Scleritis

Scleritis is inflammation of the sclera, which is the strong white wall of the eye. The sclera gives the eye its firm shape and protects the delicate parts inside the eye. When the sclera becomes inflamed, it swells, gets very tender, and triggers deep pain. The redness often looks deep and violet-red instead of bright red, because the inflamed blood vessels are deeper in the eye wall. This inflammation can happen in the front part of the eye that you can see in the mirror, or it can happen in the back part of the eye that you cannot see. Scleritis is not just a “red eye.” It is a serious condition because the inflammation can damage the eye wall, the cornea, the uvea, and even the optic nerve. If not treated properly, it can cause permanent vision loss. Doctors also care a lot about scleritis because, in many people, it is linked to a whole-body immune disease, like rheumatoid arthritis or a blood vessel inflammation disorder. In short, scleritis is a painful, deep inflammation of the eye wall that needs careful evaluation and treatment.

Scleritis means deep inflammation of the white coat of the eye (the sclera). The sclera is a tough, collagen-rich shell that gives the eye its shape and protects the inner parts. In scleritis, the inflammation sits below the surface layer (episclera) and involves the scleral tissue itself. That is why the pain is deep, boring, and often wakes people at night or hurts with eye movement. The eye looks diffusely red or purple, not just with a few surface vessels. Because the inflammation is deep, it can spread to the cornea, uvea (iris/ciliary body), and retina, and it can thin the sclera so much that perforation or severe vision loss can occur if it is not treated quickly. About half of cases are linked to a whole-body disease, most often autoimmune conditions such as rheumatoid arthritis or granulomatosis with polyangiitis; some cases are due to infection (bacteria, viruses, fungi), trauma, or follow eye surgery. Scleritis is an emergency for the eye and needs rapid care by an ophthalmologist. EyeWikiAAO-HNS

Types of scleritis

Doctors classify scleritis by where it is and how it looks. The main split is into anterior scleritis (in the front) and posterior scleritis (in the back). Anterior scleritis is most common and is further broken down by appearance into diffuse, nodular, and necrotizing forms. Posterior scleritis affects the back of the eye and can quietly threaten vision because it is hidden and harder to spot without imaging. These groupings are useful because they guide both urgency and treatment choices. NCBIEyeWiki

1. Anterior diffuse scleritis. In this type, the front of the sclera looks evenly swollen and deeply red or violaceous. A larger area may be involved, and the eye is very tender. People often report a dull, boring ache that can wake them from sleep. The inflammation can spill into nearby tissues, sometimes irritating the cornea or the uvea.
2. Anterior nodular scleritis. Here, one or more tender, elevated, immobile nodules form on the sclera. The nodules feel sore to touch. The redness around them is deep and does not move with the overlying conjunctiva. The pain is similar to diffuse scleritis but may be more localized to the lump. EyeWiki
3. Anterior necrotizing scleritis with inflammation. This is the most severe anterior form. Areas of sclera become so inflamed that the tissue starts to thin and die (necrosis). The eye can develop patches where the dark uveal layer shows through the thinned sclera. Pain can be extreme. This form is strongly linked with systemic autoimmune disease, and it carries a high risk of vision loss and perforation if it is not treated quickly and intensively. Medscape
4. Anterior necrotizing scleritis without obvious inflammation (scleromalacia perforans). This form is classically seen in people with long-standing rheumatoid arthritis. The sclera thins silently with little redness or pain. Because there is little inflammation on the surface, the condition can be missed until the eye becomes dangerously thin. Medscape
5. Posterior scleritis. This form affects the back of the eye. People may feel deep pain and reduced vision, but the front of the eye can look relatively normal. Posterior scleritis can cause fluid under the retina, choroidal folds, or optic disc swelling. On ultrasound, doctors often see a classic “T-sign,” which shows fluid collecting around the back of the eye. Because it is hidden, imaging is crucial to detect it and to prevent permanent vision loss. Review of OphthalmologyPubMedPMC

Common causes of scleritis

Scleritis has many possible causes. In many people, the immune system is overactive and attacks the eye wall by mistake. In others, a germ (bacteria, fungus, virus, or parasite) infects the sclera, often after trauma or surgery. Sometimes a medicine triggers it. Below are 20 important causes, grouped for clarity.

