Superior Limbic Keratoconjunctivitis

Superior Limbic Keratoconjunctivitis—often shortened to SLK—is a long-lasting, on-and-off eye surface problem that mainly irritates the upper part of the eye where the white part (conjunctiva), the clear dome (cornea), and their border (the limbus) meet. In SLK, that upper area gets inflamed and sore. The thin skin that lines the inner eyelid (the tarsal conjunctiva) can become bumpy, and the clear surface over the white of the eye (the superior bulbar conjunctiva) becomes red, thickened, and a bit loose. The top edge of the cornea can show tiny surface scratches. Doctors think the trouble happens because of mechanical rubbing and friction between the upper lid and the eye surface, often made worse by a dry or unstable tear film and by conditions that make the eye stick out or the eyelid fit too tightly. SLK tends to come and go over many years, usually doesn’t harm vision permanently, but causes chronic discomfort that feels out of proportion to how the eye looks. PubMedEyeWikiPMC

Superior Limbic Keratoconjunctivitis—often called SLK of Theodore—is a chronic irritation and inflammation of the upper white part of the eye (superior bulbar conjunctiva) and the upper cornea. The surface becomes dry, inflamed, and mechanically rubbed by the upper eyelid during every blink. That repeated friction keeps the surface angry and sore. SLK is not contagious. It often flares and remits over months or years. Many patients are middle-aged women, and a subset have thyroid disease (especially Graves’/thyroid eye disease). The main goals of care are to reduce friction, restore tear film, calm surface inflammation, and treat any related problems (dry eye, blepharitis, thyroid disease). With the right plan, most people get substantial relief. Vagelos CollegePubMed

Superior Limbic Keratoconjunctivitis (often called “SLK of Theodore”) is a chronic, on-and-off inflammation of the upper white part of the eye (superior bulbar conjunctiva), the inner surface of the upper eyelid (superior tarsal conjunctiva), and the top edge of the cornea (superior limbus). People typically feel burning, foreign-body sensation, grittiness, stringy mucus, light sensitivity, and redness that’s worst at the top of the eye. On exam, doctors often see fine surface scratches and stains at 12-o’clock on the cornea, a papillary reaction on the upper lid, and thickened or redundant superior conjunctiva; rose-bengal/lissamine-green stain highlights the damaged, unprotected ocular surface. SLK tends to flare and remit over years, is more common in middle-aged women, and often co-exists with dry eye disease and thyroid eye disease (a sizable minority of SLK patients show thyroid dysfunction). The most accepted explanation is mechanical friction—a tight upper lid and a dry, unstable tear film “rub” the superior ocular surface during blinking, triggering micro-injury, inflammation, and filaments. Treating SLK therefore focuses on reducing friction, stabilizing tears, and calming inflammation; stubborn cases may need office procedures or surgery. EyeWikiWebEye+1

A classic set of exam signs was described by Theodore: (1) a papillary reaction on the upper inner eyelid, (2) redness of the upper white of the eye, and (3) fine surface staining or scratches on the upper cornea. These signs together help confirm the diagnosis when the doctor flips the lid and looks under the microscope light. PMC

SLK often appears in middle-aged adults, and many patients also have thyroid eye disease or other tear-film problems; however, the exact cause is not fully known. ScienceDirect

Pathophysiology

• The upper lid slides over the upper eyeball each time you blink. In SLK, the tissue here becomes loose or thickened, the tears may not protect the surface well, and the rubbing becomes excessive. Over time this micro-trauma triggers inflammation, soreness, and the typical staining patterns doctors see with diagnostic dyes. PubMedNature

• Thyroid eye disease (especially when the eyes are more prominent or the lids are tight) and dry eye disease are common partners that raise the risk and worsen friction. Genetic & Rare Diseases CenterWebEye

• Lab and tissue studies suggest inflammatory chemicals and cells (including mast cells and the cytokine TSLP) may amplify the problem once friction has started, which helps explain flare-ups and remissions. PubMedWebEye

Types

Doctors do not divide SLK into strict textbook “types,” but in day-to-day care the condition is often discussed in helpful subgroups. This makes it easier to think about triggers and plan testing.

