemic and local ocular inflammation. Review of Optometry

  19. Oxidative stress in aging glands: The glands accumulate oxidative damage over time, making them less resistant to immune attack and dysfunction. PMC

  20. Genetic predisposition (HLA associations and others): Certain genes make a person more likely to develop Sjögren’s and its dry eye manifestations, influencing immune behavior. PMC


Symptoms of Dry Eye in Sjögren’s Syndrome

  1. Dryness or gritty feeling: People often say the eyes feel like there is sand or something stuck in them. This is caused by less tear coverage. Mayo ClinicPubMed

  2. Burning or stinging: The irritated surface sends discomfort signals, often described as burning, especially after reading or screen use. Review of Optometry

  3. Redness: Inflammation causes blood vessels on the white of the eye to widen, making the eye look red. PubMed

  4. Blurred or fluctuating vision: Tears help focus light. When tear film breaks up quickly, vision becomes unstable, especially during tasks like reading. PubMed

  5. Light sensitivity (photophobia): A damaged or irregular surface scatters light, making bright conditions uncomfortable. Review of Optometry

  6. Feeling of a foreign body: The damaged surface or unstable tear film tricks the brain into thinking something is in the eye. Mayo ClinicPubMed

  7. Stringy mucus discharge: In response to irritation, the eye may produce sticky mucus that appears as strings. PubMed

  8. Excessive tearing (reflex tearing): Paradoxically, the eye may water because irritation triggers reflex tears, but these are poor quality and don’t reliably relieve dryness. PubMed

  9. Eye fatigue or heaviness: Constant discomfort and need to blink more can make eyes feel tired. PubMed

  10. Difficulty wearing contact lenses: Dry surface and unstable film reduce comfort and retention of contacts. PubMed

  11. Pain or soreness, especially with changes in weather or wind: The irritated surface reacts strongly to environmental changes. Review of Optometry

  12. Difficulty reading or concentrating: Vision instability and discomfort interfere with close work. PubMed

  13. Eye surface sensitivity (sometimes paradoxically reduced): Due to nerve changes, some people feel more pain, others feel less, creating a mismatch between signs and symptoms. PMCPMC

  14. Eyelid crusting or irritation: Chronic dryness can change eyelid margins and promote mild blepharitis-like symptoms. TFOS Report

  15. Mucous filaments or epithelial debris: The surface may shed small bits that float in the tear film, worsening discomfort. TFOS Report


Diagnostic Tests

A. Physical Examination

  1. Slit-lamp examination with ocular surface evaluation: A bright microscope (slit lamp) lets the doctor look at the cornea, conjunctiva, eyelid margins, tear meniscus, and blink. They can see signs of dryness, redness, inflammation, and damage. reviewofcontactlenses.comTFOS Report

  2. Ocular surface staining (fluorescein, lissamine green): Special dyes are placed in the eye to highlight damaged cells on the cornea and conjunctiva. Patterns of staining help show severity and location of damage. Reliability of these scores has been studied to improve consistent diagnosis. ACS Publications

  3. Eyelid margin and meibomian gland inspection: The eyelid edges are checked for inflammation, clogged oil glands, and structural problems. Blocked or abnormal meibomian glands worsen tear quality by affecting the oil layer. Review of OptometryPubMed

  4. Tear meniscus height observation: The thin strip of tear at the lower eyelid is inspected as a rough visual gauge of tear volume; very low height suggests low tear amount. TFOS Report

  5. Assessment of blink quality and completeness: Incomplete or infrequent blinks reduce tear spread and renewal, worsening dryness. This is evaluated during examination. TFOS Report

B. Manual / Bedside Functional Tests

  1. Schirmer test (without anesthesia or with): Small strips of paper are placed under the lower eyelid to measure how much tear is produced over five minutes. Low wetting means low tear production. PMCMerck Manuals

  2. Tear break-up time (TBUT): After placing a dye, the time until the tear film breaks in patches is measured. Short times mean the film is unstable. reviewofcontactlenses.com