1) Rheumatoid arthritis (RA). RA is the most common systemic association of scleritis. The same immune attack that inflames joints can inflame the eye wall. Necrotizing forms are particularly linked to RA, and scleritis can signal active, dangerous inflammation elsewhere in the body. ScienceDirect

2) Granulomatosis with polyangiitis (GPA). This is an autoimmune disease that inflames blood vessels (vasculitis). The small vessels in the sclera can be attacked, causing severe scleritis, sometimes necrotizing. It can also involve the sinuses, lungs, and kidneys. Cleveland Clinic

3) Relapsing polychondritis. This autoimmune disease inflames cartilage in the ears, nose, and airway. It can also inflame the eye, including the sclera, leading to painful episodes that flare and settle. Cleveland Clinic

4) Systemic lupus erythematosus (SLE). In lupus, immune complexes can inflame many tissues. The eye wall can become involved, sometimes with other eye tissues such as the uvea. Cleveland Clinic

5) Inflammatory bowel disease (Crohn’s disease and ulcerative colitis). Gut inflammation can be linked with eye inflammation. Scleritis may flare with bowel flares or run on its own track. Cleveland Clinic

6) Sarcoidosis. Sarcoid forms immune cell clusters called granulomas in organs such as the lungs or lymph nodes. The eye can also be affected. Scleritis can occur alone or with uveitis. Cleveland Clinic

7) Ankylosing spondylitis and other HLA-B27–related disease. These spinal and joint conditions are famous for uveitis, but the sclera can be inflamed too. The eye pain can be intense and may come with back or joint stiffness.

8) Psoriatic arthritis. This is another immune-mediated joint disease that can involve the eyes. Eye inflammation can show up even when skin psoriasis is mild. PMC

9) Behçet disease. This blood-vessel inflammation causes mouth and genital ulcers and can inflame many eye tissues, including the sclera. Attacks can be explosive and sight-threatening.

10) IgG4-related disease. This is a newer immune condition that can create firm inflammatory masses in different organs. It can involve the orbit and, rarely, present as scleritis, including posterior disease, and usually responds to immunosuppression. PMC+1

11) Infectious scleritis from bacteria. Bacteria can directly infect the sclera, especially after trauma or surgery. Pseudomonas aeruginosa is a leading cause in many series and can be aggressive, often after pterygium surgery; early recognition and antibiotics are critical. PMC

12) Infectious scleritis from fungi. Fungal scleritis can follow injuries with plant matter or occur in hot, humid climates and agricultural settings. It is often slow and stubborn. In some regions, fungi are a leading cause after trauma. Lippincott Journals

13) Infectious scleritis from viruses (herpes simplex or herpes zoster). Herpes viruses can inflame the sclera directly or by triggering immune reactions. Shingles (zoster) around the eye can precede a painful scleritis.

14) Infectious scleritis from tuberculosis. TB can involve the eye by spreading through the blood or by immune reaction. Doctors test for TB when scleritis is severe, recurrent, or when other risk factors exist.

15) Infectious scleritis from syphilis or Lyme disease. These systemic infections can cause many eye problems, including scleritis, and must be tested for because they require specific antibiotics.

16) Surgically-induced necrotizing scleritis (SINS). This severe form can appear days to years after eye surgery such as pterygium removal, cataract surgery, trabeculectomy, scleral buckle, strabismus surgery, or vitrectomy. It is believed to be an autoimmune reaction around the surgical site and can progress rapidly if missed. EyeWikiAAO-HNSSpringerOpen

17) Ocular trauma. Blunt or penetrating injuries can damage the sclera and set off inflammation or allow germs to enter. Later thinning and inflammation may appear long after the initial injury, especially if the wound involved the sclera. Lippincott Journals

18) Drug-induced scleritis (especially bisphosphonates). Medicines used for osteoporosis, such as pamidronate, zoledronate, alendronate, and risedronate, have been linked to episcleritis and scleritis. Stopping the drug and treating the inflammation usually leads to recovery. New England Journal of MedicinePubMed

19) Gout and crystal disease. High uric acid and crystal deposits can irritate tissues. While uncommon, they can contribute to scleral inflammation, especially when other risk factors exist.

20) “Idiopathic” immune scleritis. In a sizable group, no definite trigger is found even after careful testing. Doctors still treat the eye inflammation and watch closely for any later clues of a systemic disease. Notably, about 36–44% of all scleritis cases are associated with a systemic condition, most often rheumatoid arthritis, so the search is important. Cleveland Clinic

Common symptoms

1) Deep, boring eye pain. The pain feels like it sits inside the eye, not on the surface. It can radiate to the brow, temple, jaw, or teeth and may wake you from sleep.