1. Classic (idiopathic) SLK of Theodore – the typical, long-running version with the three hallmark signs; the exact cause is unknown, and symptoms wax and wane. JAMA Network

2. Thyroid-associated SLK – SLK occurring with thyroid eye disease; lid tightness, proptosis, or eye surface exposure increase friction. PMCIOVS

3. Contact lens–related SLK (CL-SLK) – looks like classic SLK but triggered or worsened by soft contact lenses and sometimes by preservatives like thimerosal in older care systems. Stopping lens wear usually helps. PubMedAAO JournalReview of Optometry

4. Dry-eye–predominant SLK – SLK in people with tear film instability or keratoconjunctivitis sicca, where poor tear protection increases lid–eye friction. EyeWiki

5. SLK-like inflammation with superior conjunctivochalasis – loose, wrinkled conjunctiva above the cornea (superior CCh) can mimic or accompany SLK; treating the lax tissue can improve symptoms. PubMed+1

6. SLK-like changes in ocular graft-versus-host disease (oGVHD) – some patients with oGVHD have SLK-like superior inflammation as part of the broader ocular surface disease. PMC

Causes and contributors

Important note: No single “root cause” explains all SLK. The items below are risk factors and contributors that either start the process or make it worse. The strongest evidence supports mechanical friction, tear-film problems, thyroid eye disease, conjunctival laxity, and contact lens factors. PubMed+1EyeWikiGenetic & Rare Diseases Center

1. Mechanical friction from blinking
   Every blink sweeps the upper lid across the superior eye surface; in SLK this contact is too rough or too frequent, so the surface gets irritated and inflamed over time. PubMed

2. Lax, redundant superior conjunctiva
   The thin tissue over the white of the eye can become loose and folded; these folds rub against the lid and increase friction, especially when looking up. Genetic & Rare Diseases Center

3. Tight upper eyelids
   A snug or stiff upper lid presses harder on the eye, so each blink scrapes the surface a bit more than normal, feeding the cycle of irritation. Genetic & Rare Diseases Center

4. Prominent eyes (proptosis)
   Eyes that sit farther forward, as in some thyroid conditions, expose the upper surface and make friction with the lid more likely. Genetic & Rare Diseases Center

5. Thyroid eye disease and autoimmune thyroiditis
   Thyroid eye changes alter lid position and eye exposure; many SLK patients have or develop thyroid issues. Screening the thyroid is often recommended. WebEyeIOVS

6. Dry eye disease / tear-film instability
   Thin, unstable tears cannot cushion the eye; the lid then rubs more directly on the tissue, causing soreness and surface staining. EyeWiki

7. Keratoconjunctivitis sicca (aqueous deficiency)
   When the lacrimal glands do not make enough tears, the upper cornea and conjunctiva dry out, raising friction and staining in the SLK zone. EyeWiki

8. Contact lens wear (especially soft lenses)
   Lens edges and solutions can irritate the upper ocular surface and mimic or trigger SLK, particularly in older care systems with thimerosal. Stopping lens wear often improves signs. AAO JournalPubMed

9. Preservative sensitivity (e.g., thimerosal in older solutions)
   Some CL-SLK cases were tied to thimerosal; removing the preservative exposure reduced inflammation. PubMed

10. Superior conjunctivochalasis (CCh)
    Loose, wrinkled tissue above the cornea can behave like SLK and shares the same friction-driven mechanism; treating the lax tissue can relieve symptoms. PubMed+1

11. Meibomian gland dysfunction (oily tear layer problems)
    Poor oil layer quality lets tears evaporate quickly, leaving the surface unprotected and easier to irritate. (General dry-eye mechanism that can worsen SLK.) PMC

12. Autoimmune surface inflammation (amplifiers)
    Studies show mast cells and TSLP are upregulated in SLK tissue, suggesting that once friction starts, immune signals can keep inflammation going. WebEye

13. Chronic eye rubbing or frequent squinting
    Repeated pressure and movement across the upper surface can worsen micro-trauma and trigger flares. (Mechanism consistent with friction hypothesis.) PubMed

14. Blink pattern changes (fewer, harder, or incomplete blinks)
    Long screen time or stress can reduce blink rate or quality, which dries the surface and increases rubbing in the superior zone. (General dry-eye contributor.) EyeWiki

15. Exposure from incomplete eyelid closure (nocturnal lagophthalmos)
    If the eye doesn’t close fully, the upper cornea and conjunctiva dry out, making friction worse. (Common in thyroid eye disease.) Genetic & Rare Diseases Center

16. Age-related tissue changes
    With age, conjunctiva can become looser and goblet cells can decline, reducing mucin protection and making the upper surface more vulnerable. Nature

17. Goblet cell loss / mucin deficiency
    Loss of the “mucin coat” means the lid glides less smoothly; vital dyes like rose bengal highlight these unprotected cells. AAO