  3. Phenol red thread test: A thin cotton thread treated to change color with tears is placed briefly in the lower lid, giving a quick measure of tear volume. arXiv

  4. Meibomian gland expression (manual): Gentle pressure is applied to the eyelid to see if oil comes out and what its quality is. Thick, cloudy, or absent secretion suggests meibomian dysfunction. Review of Optometry

  5. Corneal esthesiometry: Tests like the Cochet-Bonnet or Belmonte aesthesiometers measure corneal nerve sensitivity. Abnormal sensation helps identify neurosensory contributions and differentiates pain sources. PMCScienceDirectPMC

C. Laboratory and Pathological Tests

  1. Tear osmolarity measurement: Tears are sampled to measure salt concentration. High osmolarity is a key sign of dry eye and contributes to inflammation and damage. PMC

  2. MMP-9 (InflammaDry) point-of-care test: Measures matrix metalloproteinase-9, a marker of surface inflammation. Elevated MMP-9 shows ongoing inflammatory damage and helps decide anti-inflammatory therapy. PMCPubMedTVSTSpringerLink

  3. Conjunctival impression cytology: A small filter paper touches the conjunctiva to collect cells. Lab analysis shows loss of goblet cells or abnormal epithelial changes, reflecting chronic surface disease. PubMed

  4. Autoantibody testing (anti-SSA/Ro, anti-SSB/La, ANA, rheumatoid factor): These blood tests help confirm Sjögren’s syndrome systemically and support the diagnosis of autoimmune dry eye. PMCScienceDirectMerck Manuals

  5. Salivary gland biopsy (focus score): Though not an eye test, this tissue test helps confirm Sjögren’s syndrome. Finding clusters of immune cells in a lip biopsy adds weight to the diagnosis that explains the ocular dry eye. PMCPMC

D. Electrodiagnostic / Neurosensory Tests

  1. Corneal nerve imaging and functional testing (e.g., confocal microscopy): In vivo confocal microscopy visualizes small nerve fibers in the cornea that may be altered in dry eye and neuropathic-like pain. Changes correlate with symptom patterns and help explain mismatches between signs and discomfort. IOVSAAO

  2. Quantitative sensory testing (mechanical/thermal): Advanced neurosensory evaluation (often research/clinical trial context) assesses how the cornea perceives different stimuli; abnormalities indicate nerve dysfunction contributing to pain or reduced reflex tearing. PMCNature

E. Imaging Tests

  1. Meibography (infrared imaging of meibomian glands): Noninvasive pictures of the oil glands show their structure, dropout, or atrophy. This helps detect evaporative contributors and motivates patients. Review of OptometryPubMedReview of Optometry

  2. Anterior segment optical coherence tomography (OCT) of tear meniscus: High-resolution imaging measures tear volume and distribution by visualizing the tear strip; it helps quantify deficiency without touching the eye. arXiv

  3. High-speed videokeratoscopy / tear film dynamics imaging: Non-contact imaging watches how the tear film behaves over time, revealing instability patterns and supporting diagnosis of loss of tear film homeostasis. arXiv

Non-Pharmacological Treatments

Each of these approaches helps the eye in a different way—by increasing moisture, reducing evaporation, calming inflammation, or protecting the surface.

  1. Eyelid Hygiene with Warm Compresses and Lid Massage
    Gently warming the eyelids and massaging helps open clogged meibomian glands (which contribute the oily layer of tears) and improves the quality of the tear film. This reduces evaporation and soothes irritation. Warm compresses also increase local circulation and help loosen debris. ScienceDirect

  2. Blinking Exercises / Conscious Blinking
    Many people blink incompletely during screen use, reducing tear spread. Deliberate full blinking improves tear distribution and prevents rapid drying, especially during prolonged device use. ScienceDirect

  3. Environmental Control (Humidifiers and Avoiding Drafts)
    Using a room humidifier adds moisture to dry air, slowing tear evaporation. Avoiding direct wind, fans, or air conditioning on the face also helps preserve the tear film. ScienceDirect