2) Pain worse with eye movement. Moving the eye pulls on the inflamed sclera, so looking left, right, up, or down can make the pain spike.

3) Redness with a violet-red hue. The color looks deeper than a simple pink eye because the inflamed blood vessels are deep in the eye wall.

4) Tenderness to touch. Gently pressing the eyelid over the sore area can be quite painful because the sclera under it is inflamed.

5) Light sensitivity (photophobia). Bright light causes discomfort because the inner eye tissues are irritated.

6) Tearing or watery eye. The irritated eye may water as a reflex response to the inflammation.

7) Blurry vision. Swelling and inflammation can affect the cornea, the uvea, or the retina (especially in posterior scleritis), leading to blurred sight.

8) Reduced vision. If the inflammation is strong or reaches the back of the eye, vision can drop noticeably and may not fully return unless treated quickly.

9) Headache or facial pain. Pain from the sclera can spread to nearby nerves, causing headache or pain in the cheek or jaw.

10) Pain at night or on waking. The deep ache often feels worse at night or early morning.

11) A visible nodule on the white of the eye. In nodular scleritis, a firm, tender bump appears that does not move when the outer membrane is pushed with a cotton swab.

12) A sense of “eye fullness” or pressure. In posterior scleritis, swelling behind the eye can give a feeling of fullness or deep pressure.

13) Double vision or painful eye movements. If the tissues around the extra-ocular muscles are inflamed, eye movements can be painful or slightly restricted, rarely causing diplopia.

14) Blue-grey or dark patch on the white of the eye. Severe thinning can reveal the darker uveal layer, creating a bluish area.

15) Flashes, floaters, or distorted lines. Posterior scleritis can cause fluid under the retina or choroidal folds, which may distort straight lines or cause new floaters. PMC

Diagnostic tests

Doctors don’t rely on just one sign. They combine examination, simple office maneuvers, lab tests, electrodiagnostic tests (when the back of the eye is involved), and imaging to confirm scleritis, rule out episcleritis, and search for the cause.

A) Physical examination

1) Visual acuity testing. Reading an eye chart measures how much the inflammation is affecting sight. Any drop in vision raises the urgency for imaging and treatment.

2) Slit-lamp examination of the anterior eye. The doctor uses a microscope and light to look at the sclera, episclera, cornea, and anterior chamber. They look for deep, immobile vessels, nodules, scleral edema, thinning, and any corneal inflammation or peripheral ulcerative keratitis that can travel with necrotizing scleritis.

3) Dilated fundus examination. Drops widen the pupil so the back of the eye can be checked for retinal fluid, choroidal folds, or optic disc swelling, which suggest posterior scleritis and push the team to order an ultrasound or OCT. PMC

4) Intraocular pressure measurement (tonometry). Pressure can go up or down depending on inflammation patterns. An unexpected pressure change adds to the picture and helps guide therapy.

5) Pupillary and ocular motility testing. Checking pupil responses and eye movements helps detect inflammation affecting the optic nerve or tissues behind the eye, which is especially relevant in posterior scleritis.

B) Manual office maneuvers

6) Phenylephrine blanching test. A drop of 2.5% phenylephrine blanches the superficial conjunctival and episcleral vessels. In episcleritis, redness fades because those surface vessels constrict. In scleritis, the deep scleral vessels do not blanch, so the redness stays. This simple test helps distinguish a benign condition from a serious one. Review of OptometryEyeWikiNCBI

7) Cotton-swab vessel mobility test. Gently moving the conjunctiva with a moistened swab can slide superficial vessels in episcleritis, but the deep scleral vessels in scleritis do not move, supporting the deeper diagnosis. Taming the SRU

8) Palpation for focal tenderness. Lightly pressing over the red area often produces marked tenderness in scleritis but only mild or no tenderness in episcleritis, helping separate the two.

9) Seidel test (fluorescein leak test) when corneal involvement is suspected. If the cornea has a peripheral ulcer from associated disease, fluorescein dye checks for leaks, because necrotizing scleritis can travel to the cornea.