18. Rheumatoid arthritis and other systemic autoimmune disease
    Some patients with RA or Sjögren-type dryness develop SLK, reflecting systemic dryness and inflammation. EyeWiki

19. Ocular graft-versus-host disease (oGVHD)
    In oGVHD, severe surface dryness and inflammation can produce SLK-like superior changes. PMC

20. Environmental dryness and low humidity
    Air-conditioned, windy, or arid settings thin the tear film, increasing upper-surface friction during blinking. (General dry-eye mechanism relevant to SLK.) EyeWiki

Common symptoms

1. Burning – a steady heat-like irritation on the upper part of the eye that gets worse when you blink or when the air is dry; it reflects surface inflammation and friction. Genetic & Rare Diseases Center

2. Foreign-body sensation – the feeling that something is in the eye even when nothing is there; it comes from roughened tissue under the upper lid. Vagelos College

3. Redness (upper eye) – redness is most obvious on the top white of the eye where the problem lives. Vagelos College

4. Itching or scratchiness – persistent urge to rub the eye because the lid and surface are not gliding smoothly. Genetic & Rare Diseases Center

5. Light sensitivity (photophobia) – bright light stings because the upper cornea is irritated. Vagelos College

6. Tearing – the eye may water in response to surface irritation, though baseline tear quality is often poor. Genetic & Rare Diseases Center

7. Stringy mucus – mild mucoid discharge can appear as the surface becomes inflamed and dry. PMC

8. Pain on blinking – each blink can rub the sore area and make pain or awareness of the lid worse. PubMed

9. Fluctuating blur – vision may go in and out because the tear film is unstable over the upper cornea. EyeWiki

10. Contact lens intolerance – soft lenses may feel uncomfortable or worsen symptoms, especially with certain solutions. AAO Journal

11. Morning or end-of-day worsening – symptoms may be worse after dry sleep or after long days of blinking and screen time. (Typical dry-eye pattern that fits SLK.) EyeWiki

12. Grittiness – a sandy feeling from tiny surface defects on the upper cornea. Vagelos College

13. Sensitivity to wind or fans – air movement evaporates tears, exposing the sore superior surface. EyeWiki

14. Recurrent flares – symptoms often come and go over months to years, which is typical of SLK’s relapsing course. Genetic & Rare Diseases Center

15. Often little loss of vision – vision usually remains intact, even when discomfort is significant. Genetic & Rare Diseases Center

Diagnostic tests

Big picture: SLK is largely a clinical diagnosis made at the slit lamp by an eye-care professional who looks high on the eye and everts the upper lid. Dyes that stain damaged cells are very helpful. Extra tests help grade severity, search for causes (like thyroid disease or dry eye), and rule out mimics. EyeWiki

A) Physical exam at the slit lamp (core tests)

1. Careful slit-lamp exam of the superior bulbar conjunctiva
   The doctor looks for redness, thickening, redundancy, and filaments on the upper white of the eye, often asking you to look down while the examiner looks up. This is the anchor exam for SLK. EyeWiki

2. Upper lid eversion to inspect the tarsal conjunctiva
   Flipping the lid shows fine papillary bumps on the upper inner lid that rub the eye; this supports the diagnosis and helps rule out other causes of irritation. PMC

3. Vital-dye staining with fluorescein
   A drop of fluorescein highlights tiny scratches on the upper cornea and limbus; in SLK these are superior and may include filaments. WebEye

4. Vital-dye staining with rose bengal or lissamine green
   These dyes stain unprotected or damaged surface cells of the upper bulbar conjunctiva and limbus, often producing a very distinctive superior pattern that is highly suggestive of SLK. EyeWikiAAO

5. Assessment for superior corneal filaments
   The examiner gently looks for thin, string-like filaments stuck to the upper cornea that cause pain with blinking; their presence supports SLK and related dry-eye disease. Vagelos College

6. Baseline vision and refraction check
   Vision is usually normal, but measuring it provides a baseline and helps rule out other issues. Genetic & Rare Diseases Center

7. External inspection of lid position and blink
   The doctor notes tight lids, proptosis, incomplete blink, or frequent rubbing, which all increase friction over the superior surface. Genetic & Rare Diseases Center

8. Hertel exophthalmometry (simple office measurement)
   If thyroid eye disease is suspected, this device measures how far the eyes protrude, which relates to exposure and friction risk. IOVS

B) Manual and chair-side functional tests

9. Schirmer tear test (without anesthesia)
   A small paper strip under the lower lid measures tear production; low numbers point to aqueous-deficient dry eye that can worsen SLK. EyeWiki