  4. Protective Eyewear / Moisture Chamber Goggles
    Wraparound glasses or specially designed moisture-retaining goggles reduce air exposure, trapping humidity around the eye and lowering evaporation. These are especially helpful in windy/dry environments or during sleep. ScienceDirect

  5. Screen Time Management (20-20-20 Rule)
    Reducing continuous focus on digital screens by looking away every 20 minutes at something 20 feet away for 20 seconds encourages blinking and lessens eye strain and evaporation. ScienceDirect

  6. Omega-3 Rich Diet / Dietary Anti-Inflammation
    Eating foods high in omega-3 fatty acids (like fatty fish) has mild anti-inflammatory effects and can improve tear quality and reduce ocular surface inflammation. PMCSjögren’s Foundation

  7. Hydration (Adequate Fluid Intake)
    Proper body hydration supports tear production. Dehydration can worsen dryness; sipping water regularly helps maintain baseline tear volume. ScienceDirect

  8. Avoiding Desiccating Medications and Triggers
    Being aware of and minimizing use of antihistamines, decongestants, certain antidepressants, and other drugs that dry mucous membranes can reduce worsening of symptoms. ScienceDirect

  9. Smoking Cessation
    Tobacco smoke irritates the ocular surface and increases inflammation and tear film instability. Quitting smoking helps reduce these effects. ScienceDirect

  10. Warmth-Based Meibomian Gland Expression Devices (e.g., Thermal Pulsation / LipiFlow)
    These office or home procedures apply heat and gentle pressure to unclog meibomian glands more effectively than manual massage, improving lipid layer thickness and reducing evaporation. ScienceDirect

  11. Intense Pulsed Light (IPL) Therapy
    IPL targets abnormal blood vessels and inflammation around the eyelids in meibomian gland dysfunction, helping normalize gland function and reduce surface inflammation. PMC

  12. Scleral or Specialty Contact Lenses (e.g., PROSE)
    These lenses vault over the cornea and create a fluid reservoir of tears, protecting the surface and providing continuous lubrication, especially useful in severe cases. ScienceDirect

  13. Autologous Serum Eye Drops (Biologic Tear Substitute)
    Made from the patient’s own blood, these drops contain growth factors and vitamins that help heal and nourish the ocular surface, acting like natural tears. PMC

  14. Platelet-Rich Plasma (PRP) Eye Drops
    Similar to autologous serum, PRP is richer in healing cytokines and can reduce inflammation and promote corneal epithelial repair in persistent dry eye. PMC

  15. Cold Compresses for Flare Management
    Applying cold can soothe acute irritation and reduce inflammation when the eye is inflamed, especially in combination with other therapies. PMC

  16. Sleep Position Optimization (Prevent Nocturnal Exposure)
    Elevating the head or using moisture-retentive eye protection at night can prevent exposure-related drying or incomplete eyelid closure during sleep. ScienceDirect

  17. Systemic Inflammation Control through Lifestyle (Exercise, Stress Reduction)
    Regular moderate exercise and stress management lower systemic inflammatory mediators, indirectly improving autoimmune dry eye by reducing immune activation. EatingWell

  18. Nutrition Timing and Anti-Oxidant Support
    Spacing intake of anti-inflammatory foods and antioxidants helps continuously supply protective nutrients to ocular tissues. Prevention

  19. Education and Self-Monitoring
    Teaching patients to recognize early flare signs, proper drop technique, and adherence improves outcomes. ScienceDirect

  20. Avoiding Overuse of Contact Lenses and Cosmetic Eye Products
    Limiting use when dryness is active and ensuring all products are non-irritating prevents additional surface stress. ScienceDirect


Drug Treatments

  1. Topical Cyclosporine A (e.g., Restasis, Cequa)

    • Class: Calcineurin inhibitor / immunomodulator

    • Dosage: Typically twice daily in each eye. Cequa uses nanomicellar technology for better penetration.