10) Schirmer test for dry eye in suspected Sjögren’s or RA overlap. Measuring tear production is not a test for scleritis itself, but it helps evaluate autoimmune context that often coexists.

C) Laboratory and pathological testing

11) Inflammation markers (ESR and CRP). These blood tests show how active body-wide inflammation is. High levels support an immune cause and help monitor response to treatment.

12) Rheumatologic panel (RF and anti-CCP for RA). Because RA is the most common association, these tests matter whenever scleritis appears, especially if joints are stiff or painful. ScienceDirect

13) ANCA (c-ANCA/PR3 and p-ANCA/MPO). These help detect vasculitis such as GPA, which can cause severe, necrotizing eye disease and needs systemic therapy. Cleveland Clinic

14) ANA and other autoimmune screens. These look for lupus or related connective tissue disease when symptoms or exam findings suggest them. Cleveland Clinic

15) Infectious work-up when indicated. Tests include syphilis serology, TB testing (IGRA/TST), and Lyme serology based on risk and geography. Because infections require antimicrobials and steroids may worsen them, this step is critical. In suspected infectious scleritis or when necrosis is present, doctors may perform scleral scrapings or biopsy for culture (bacterial, fungal, mycobacterial) to identify the organism. NCBIPMC

D) Electrodiagnostic testing

16) Visual evoked potential (VEP). If the optic nerve might be affected—especially in posterior scleritis with disc swelling—VEP can measure how well signals travel from the retina to the brain, helping distinguish optic nerve involvement from other causes of vision loss.

17) Full-field electroretinography (ERG). If the retina seems involved—for example, with serous retinal detachment—ERG can check global retinal function and set a baseline when disease is severe or prolonged.

E) Imaging tests

18) B-scan ocular ultrasonography. This is the key test when posterior scleritis is suspected. It can show scleral thickening and the classic “T-sign,” which represents fluid in Tenon’s space behind the eyeball. It also detects choroidal folds and serous retinal detachments, explaining vision changes and guiding urgent therapy. Review of OphthalmologyPubMedPMC

19) Optical coherence tomography (OCT). OCT provides a high-resolution cross-section of the retina and can reveal subretinal fluid, macular edema, and choroidal folds caused by posterior scleritis, allowing precise monitoring over time. PMC

20) CT or MRI of the orbits (with contrast). When ultrasound is inconclusive or when the clinician needs to look for orbital inflammation, abscess, tumor, or wider spread, cross-sectional imaging helps map the full extent of disease and exclude other causes of pain and swelling.

Non-pharmacological treatments

These measures support, not replace, medical therapy. They reduce pain, protect the eye, lower inflammation triggers, and improve safety of drug treatment.

1. Urgent specialist care and monitoring — Purpose: prevent scleral thinning, uveitis, glaucoma, or perforation. Mechanism: early diagnosis, right drug choice (e.g., NSAID vs steroids vs immunosuppression; antimicrobials when infectious), and serial exams (including B-scan for posterior scleritis). NCBISAGE Journals

2. Treat the underlying systemic disease — Purpose: stop the driver. Mechanism: coordinating with rheumatology/infectious-disease to control rheumatoid arthritis, vasculitis, gout, TB, syphilis, zoster, etc., which reduces scleral inflammation relapses. EyeWiki

3. Cold compresses for pain — Purpose: pain relief and vessel constriction. Mechanism: reduces neurogenic vascular dilation in inflamed tissues (adjunct only; does not treat cause).

4. Strict contact lens holiday — Purpose: avoid mechanical irritation and microtrauma. Mechanism: reduces local friction and infection risk while the sclera is inflamed and thinned.

5. Protective eyewear — Purpose: prevent minor trauma on a thinned sclera. Mechanism: physical barrier during flares and daily activities.

6. Artificial tears / ocular surface care — Purpose: reduce surface inflammation spillover & photophobia. Mechanism: lubricants dilute inflammatory mediators; lid hygiene controls blepharitis that can worsen ocular surface inflammation.

7. Smoking cessation — Purpose: lower systemic inflammation and vascular risk that worsens scleral ischemia. Mechanism: reduces oxidative stress and neutrophil activation.

8. Alcohol moderation (especially on methotrexate) — Purpose: protect the liver. Mechanism: lowers hepatotoxicity risk when using immunomodulators.