10. Tear film breakup time (TBUT) with fluorescein
    After a fluorescein drop, the doctor times how fast the tear film breaks up; a short TBUT means unstable tears that make friction worse. EyeWiki

11. Meibomian gland expression
    Gentle pressure on the lid margin checks the quality and flow of meibum (the oily tear layer); poor quality suggests evaporative dry eye. PMC

12. Standardized surface-staining scoring (e.g., NEI or van Bijsterveld)
    The clinician scores how much the dyes stain the cornea and conjunctiva to track severity and response over time. Nature

13. Lid eversion with cotton-tip “sweep” to gauge friction
    A gentle sweep helps visualize how the loose superior conjunctiva rubs the lid and whether filaments are present—useful to localize symptoms to the superior zone. EyeWiki

C) Laboratory and pathological tests (to look for causes and tissue change)

14. Thyroid function tests (TSH, free T4 ± T3)
    Because of the strong link between SLK and thyroid eye disease, checking the thyroid helps find a treatable driver of friction and exposure. WebEye

15. Thyroid autoantibodies (e.g., TSI/TSHR, TPO, Tg)
    These tests flag autoimmune thyroid disease when eye findings suggest SLK plus thyroid involvement. IOVS

16. Tear osmolarity
    A tiny tear sample shows how concentrated the tears are; higher osmolarity reflects dry eye stress that worsens SLK. (Common dry-eye metric.) EyeWiki

17. MMP-9 point-of-care test
    This quick test detects inflammatory enzyme MMP-9 on the surface; a positive result supports ocular surface inflammation consistent with SLK flares. (General dry-eye inflammation tool.) EyeWiki

18. Impression cytology of the superior conjunctiva
    A gentle filter paper lifts the top cell layer to check for squamous metaplasia and goblet-cell loss—changes that explain why vital dyes stick and why the surface is unprotected in SLK. PMCNature

19. Histopathology (if tissue is removed during surgery)
    When surgeons resect loose superior conjunctiva, the specimen often shows keratinization and mast cells, supporting the friction-inflammation model. PubMed

D) Electrodiagnostic tests (rarely used for SLK)

20. Electrodiagnostic studies
    There are no routine electrodiagnostic tests for SLK; tests like ERG or VEP are not indicated. SLK is diagnosed clinically with dyes and the slit lamp, plus tear and thyroid evaluation as needed. (This point helps avoid unnecessary testing.) EyeWiki

E) Imaging tests (helpful when available, not mandatory)

1. Anterior-segment OCT (AS-OCT)
   High-resolution scans can document thickening or surface irregularity at the superior limbus and track changes over time; this is supportive, not required for diagnosis. PMC

2. External or slit-lamp photography with vital dyes
   Photos taken after fluorescein, lissamine green, or rose bengal help record the classic superior staining pattern for follow-up and teaching. WebEyeEyeWiki

3. Meibography (infrared imaging of meibomian glands)
   This imaging shows gland dropout in evaporative dry eye, which can co-exist with SLK and explain symptoms. PMC

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Non-pharmacological treatment

1. Blink hygiene and “20-20-20” breaks
   Gently train yourself to blink fully and regularly; every 20 minutes, look 20 feet away for 20 seconds. Purpose: decrease evaporative dryness and friction. Mechanism: fuller blinks refresh the tear film and spread meibum (oil), lowering shear on the superior cornea. (Supportive dry-eye guidance.) TIME

2. Humidify your air & avoid direct fans/AC to the face
   Purpose: raise ambient humidity to slow tear evaporation. Mechanism: more moisture in the room = longer-lasting tear film, less blink-related rubbing. TIME

3. Moisture-chamber glasses or wraparound eyewear
   Purpose: create a “mini-humid environment” in front of the eyes. Mechanism: traps humidity, reduces airflow, stabilizes tears, and eases friction at the superior limbus. (Dry-eye standard.) TIME

4. Contact-lens holiday (pause soft lenses)
   Purpose: remove a trigger when SLK flares, especially if lenses or their solutions irritate. Mechanism: reduces mechanical contact and preservative exposure on an already sensitive surface. EyeWiki

5. Therapeutic bandage soft contact lens (in-office fitting)
   Purpose: act as a friction shield over the cornea during a flare. Mechanism: the lens smooths the ocular surface, decreasing micro-trauma with each blink. (Commonly used in SLK.) EyeWiki