    • Time: Ongoing long-term use; benefits usually appear after several weeks to months.

    • Purpose: Reduce ocular surface inflammation by inhibiting T-cell activation and cytokine release.

    • Mechanism: Blocks calcineurin pathway, decreasing inflammatory mediators that damage lacrimal glands and tear film.

    • Side Effects: Burning or stinging at application, transient redness, rare hypersensitivity. Lippincott Journals

  2. Topical Lifitegrast (Xiidra)

    • Class: Lymphocyte function-associated antigen-1 (LFA-1) antagonist

    • Dosage: Twice daily in each eye.

    • Time: Chronic for symptom control; effects may be noticed within weeks.

    • Purpose: Decrease inflammation and improve symptom scores.

    • Mechanism: Blocks interaction between LFA-1 and ICAM-1, reducing T-cell mediated inflammation on ocular surface.

    • Side Effects: Dysgeusia (altered taste), eye irritation, transient blurred vision. PMC

  3. Topical Corticosteroids (e.g., Loteprednol)

    • Class: Anti-inflammatory steroid

    • Dosage: Short course—often 1 to 4 times daily for days to weeks, then tapered.

    • Time: Used for flares due to rapid effect; not for long-term continuous use because of risks.

    • Purpose: Quickly reduce surface inflammation and symptom flares.

    • Mechanism: Broad suppression of inflammatory gene expression.

    • Side Effects: Increased intraocular pressure (glaucoma), cataract formation, risk of infection if prolonged. PMC

  4. Oral Secretagogues – Pilocarpine and Cevimeline

    • Class: Muscarinic receptor agonists

    • Dosage:

      • Pilocarpine: 5 mg orally 3–4 times daily.

      • Cevimeline: 30 mg orally three times daily.

    • Time: Daily systemic therapy to stimulate glandular secretion.

    • Purpose: Increase residual tear and saliva production in Sjögren’s.

    • Mechanism: Stimulates muscarinic receptors on exocrine glands to promote fluid secretion.

    • Side Effects: Sweating, gastrointestinal upset, urinary frequency, bradycardia, bronchospasm (caution in asthma). PMC

  5. Oral Hydroxychloroquine

    • Class: Antimalarial with immune-modulating properties

    • Dosage: Typically 200–400 mg daily (adjusted by weight and ophthalmologic screening).

    • Time: Long-term for systemic autoimmune control; limited direct effect on dry eye but helps overall disease activity.

    • Purpose: Reduce systemic autoimmunity and inflammatory drive that exacerbates ocular surface inflammation.

    • Mechanism: Modulates toll-like receptor signaling and antigen presentation.

    • Side Effects: Retinopathy (requires baseline and periodic eye exams), gastrointestinal upset, rash. Lippincott Journals

  6. Low-Dose Oral Doxycycline

    • Class: Tetracycline antibiotic with anti-inflammatory effects

    • Dosage: 20–50 mg once or twice daily (sub-antimicrobial dose).

    • Time: Weeks to months for improvement in meibomian gland dysfunction.

    • Purpose: Reduce eyelid margin inflammation and improve lipid secretion quality.

    • Mechanism: Inhibits matrix metalloproteinases and inflammatory cytokines.

    • Side Effects: Gastrointestinal upset, photosensitivity, possible microbiome alteration. PMC

  7. Topical Secretagogues (e.g., Diquafosol – where available)

    • Class: P2Y2 receptor agonist

    • Dosage: Often 6 times daily (varies by formulation).

    • Time: Ongoing for tear film stabilization.

    • Purpose: Stimulate mucin and aqueous secretion to stabilize tear film.

    • Mechanism: Activates P2Y2 receptors on ocular surface epithelium to promote fluid and mucin release.

    • Side Effects: Mild irritation, unclear availability in all regions. ScienceDirect

  8. Topical Omega-3 Derived or Specialized Tear Lubricants

    • Class: Tear film augmenting agents with lipid components

    • Dosage: Per product instructions (several times daily).