9. Vaccination review before biologics — Purpose: reduce severe infections during immunosuppression. Mechanism: pre-biologic immunization (e.g., zoster, pneumococcal, influenza) reduces infectious complications that can mimic or trigger scleral disease; live vaccines are avoided on active high-dose immunosuppression.

10. Blood pressure, glucose, and lipid control — Purpose: lower steroid complications and vascular events. Mechanism: reduces steroid-induced hypertension/hyperglycemia and vasculitic risk.

11. Bone protection plan — Purpose: prevent steroid-induced osteoporosis. Mechanism: weight-bearing exercise, calcium-rich diet, vitamin D sufficiency; DEXA scans if long steroid courses.

12. Gastroprotection with high-dose NSAIDs — Purpose: prevent ulcers/bleeding. Mechanism: PPI or H2 blocker when NSAIDs are required; take NSAIDs with food and avoid duplicate OTC NSAIDs. (Drug specifics below.) NCBI

13. Sun and wind protection — Purpose: comfort; reduce photophobia and tear evaporation. Mechanism: wraparound sunglasses and hats.

14. Stress-sleep management — Purpose: reduce flares triggered by systemic stress. Mechanism: calmer autonomic tone dampens inflammatory signaling.

15. Nutrition pattern: anti-inflammatory base — Purpose: lower systemic inflammatory tone. Mechanism: omega-3-rich fish, extra-virgin olive oil, legumes, vegetables, nuts, fermented foods emphasize pro-resolving lipid mediators and antioxidant balance (details in diet section). FASEB JournalPMC

16. Avoid vasoconstrictor “get-the-red-out” drops — Purpose: prevent rebound redness and masking of disease severity. Mechanism: temporary alpha-agonist vasoconstriction can hide progression.

17. Medication reconciliation — Purpose: avoid drug interactions (e.g., cyclosporine + grapefruit; methotrexate + sulfonamides). Mechanism: pharmacist and clinician review.

18. Eye surgery timing — Purpose: avoid SINS (surgically induced necrotizing scleritis) and poor healing. Mechanism: defer elective surgery until disease is quiet; use peri-operative immunosuppression plans. AAO-HNSEyeWiki

19. Infection control when infectious scleritis is suspected — Purpose: sight-saving. Mechanism: urgent cultures and early debridement plus intensive topical/systemic antimicrobials; topical steroids only with antimicrobial cover once pathogen is controlled. NCBIPMCSAGE Journals

20. Shared “flare plan” — Purpose: speed to care. Mechanism: you and your clinicians agree on warning signs, who to call, and how to escalate (e.g., same-day clinic, ED if severe pain/vision drop).

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Drug treatments

Doses below are typical and must be individualized by your ophthalmologist/rheumatologist with lab monitoring. Infectious scleritis requires antimicrobials first (see note after #10).

1. Indomethacin (NSAID)
   Dose: 50 mg by mouth 2–3×/day (or 25–50 mg TID). Timing: first-line for mild/moderate non-necrotizing anterior scleritis. Purpose: reduce pain and inflammation. Mechanism: COX inhibition lowers prostaglandins. Side effects: stomach irritation/ulcer, kidney stress, fluid retention; use PPI if high risk. NCBI

2. Naproxen (NSAID)
   Dose: 500 mg by mouth 2×/day. Timing: alternative when indomethacin not tolerated/effective. Purpose/Mechanism: as above; longer half-life helps adherence. Side effects: as NSAIDs. NCBI

3. Prednisone (systemic glucocorticoid)
   Dose: ~0.5–1 mg/kg/day (often 60–80 mg/day), then slow taper once quiet. Timing: for cases not controlled with NSAIDs, posterior scleritis, or necrotizing disease. Purpose: fast control to protect vision. Mechanism: broad cytokine gene suppression. Side effects: sleep/mood change, high glucose/BP, infection risk, osteoporosis, cataract, glaucoma; taper guided by specialist. NCBIWebEye

4. Methotrexate (antimetabolite/DMARD)
   Dose: 7.5–25 mg once weekly PO/SC + folic acid; monitor CBC/LFTs. Timing: steroid-sparing for recurrent/noninfectious scleritis. Purpose: maintain remission with lower steroid doses. Mechanism: inhibits dihydrofolate-dependent pathways; immunomodulates adenosine signaling. Side effects: liver toxicity, cytopenias, GI upset; avoid alcohol and pregnancy. Medscape