6. Scleral lens / PROSE device
   Purpose: vault the cornea under a fluid reservoir for all-day lubrication and mechanical protection. Mechanism: a tear reservoir between lens and cornea eliminates blink shear; helpful in severe ocular-surface disease, and used as part of SLK care in select cases. EyeWiki

7. Warm compresses + lid massage (daily)
   Purpose: melt and express meibomian oils to improve tear stability. Mechanism: better meibum reduces evaporative dry eye, lowering friction on the superior cornea (important because dry eye and SLK often travel together). Review of Ophthalmology

8. Lid hygiene (gentle foam/cleanser)
   Purpose: reduce biofilm and lid margin inflammation that destabilize tears. Mechanism: cleaner lids → healthier meibum → smoother blink mechanics. Review of Ophthalmology

9. Digital ergonomics (screen below eye level)
   Purpose: encourage more complete blinks. Mechanism: looking slightly downward naturally increases blink rate and completeness, improving tear spread. (Dry-eye ergonomics.) TIME

10. Allergen reduction (HEPA filter, avoid triggers)
    Purpose: lower allergic papillary response on the upper lid that can worsen rubbing. Mechanism: less allergic edema = less mechanical contact. EyeWiki

11. Temporary punctal plugs (trial)
    Purpose: conserve natural tears by slowing drainage. Mechanism: raises tear volume and contact time, improving lubrication and reducing friction; used when aqueous deficiency contributes. PMC

12. Permanent punctal cautery (for severe, proven benefit)
    Purpose: long-term tear conservation when plugs fail or fall out. Mechanism: thermally closes the punctum to retain tears; evidence suggests symptom and sign improvement in severe dry eye (a common SLK partner). PMCEyeWiki

13. Environment tweaks: smoke-free, wind protection, hydrate
    Purpose: minimize tear evaporation and irritants. Mechanism: reduces surface inflammation and micro-injury during blinks. TIME

14. Treat systemic thyroid disease (co-management)
    Purpose: in patients with thyroid eye disease (TED), control of thyroid status and orbitopathy can reduce lid tension and exposure that aggravate SLK. Mechanism: less proptosis/lid retraction → less superior friction. NCBI

15. Filament debridement (in-office)
    Purpose: carefully remove painful mucus filaments that stick to the cornea. Mechanism: immediate relief and less traction on epithelium; usually combined with lubricants/N-acetylcysteine. EyeWiki

16. Botulinum-toxin–induced protective ptosis (refractory cases)
    Purpose: temporarily reduce blink force/upper-lid contact to let the surface heal. Mechanism: weakening levator/pretarsal orbicularis changes lid dynamics and reduces friction; used for stubborn filamentary keratitis and reported for SLK in select patients; benefits must be weighed against transient lid droop. PubMedPMCIOVS

17. Intense pulsed light (IPL) or vectored thermal pulsation for MGD
    Purpose: treat meibomian gland dysfunction driving evaporative dry eye. Mechanism: improves meibum quality/expressibility, indirectly reducing friction that fuels SLK flares. PMC+1

18. Protective sleep strategies
    Purpose: if lids don’t fully close (nocturnal lagophthalmos), use sleep masks or medical tape as directed. Mechanism: prevents overnight drying of the superior cornea and conjunctiva. (Standard dry-eye care.) EyeWiki

19. Counsel to avoid preserved drops where possible
    Purpose: reduce benzalkonium chloride (BAK)-related surface toxicity. Mechanism: fewer preservatives = less epithelial damage and staining at the superior limbus. EyeWiki

20. Education + relapse plan
    Purpose: SLK relapses; knowing early signs and having a home plan (frequent PF tears, cool compresses, break from lenses) shortens flares. Mechanism: early lubrication and trigger control break the friction-inflammation cycle. EyeWiki

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Drug treatments

(Doses are typical starting points—final decisions are individualized by your eye doctor. Many are off-label for SLK but used for its drivers: friction, inflammation, dry eye, allergy.)