    • Purpose: Supplement deficient lipid layer to reduce evaporation.

    • Mechanism: Replace or bolster tear film lipids to improve stability.

    • Side Effects: Minimal; some users report mild vision blur temporarily. ScienceDirect

  9. Systemic Immunosuppressants (e.g., Methotrexate, Mycophenolate mofetil)

    • Class: Disease-modifying agents

    • Dosage: Depends on specific drug and protocol; used when systemic manifestations are severe.

    • Time: Long-term, under rheumatologist supervision.

    • Purpose: Control systemic autoimmune inflammation that may secondarily worsen ocular disease.

    • Mechanism: Broad suppression of immune cell proliferation and activation.

    • Side Effects: Vary widely—liver toxicity, bone marrow suppression, infection risk; requires monitoring. Lippincott Journals

  10. Topical Nonsteroidal Anti-Inflammatory Drops (NSAIDs)

    • Class: COX inhibitors

    • Dosage: Often used short-term under supervision.

    • Purpose: Reduce mild inflammation and discomfort.

    • Mechanism: Inhibit prostaglandin synthesis.

    • Side Effects: Rare corneal complications if overused; mild burning. PMC


Dietary Molecular Supplements (Dosage, Function, Mechanism)

  1. Omega-3 Fatty Acids (EPA/DHA)

    • Dosage: 1000–3000 mg combined EPA/DHA daily (often in fish oil).

    • Function: Anti-inflammatory support for ocular surface and meibomian gland function.

    • Mechanism: Modulate cytokine production, reduce inflammatory mediators, improve lipid composition of meibum.

    • Evidence: Shown to reduce dry eye symptoms in many studies, though some trials have mixed results. PMCSjögren’s Foundation

  2. Flaxseed Oil (Alpha-linolenic acid)

    • Dosage: 1–2 tablespoons of flaxseed oil daily or equivalent capsule.

    • Function: Precursor to anti-inflammatory omega-3 derivatives.

    • Mechanism: Converted in the body to EPA/DHA (inefficiently), contributes to reducing inflammation.

    • Evidence: Some benefit as adjunct in dry eye and systemic inflammation. PMC

  3. Borage Oil (Gamma-Linolenic Acid, GLA)

    • Dosage: 500–1000 mg daily.

    • Function: Anti-inflammatory support to reduce surface inflammation.

    • Mechanism: GLA is metabolized to anti-inflammatory prostaglandins (e.g., PGE1).

    • Evidence: May help in inflammatory conditions including dry eye when combined with other fatty acids. PMC

  4. Vitamin D

    • Dosage: 1000–4000 IU daily (adjust for deficiency by testing).

    • Function: Immune modulation and reduced ocular surface inflammation.

    • Mechanism: Influences regulatory T cells, reduces pro-inflammatory cytokines.

    • Evidence: Deficiency is associated with worse dry eye; supplementation may improve symptoms in deficient individuals. EatingWell

  5. Vitamin A (Beta-Carotene precursor)

    • Dosage: As part of diet or supplement within recommended daily allowances (e.g., 700–900 mcg RAE).

    • Function: Supports mucin production and epithelial health.

    • Mechanism: Essential for normal differentiation of ocular surface epithelial cells and goblet cells.

    • Evidence: Deficiency leads to surface dryness; supplementation in deficient states restores ocular surface integrity. Prevention

  6. Vitamin E

    • Dosage: 15 mg (22.4 IU) daily, usually from diet or supplements.

    • Function: Antioxidant protection reducing oxidative stress on the ocular surface.

    • Mechanism: Scavenges free radicals, stabilizes cell membranes.

    • Evidence: Supports general eye health and may complement other anti-inflammatory nutrients. Prevention

  7. Lactoferrin

    • Dosage: Often 100–200 mg orally or via specialized eye formulas (varies by product).

    • Function: Anti-microbial, anti-inflammatory, and tear film stabilizing.