5. Azathioprine (antimetabolite)
   Dose: ~1–2.5 mg/kg/day PO; consider TPMT/NUDT15 status. Timing: steroid-sparing or with vasculitic disease. Mechanism: purine synthesis inhibition reduces lymphocyte activity. Side effects: leukopenia, liver toxicity, nausea; infection risk. Medscape

6. Mycophenolate mofetil (antimetabolite)
   Dose: 1.0–1.5 g PO twice daily. Timing: steroid-sparing alternative to AZA/MTX. Mechanism: inhibits inosine monophosphate dehydrogenase; T/B-cell suppression. Side effects: GI upset, leukopenia; teratogenic. Medscape

7. Cyclosporine (calcineurin inhibitor)
   Dose: often 2–5 mg/kg/day divided; monitor drug levels, BP, creatinine. Timing: refractory noninfectious scleritis or with posterior involvement. Mechanism: blocks calcineurin-NFAT → lowers IL-2/T-cell activation. Side effects: nephrotoxicity, hypertension, gingival hyperplasia; avoid grapefruit (raises levels). SAGE Journals

8. Cyclophosphamide (alkylator)
   Dose: ~1.5–3 mg/kg/day PO or IV pulses in severe vasculitis-linked scleritis. Timing: limb/organ-threatening vasculitis (e.g., GPA) with necrotizing scleritis. Mechanism: DNA cross-linking → potent immunosuppression. Side effects: cytopenias, hemorrhagic cystitis, infertility, malignancy risk; requires close specialist oversight. MedscapeAAO-HNS

9. Infliximab (anti-TNF-α biologic, IV)
   Dose: ~5 mg/kg IV at weeks 0, 2, 6, then q8 weeks (individualized). Timing: refractory noninfectious scleritis after antimetabolite failure/intolerance. Mechanism: neutralizes TNF-α to interrupt inflammatory cascade. Side effects: infusion reactions, infection risk (screen TB/hepatitis), drug antibodies. Evidence: case series and small cohorts show high rates of quiescence in refractory scleritis. PMC+1AAO-HNS

10. Rituximab (anti-CD20 biologic, IV)
    Dose: either 375 mg/m² weekly ×4 or 1000 mg on days 1 & 15; reinfusion for relapse. Timing: refractory, sight-threatening noninfectious scleritis (often vasculitic or RA-related). Mechanism: B-cell depletion reduces autoantibody and antigen-presentation activity. Side effects: infusion reactions, hypogammaglobulinemia, infection risk; pre-screening and vaccines recommended. Evidence: multiple case series and small trials show benefit when other IMT/anti-TNF fail. AAO JournalSpringerOpenTaylor & Francis Online

Special note — infectious scleritis: When infection is suspected or proven (e.g., after pterygium surgery, trauma, or zoster), the primary therapy is antimicrobial: intensive topical fortified antibiotics, targeted systemic antibiotics/antivirals/antifungals, and often early surgical debridement of necrotic tissue to let drugs penetrate. Steroids are used only with antimicrobial cover and specialist guidance. NCBIPMCSAGE Journals

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Dietary molecular supplements

No supplement treats scleritis on its own. The goal is to support resolution of inflammation and overall safety of therapy. Always review supplements with your clinicians for interactions (e.g., anticoagulants).

1. Omega-3 EPA/DHA — Dose: ~1–2 g/day combined EPA+DHA (higher only if approved). Function: supports “pro-resolving” lipid mediators (SPMs). Mechanism: precursors of resolvins/protectins/maresins that actively turn off inflammation. FASEB JournalPMC

2. Curcumin (with piperine or high-bioavailability form) — Dose: 500–1000 mg/day (divided), evidence for ocular inflammation mostly from uveitis/dry eye studies. Function: antioxidant/anti-NF-κB effects. Mechanism: lowers IL-1β, TNF-α, COX-2 signaling. PubMedPMCEuropean Review

3. Vitamin D3 — Dose: typically 1000–2000 IU/day (personalize to serum 25-OH D). Function: immune tolerance support. Mechanism: shifts Th17/Treg balance toward tolerance; improves antimicrobial peptides. PMCMDPI

4. Lutein + Zeaxanthin — Dose: ~10–20 mg lutein + 2–4 mg zeaxanthin/day. Function: ocular antioxidant network. Mechanism: quenches reactive oxygen species; small ocular trials show anti-inflammatory signals in dry eye; extrapolation only. Frontiers

5. N-Acetylcysteine (NAC) — Dose: 600–1200 mg/day. Function: glutathione precursor. Mechanism: reduces oxidative stress linked to inflammatory signaling.