1. Topical corticosteroid (e.g., loteprednol 0.2–0.5%)
   Class: anti-inflammatory steroid. Dose/Time: short courses (e.g., 2–4×/day for 1–2 weeks, then taper). Purpose: quickly quiet a hot flare. Mechanism: suppresses surface inflammation and papillary response. Side effects: pressure rise, cataract risk with longer use—needs monitoring. (Listed in SLK management.) EyeWiki

2. Cyclosporine A ophthalmic 0.05% (Restasis®) or higher compounded
   Class: calcineurin inhibitor (immunomodulator). Dose/Time: 1 drop BID, long-term. Purpose: chronic anti-inflammatory for dry eye/SLK maintenance. Mechanism: reduces T-cell–driven inflammation, increases tear production. Side effects: stinging, delayed onset (weeks). Note: 0.05% is FDA-approved for dry eye; higher strengths sometimes compounded by specialists. FDA Access Data

3. Tacrolimus ophthalmic ointment 0.02–0.03% (off-label)
   Class: calcineurin inhibitor. Dose/Time: thin ribbon QD–BID, taper per response. Purpose: steroid-sparing control of ocular-surface inflammation. Mechanism: inhibits T-cell cytokines; helpful in refractory surface disease. Side effects: transient burn/tingle. MDPIAAO Journal

4. Rebamipide 2% ophthalmic suspension (Japan)
   Class: mucin secretagogue/epitheliotrophic. Dose/Time: QID. Purpose: improve mucin layer and heal staining. Mechanism: boosts mucin, stabilizes tear film, improves epithelium. Side effects: mild irritation; availability limited outside Japan. PubMedPMC

5. Antihistamine/mast-cell stabilizer (e.g., olopatadine/ketotifen/cromolyn)
   Class: anti-allergy. Dose/Time: typically BID (products vary). Purpose: calm papillary lid reaction that increases friction. Mechanism: blocks histamine and stabilizes mast cells. Side effects: mild sting, dryness. (Included among SLK options.) EyeWiki

6. N-Acetylcysteine (NAC) 5–10% drops (compounded; off-label)
   Class: mucolytic. Dose/Time: QID (regimens vary). Purpose: dissolve sticky filaments and mucus strands that tug on the cornea. Mechanism: breaks disulfide bonds in mucus; reduces filament formation and pain. Side effects: transient burn; needs compounding. EyeWikiScienceDirect

7. Hypertonic sodium chloride 2% drops / 5% ointment (night)
   Class: hypertonic agents. Dose/Time: drops QID, ointment QHS. Purpose: reduce epithelial edema and help filaments adhere less. Mechanism: draws out corneal fluid; helps epithelial adhesion. Side effects: sting. EyeWiki

8. Vitamin A ophthalmic ointment (off-label)
   Class: epitheliotrophic nutrient. Dose/Time: QHS. Purpose: aid surface healing where rose-bengal stains. Mechanism: normalizes epithelial differentiation; studied historically in SLK. Side effects: blur after application. Nature

9. Short courses of oral doxycycline or pulsed oral azithromycin (for MGD/rosacea drivers)
   Class: tetracycline/macrolide (anti-inflammatory dosing). Dose: doxycycline 20–50 mg BID or tapered protocols; azithromycin 500 mg once weekly ×3 weeks (examples from trials). Purpose: improve meibum and lid inflammation to stabilize tears. Mechanism: down-regulates matrix metalloproteinases and alters meibum composition. Side effects: GI upset, sun sensitivity (doxy), taste disturbance (azithro). PMCJAMA NetworkEyeWiki

10. Lifitegrast 5% (off-label for SLK; approved for dry eye)
    Class: LFA-1 antagonist (anti-inflammatory). Dose/Time: BID. Purpose: reduce ocular-surface inflammation in chronic dry eye that co-drives SLK. Mechanism: blocks T-cell adhesion signaling. Side effects: dysgeusia, irritation. (Dry-eye–directed option; not SLK-specific.) EyeWiki

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Dietary molecular supplements

1. Omega-3 (EPA/DHA) 1,000–2,000 mg/day
   Function: supports oil layer quality. Mechanism: anti-inflammatory lipid mediators; trial results are mixed—some benefit, some neutral. PMC

2. Gamma-linolenic acid (GLA) 240–300 mg/day (evening primrose/borage)
   Function: may reduce ocular-surface inflammation. Mechanism: converts to anti-inflammatory eicosanoids; evidence variable. (Supportive.) MDPI

3. Vitamin D (per deficiency, e.g., 1,000–2,000 IU/day)
   Function: immunomodulation; deficiency is linked to worse dry eye in some studies. Mechanism: influences epithelial and immune health. MDPI

4. Vitamin A (dietary; avoid excess supplements)
   Function: epithelial health. Mechanism: supports goblet cells and differentiation; avoid hypervitaminosis A. Nature

5. Lactoferrin (100–250 mg/day)
   Function: tear protein support; antioxidant/antimicrobial. Mechanism: may improve tear stability in some dry-eye cohorts. MDPI