    • Mechanism: Binds iron, reduces bacterial growth, and modulates local immune response.

    • Evidence: Reduced levels found in dry eye; supplementation may help restoration. PMC

  8. Curcumin (Turmeric Extract)

    • Dosage: 500–1000 mg standardized extract daily, ideally with black pepper (piperine) for absorption.

    • Function: Strong anti-inflammatory and antioxidant.

    • Mechanism: Inhibits NF-κB and other inflammatory pathways, reducing cytokine production.

    • Evidence: Supports systemic inflammation reduction, indirectly benefiting Sjogren’s-related dryness. EatingWell

  9. Green Tea Polyphenols (EGCG)

    • Dosage: Equivalent of 2–3 cups of green tea daily or standardized supplement.

    • Function: Anti-inflammatory and anti-oxidative ocular surface support.

    • Mechanism: Reduces inflammatory signaling and oxidative damage to surface cells.

    • Evidence: May help in chronic inflammatory conditions including dry eye. EatingWell

  10. Probiotics

    • Dosage: Varies by strain; common formulations contain billions of CFUs daily.

    • Function: Modulate gut-immune axis to reduce systemic autoimmunity/inflammation.

    • Mechanism: Support regulatory immune responses, decrease systemic inflammatory mediators that can affect the ocular surface.

    • Evidence: Emerging support for autoimmune diseases; indirect benefit anticipated for inflammatory dry eye. EatingWell


Regenerative / Immune-Modulating / Stem Cell–Related Therapies

  1. Allogeneic Mesenchymal Stem Cell Therapy (Systemic or Ocular Delivery)

    • Dosage: Protocols vary; clinical trials often use cellular doses based on weight, delivered via injection or eye drops over several sessions.

    • Function: Immune modulation and repair of ocular surface tissues.

    • Mechanism: MSCs secrete anti-inflammatory cytokines, promote regulatory immune cells, and inhibit pathological immune activation.

    • Evidence: Randomized trials in Sjögren’s dry eye show symptom improvement and reduced inflammation. PubMed

  2. Autologous Mesenchymal Stem Cell–Derived Eye Drops / Local MSC Application

    • Dosage: Experimental; drops prepared from patient-derived or donor MSC secretome applied topically in trials.

    • Function: Direct ocular surface healing and immune calming.

    • Mechanism: Growth factors and exosomes from MSCs promote epithelial regeneration and reduce autoimmunity locally.

    • Evidence: Preclinical and early human studies show promise in refractory dry eye. PMCBioMed Central

  3. Autologous Serum Eye Drops

    • Dosage: Typically 20–100% dilution of patient serum, instilled several times daily.

    • Function: Replace deficient tear components and support healing.

    • Mechanism: Contains natural growth factors, vitamins, and anti-inflammatory proteins to nourish and regenerate the ocular surface.

    • Evidence: Beneficial in severe dry eye, especially where conventional tears fail. PMC

  4. Platelet-Rich Plasma (PRP) Drops

    • Dosage: Prepared from patient’s blood and used multiple times daily as prescribed.

    • Function: Enhance epithelial repair and decrease inflammation.

    • Mechanism: High concentration of platelets releases growth factors (PDGF, TGF-β) that support tissue regeneration.

    • Evidence: Shows improvement in persistent dry eye and epithelial defects. PMC

  5. Amniotic Membrane–Derived Therapy (e.g., PROKERA)

    • Dosage: Applied as a biological bandage for a few days to weeks depending on severity.

    • Function: Provide regenerative scaffold, reduce inflammation, and encourage healing of the corneal surface.

    • Mechanism: Contains anti-inflammatory proteins and growth factors; the physical membrane protects and promotes epithelial cell migration.

    • Evidence: Used in severe ocular surface disease including Sjögren’s complications. ScienceDirect

  6. Recombinant Human Nerve Growth Factor (Cenegermin)

    • Dosage: Eye drops, typically 6 times daily for 8 weeks (approved for neurotrophic keratitis but conceptually valuable in severe surface disease).