6. Boswellia serrata extract (AKBA-standardized) — Dose: 300–500 mg 2–3×/day. Function: leukotriene pathway modulation. Mechanism: 5-LOX inhibition may reduce inflammatory cell recruitment.

7. Green tea catechins (EGCG) — Dose: 200–400 mg/day (as decaf extract if caffeine-sensitive). Function: antioxidant/anti-NF-κB. Mechanism: dampens cytokine production.

8. Quercetin — Dose: 500–1000 mg/day. Function: mast-cell stabilization; antioxidant. Mechanism: modulates MAPK/NF-κB; evidence mostly systemic.

9. Probiotics (multi-strain Lactobacillus/Bifidobacterium) — Dose: as labeled daily. Function: gut–immune crosstalk. Mechanism: improves barrier and short-chain fatty acids that favor Treg tone.

10. Ginger extract (standardized) — Dose: 500–1000 mg/day. Function: COX/LOX modulation and anti-nausea (helpful if on MTX). Mechanism: gingerols/shogaols reduce eicosanoid synthesis.

Regenerative / stem cell drugs

Important safety note: There are no approved “stem cell drugs” for scleritis. Some cell-based therapies are being studied for autoimmune eye disease in research settings; they are experimental and not standard of care. Below is a practical, safety-first view:

1. Recombinant zoster vaccine (Shingrix®) — Use: adults meeting local guidelines, ideally before high-level immunosuppression. Function/Mechanism: primes VZV immunity to lower shingles risk, which can cause ocular disease including scleritis. Not for acute treatment; reduces preventable infectious flares. (Non-live vaccine; schedule per country guidance.)

2. Pneumococcal & annual influenza vaccines — Use: before or during long-term IMT/biologics to cut severe infections. Mechanism: reduces infections that can mimic/worsen ocular inflammation; live vaccines avoided on strong immunosuppression.

3. Intravenous immunoglobulin (IVIG) — Use: selected autoimmune disorders; not routine for scleritis but occasionally considered off-label in refractory immune disease by subspecialists. Mechanism: Fc-mediated immune modulation; risks include headache, thrombosis, cost; specialist only.

4. Autologous hematopoietic stem-cell transplantation (AHSCT) — Use: not for isolated scleritis; reserved for life-threatening, refractory systemic autoimmune diseases in trials/centers. Mechanism: immune “reset.” Significant morbidity; not recommended for typical scleritis.

5. Mesenchymal stromal cell therapies (investigational) — Use: research for autoimmune uveitis/systemic disease; not approved for scleritis. Mechanism: paracrine immune modulation; unknown long-term safety; consider only in clinical trials. Frontiers

6. “Immune boosters” (OTC products) — Be cautious. Many products marketed as immune boosters have no proven benefit and may interfere with immunosuppressants. Discuss any product with your clinicians.

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Procedures/surgeries

Most scleritis is medical-therapy-first. Surgery is for complications (especially infectious or necrotizing disease and structural threats).

1. Surgical debridement of necrotic/infected sclera — Why: remove devitalized tissue so antibiotics/antifungals can penetrate and to decrease pathogen load. What: excision of infected scleral plaque or abscess with cultures; often combined with grafting. Evidence: early debridement improves outcomes in infectious scleritis (e.g., post-pterygium). PMCSAGE Journals

2. Scleral patch graft (lamellar, donor sclera or fascia lata) — Why: reinforce areas of severe thinning or impending perforation. What: shaped graft sutured over defect; sometimes with Tenon’s advancement or amniotic membrane overlay. Ajo

3. Amniotic membrane graft / Tenon’s advancement — Why: cover exposed sclera, promote healing, and provide a biologic bandage after debridement. What: biologic membrane secured to the ocular surface to reduce inflammation and pain.

4. Tectonic corneoscleral/lamellar keratoplasty — Why: when cornea and sclera thin together (keratoscleritis) or perforation occurs. What: layered corneal or corneoscleral graft to restore globe integrity. ScienceDirect

5. Posterior segment or pressure-control surgery when indicated — Why: treat complications such as retinal detachment, non-clearing vitreous hemorrhage, or secondary glaucoma once inflammation is controlled. What: pars plana vitrectomy or glaucoma surgery; timing coordinated to avoid worsening inflammation.