6. Curcumin (as curcumin phytosome per label)
   Function: systemic anti-inflammatory adjunct. Mechanism: NF-κB modulation; ocular evidence is preliminary. MDPI

7. N-Acetylcysteine (oral 600 mg/day)
   Function: antioxidant/mucolytic systemic support. Mechanism: replenishes glutathione; ocular-surface data are limited compared to topical NAC. HSHSL Archive

8. Hyaluronic-acid oral supplements (per label)
   Function: joint/skin hydration; minimal ocular evidence; harmless adjunct. Mechanism: water-binding. MDPI

9. Bilberry/anthocyanins (per label)
   Function: antioxidant support. Mechanism: capillary and epithelial antioxidant effects; evidence modest. MDPI

10. Coenzyme Q10 (100–200 mg/day)
    Function: mitochondrial antioxidant; early ocular-surface signals only. Mechanism: reduces oxidative stress. (Use as supportive, not primary therapy.) MDPI

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Regenerative” ocular-surface therapies

(These are used in severe ocular-surface disease; some are off-label for SLK; availability varies. I’ll note regulatory status.)

1. Autologous Serum Eye Drops (ASEDs; e.g., 20–50% dilution, 4–8×/day)
   Function: biologic tear substitute with growth factors. Mechanism: promotes epithelial healing and reduces inflammation; used for dry eye, filamentary keratitis, and reported in SLK. Status: prepared under sterile protocols; not a mass-market drug. Evidence supports benefit over artificial tears in moderate–severe dry eye. PubMedFrontiers

2. Platelet-Rich Plasma (PRP) eye drops (specialty prep)
   Function: concentrated platelets deliver growth factors. Mechanism: improves staining and symptoms by stimulating surface repair. Status: specialty biologic; growing evidence including network meta-analysis. PubMedbmjophth.bmj.com

3. Cryopreserved amniotic membrane (AM) onlay—e.g., PROKERA®
   Function: biologic bandage to calm inflammation and aid healing. Mechanism: provides matrix, anti-inflammatory factors, and nerve support; short placements (2–7 days) can improve signs/symptoms for months in severe dry eye. Status: regulated human tissue product; used widely for ocular surface disease. PMCAAO

4. Amniotic membrane extract eye drops (AMED/AMEED)
   Function: soluble factors from amnion for epithelium. Mechanism: growth-factor–rich drops may aid healing; early studies suggest benefit. Status: investigational in many regions; currently no FDA-approved amniotic fluid eye drops—use only within proper trials/INDs. PubMedU.S. Food and Drug Administration

5. Nerve growth factor (cenegermin) for neurotrophic epithelium (off-label in SLK)
   Function: if neurotrophic changes coexist, NGF can promote corneal healing. Mechanism: stimulates corneal nerves/epithelium. Status: approved for neurotrophic keratitis; off-label beyond that. (Advanced specialist decision.) EyeWiki

6. Matrix therapy agent (RGTA®/Cacicol)—where available
   Function: mimics heparan sulfate to protect growth factors. Mechanism: creates a favorable healing micro-environment. Status: availability limited; off-label for SLK; evidence evolving. (Specialist use only.) ScienceDirect

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Surgeries

1. Thermal cauterization of the superior bulbar conjunctiva
   What: targeted thermocautery to shrink and stiffen the loose, inflamed superior conjunctiva.
   Why: reduces redundant tissue that rubs on the cornea with each blink; decades of clinical use for SLK with symptom relief in many series. PubMed

2. Superior conjunctival resection (with/without Tenon’s excision, with/without amniotic membrane)
   What: surgically removing the diseased strip of superior conjunctiva; sometimes placing amniotic membrane.
   Why: permanently decreases the “rubbing” tissue and its inflammatory load—key procedure for recalcitrant SLK. PubMed

3. Punctal cautery (permanent tear-conservation) when severe aqueous deficiency is present
   What: thermally closing puncta to retain tears long-term.
   Why: increases ocular-surface lubrication when plugs are ineffective or lost, indirectly reducing friction that fuels SLK. PMC

4. Amniotic membrane transplantation (sutured/glued) for surface rehabilitation
   What: surgical placement of amniotic membrane to regenerate epithelium and calm inflammation.
   Why: helps restore a healthier superior ocular surface in severe or surgically treated SLK. PMC

5. Laser conjunctivoplasty/thermal conjunctivoplasty (select centers)
   What: energy delivered to shrink redundant superior conjunctiva identified by dye staining.
   Why: aims to achieve the same endpoint as cautery—less tissue redundancy and less friction—using controlled energy patterns. (Technique-dependent; limited centers.) Wikipedia