    • Function: Promote corneal nerve health and epithelial healing.

    • Mechanism: Stimulates nerve regeneration and survival, improving trophic support for epithelial cells.

    • Evidence: While officially for neurotrophic keratitis, enhanced surface healing mechanisms are relevant in damaged dry-eye corneas. ScienceDirect


Surgical / Procedural Interventions

  1. Permanent Punctal Occlusion (Thermal Cautery)

    • Procedure: Closing the tear drainage puncta permanently using heat.

    • Why Done: To retain existing tears on the ocular surface by stopping drainage, helpful when artificial tears or plugs fail.

    • Effect: Prolongs tear film residence, reducing symptom severity. ScienceDirect

  2. Tarsorrhaphy

    • Procedure: Partial sewing together of the eyelids to reduce exposure.

    • Why Done: For severe surface desiccation or exposure keratopathy when other measures fail, to physically protect and conserve moisture.

    • Effect: Reduces surface area exposed to air, helping healing. ScienceDirect

  3. Amniotic Membrane Transplantation

    • Procedure: Placement of amniotic tissue on the cornea as a biological dressing (over or under a device like PROKERA).

    • Why Done: For persistent epithelial defects and inflammation that have not healed, providing a healing environment.

    • Effect: Anti-inflammatory and regenerative support for damaged surfaces. ScienceDirect

  4. Limbal Stem Cell Transplantation

    • Procedure: Transferring healthy limbal stem cells to replace damaged corneal surface stem cells.

    • Why Done: In cases where chronic dryness has caused stem cell deficiency and the corneal surface cannot regenerate normally.

    • Effect: Restores epithelial maintenance and transparency. ScienceDirect

  5. Corneal Transplantation (Penetrating Keratoplasty)

    • Procedure: Full-thickness corneal replacement when scarring, thinning, or perforation occurs.

    • Why Done: To restore vision and structural integrity after severe surface damage from uncontrolled dry eye complications.

    • Effect: Vision rehabilitation, though underlying dryness must be managed to protect the graft. ScienceDirect


Prevention Strategies

  1. Regular Eye Exams to catch early signs before damage occurs. ScienceDirect

  2. Early Use of Lubricating Drops to interrupt the cycle of surface stress. ScienceDirect

  3. Consistent Eyelid Hygiene to maintain meibomian gland health. ScienceDirect

  4. Avoid Smoking and Air Irritants which worsen inflammation. ScienceDirect

  5. Control Screen Time and Encourage Blinking to reduce evaporative loss. ScienceDirect

  6. Maintain Adequate Hydration for baseline tear volume. ScienceDirect

  7. Use Environmental Humidification in dry climates or seasons. ScienceDirect

  8. Manage Underlying Autoimmune Activity with appropriate rheumatologic care. Lippincott Journals

  9. Anti-Inflammatory Diet (Omega-3s, Antioxidants) to reduce systemic inflammatory burden. EatingWell

  10. Review and Limit Medications that Cause Dryness (e.g., certain antihistamines). ScienceDirect


When to See a Doctor

You should seek medical evaluation if you experience any of the following: persistent burning or stinging that does not improve with over-the-counter drops, worsening blurred vision, significant light sensitivity, foreign body sensation that interferes with daily tasks, redness with discharge (possible infection), eye pain especially with corneal involvement, sudden vision changes, failure of basic self-care to control symptoms, signs of corneal surface damage (e.g., appearing as ulcer or white spot), or new systemic symptoms like joint pain, fatigue, or swelling suggesting active Sjögren’s flare or other autoimmune involvement. Early specialist input (ophthalmologist with dry eye experience and rheumatologist) prevents long-term damage. ScienceDirectLippincott Journals