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 Preventions

1. Keep blinks complete and frequent, especially on screens.

2. Use room humidifiers and avoid direct air to the face.

3. Wear wraparound/moisture-chamber glasses in wind or AC.

4. Do warm compresses and lid hygiene routinely if you have MGD/rosacea.

5. Prefer preservative-free tears if you use drops often.

6. Pause or modify contact-lens wear at early signs of irritation.

7. Manage allergies and environmental triggers.

8. Co-manage thyroid disease with your physician if present.

9. Hydrate, sleep well, protect eyes overnight if lids don’t fully close.

10. Attend regular eye check-ups—SLK relapses are common. EyeWiki

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When to see a doctor (red flags)

• Sharp or increasing pain, new light sensitivity, or vision drop.

• Persistent foreign-body sensation despite lubrication.

• Filaments or strings on the cornea that keep recurring.

• Contact-lens intolerance or redness that localizes to the top of the eye.

• Signs of thyroid eye disease (lid retraction, bulging eyes, double vision).
  Early treatment cuts friction and prevents chronic surface damage. NCBI

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What to eat and what to avoid

Eat more of:

• Fatty fish (salmon, sardine, mackerel) or omega-3–rich foods; consider supplements if diet is low (benefit is mixed but reasonable).

• Colorful vegetables (leafy greens, carrots, peppers) and vitamin-A–rich foods for epithelial health.

• Nuts, seeds, olive oil (healthy fats) and adequate water daily. PMC

Limit/avoid:

• Cigarette smoke exposure; it worsens surface inflammation.

• Very dry, windy, or dusty environments without eye protection.

• Excess alcohol and very high caffeine that can dry you out.

• Heavily preserved eye drops if you need frequent dosing—use preservative-free where possible. TIMEEyeWiki

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Frequently Asked Questions

1. Is SLK contagious?
   No. It’s an inflammatory, friction-related problem, not an infection. EyeWiki

2. Why is the top (12-o’clock) of my eye always the sore spot?
   That’s where the upper lid rubs the most during each blink; friction + dry tear film irritate that zone. EyeWiki

3. Is SLK linked to thyroid problems?
   Yes—some patients with SLK have thyroid dysfunction or thyroid eye disease; treating the thyroid issues can help. EyeWikiNCBI

4. Will it go away for good?
   It tends to flare and calm in cycles. With good habits and, if needed, procedures, flares usually become milder and less frequent over time. EyeWiki

5. What’s the single biggest thing I can do at home?
   Keep the ocular surface lubricated and reduce evaporation: blink fully, use humidifiers, protect from airflow, and follow your lid-care routine. TIME

6. Do I need steroid drops long-term?
   Usually no—steroids are for short flares. Maintenance commonly uses non-steroid immunomodulators like cyclosporine or tacrolimus (off-label). FDA Access DataMDPI

7. Are scleral lenses overkill?
   Not for tough cases. They bathe the cornea in liquid all day and cut friction dramatically. EyeWiki

8. What if filaments keep coming back?
   Topical N-acetylcysteine (compounded) can dissolve them; your doctor may also gently remove filaments in-office. EyeWiki

9. Are punctal plugs/cautery safe?
   They’re widely used to conserve tears. Plugs can fall out; cautery is more permanent and generally reserved for severe, proven benefit. PMC+1

10. Could surgery fix SLK?
    If conservative care fails, superior conjunctival cautery or resection can reduce the rubbing tissue and help a lot. PubMed

11. What about silver nitrate?
    Historically used to treat the superior tarsal conjunctiva; in many places it’s not readily available now. Your specialist may favor thermal options or surgery. PubMed

12. Is amniotic membrane safe?
    Surgeon-placed amniotic membrane is a standard tool for severe surface disease. Amniotic-fluid eye drops, however, are not FDA-approved; they should only be used within approved studies. AAOU.S. Food and Drug Administration

13. Can diet help?
    A heart-healthy, anti-inflammatory pattern with omega-3s and plenty of vegetables is reasonable, but it **supplements—not replaces—**medical care. PMC

14. Is SLK the same as Thygeson’s SPK?
    No. Both are superficial keratitis types, but SLK has a mechanical-friction driver and characteristic superior findings and conjunctival changes. WebEye

15. Who gets SLK?
    It often affects middle-aged women and people with dry eye or thyroid eye disease, but anyone can develop it. EyeWiki

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic 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 27, 2025.