What to Eat and What to Avoid

What to Eat:
Focus on an anti-inflammatory, nutrient-rich diet. Eat fatty fish (salmon, mackerel) for omega-3s; leafy green vegetables and colorful fruits for antioxidants like lutein, zeaxanthin, vitamins C and E; nuts and seeds for vitamin E and healthy fats; lean proteins such as tofu, beans, and poultry; green tea for polyphenols; turmeric with black pepper for curcumin’s anti-inflammatory boost; and foods rich in zinc and vitamin A to support ocular surface integrity. Hydrate with water and consider low-sugar probiotics like yogurt to help immune balance. Medical News TodayHealthlinePreventionEatingWell

What to Avoid:
Limit red and processed meats, fried foods, refined sugars, sodas, excessive alcohol, and refined grains that promote systemic inflammation. Avoid vegetable oils high in omega-6s (like safflower, corn, and canola) when consumed excessively, and watch for food triggers if you have sensitivities (e.g., gluten, dairy). Reduce intake of caffeine if it exacerbates dryness for you, and avoid overly salty foods that may draw water away from mucosal surfaces. Healthline


Frequently Asked Questions (FAQs)

  1. What is the difference between regular dry eye and dry eye from Sjögren’s syndrome?
    Regular dry eye can be due to environment or aging; Sjögren’s dry eye is from autoimmune destruction of tear glands, making it usually more severe and chronic. Sjögren’s Foundation

  2. Can Sjögren’s dry eye be cured?
    There is no cure for the underlying autoimmune disease yet, but symptoms can be managed effectively with a combination of therapies to preserve vision and comfort. PMC

  3. Are over-the-counter artificial tears enough?
    They help mild to moderate cases, but many patients with Sjögren’s need prescription anti-inflammatory drops, secretagogues, or biologics for adequate control. ScienceDirect

  4. Do dietary supplements really help dry eye?
    Some, especially omega-3s, vitamin D (if deficient), and anti-inflammatory nutrients, have evidence of benefit, though individual responses vary. PMCEatingWell

  5. Is it safe to use steroids for dry eye?
    Short courses of topical steroids are safe under medical supervision to control flares; long-term use risks glaucoma and cataracts. PMC

  6. How long before prescription treatments work?
    Anti-inflammatory eye drops like cyclosporine or lifitegrast often take several weeks to months to show full benefit. Lippincott Journals

  7. Can stem cell therapy help?
    Emerging evidence (especially mesenchymal stem cell therapy) shows promise in reducing inflammation and improving symptoms in refractory Sjögren’s dry eye. PubMedPMC

  8. What are autologous serum drops and when are they used?
    Drops made from the patient’s own blood, used when standard lubricants fail, to heal and restore the ocular surface. PMC

  9. Is surgery ever needed?
    Yes, in severe or nonresponsive cases—things like punctal occlusion, tarsorrhaphy, or surface reconstruction protect and help heal the eye. ScienceDirect

  10. Can controlling my overall autoimmune disease help my dry eye?
    Yes, treating systemic inflammation through rheumatologic management often improves ocular symptoms indirectly. Lippincott Journals

  11. Why do my eyes feel worse with screen use?
    Reduced blink rate and incomplete blinking when using screens cause faster tear evaporation and surface drying. ScienceDirect

  12. Are there lifestyle changes that really work?
    Yes: eyelid hygiene, environmental humidity, blinking exercises, avoiding irritants, and anti-inflammatory diet are all helpful. ScienceDirect

  13. Can dry eye cause vision loss?
    If left untreated and the corneal surface becomes severely damaged or infected, vision can be permanently affected. ScienceDirect

  14. How should I apply eye drops correctly?
    Tilt your head back, pull down the lower eyelid, instill the drop without touching the eye, close gently for 30 seconds, and press on the inner corner briefly to limit drainage. Wait 5 minutes between different drops. ScienceDirect

  15. Is smoking making my dry eye worse?
    Yes. Smoke increases surface inflammation and tear instability; quitting helps symptoms. ScienceDirect

Disclaimer: Each person’s journey is unique, treatment planlife stylefood habithormonal conditionimmune systemchronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: August 02, 2025.

 

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