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Prevention tips

1. Know your triggers — keep a flare diary (systemic disease activity, infections, stress, missed meds).

2. Take medicines exactly as prescribed — do not stop steroids/IMT suddenly.

3. Vaccinate appropriately before/while on IMT (non-live per guidance).

4. Eye-safe lifestyle — protective eyewear, contact lens breaks during redness, prompt care for eye injuries.

5. Control systemic diseases — consistent rheumatology follow-up for RA/vasculitis; treat gout and sinus disease.

6. Lab monitoring — on MTX/AZA/MMF/CsA/cyclophosphamide; act early on abnormal results.

7. Avoid smoking and limit alcohol (especially with MTX).

8. Nutrition and weight management — anti-inflammatory pattern and vitamin D sufficiency. PMC

9. Plan surgeries during quiet periods — reduces SINS risk; coordinate peri-operative immunosuppression. AAO-HNS

10. Have a rapid-response plan — same-day ophthalmology access if deep pain/vision change.

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When to see a doctor urgently

• Severe, deep eye pain (often worse at night or with eye movement)

• New vision drop, photophobia, or purple-red eye that does not blanch

• Blue/gray sclera, a white spot that looks thin, or any sign of tissue melting

• Recent eye surgery or trauma, especially with spreading tenderness/redness

• Fever or systemic symptoms (joint pain, nose/sinus issues, skin ulcers) suggesting vasculitis

• Any suspicion of infection (discharge, abscess, trauma with organic matter)

• No improvement within 24–48 hours on an NSAID or after starting therapy

(Scleritis can threaten sight and the integrity of the eye; urgent ophthalmology care is essential.) EyeWiki

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What to eat and what to avoid

What to emphasize:

1. Fatty fish (salmon, sardines) 2–3×/week or fish-oil per clinician advice → omega-3s support pro-resolving mediators. FASEB JournalPMC

2. Extra-virgin olive oil, nuts, seeds daily → monounsaturated fats & polyphenols dampen inflammatory signaling.

3. Colorful vegetables & berries → antioxidants that counter oxidative stress.

4. Legumes & whole grains (as tolerated) → fiber shapes a T-reg-friendly microbiome.

5. Fermented foods (yogurt, kefir, kimchi) → probiotic exposure that supports gut–eye immune crosstalk.

6. Spices (turmeric/ginger) in cooking or supervised supplements → mild COX/LOX/NF-κB modulation. PMC

7. Vitamin D sufficiency (diet + sun safety + supplementation as needed) → supports immune tolerance. PMC

What to limit/avoid :

1. Ultra-processed foods & refined sugars → promote dysbiosis and pro-inflammatory cytokines.
2. Excess omega-6 seed oils & trans fats → push pro-inflammatory eicosanoids; favor olive oil/omega-3s.
3. Alcohol on methotrexate; grapefruit with cyclosporine → safety interactions; follow your clinician’s plan. Medscape

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Frequently Asked Questions

1. Is scleritis the same as episcleritis?
   No. Episcleritis is a surface inflammation that is usually mild and self-limited. Scleritis is deeper, more painful, and can threaten vision, and about half of patients have an associated systemic disease. EyeWiki

2. Can scleritis go away on its own?
   It can fluctuate, but untreated scleritis risks scleral thinning and vision loss. Medical therapy is standard. EyeWiki

3. Which medicine is usually tried first?
   For milder non-necrotizing anterior scleritis, an oral NSAID (e.g., indomethacin or naproxen) is often first. If that fails or disease is severe, oral steroids and then steroid-sparing immunomodulators are used. NCBIMedscape

4. Are steroid eye drops enough?
   Usually no. Topical therapy alone is often insufficient for true scleritis; systemic therapy is commonly required. Medscape

5. What if my scleritis is linked to vasculitis or RA?
   Your team may add antimetabolites (MTX/AZA/MMF) or biologics (anti-TNF, rituximab) to control the systemic disease and protect the eye. SAGE JournalsIOVS

6. Are biologics effective?
   Evidence from case series and small studies shows infliximab and rituximab can quiet refractory scleritis; adalimumab also has supportive reports. Decisions are individualized. PMCAAO JournalMDPI

7. When is surgery needed?
   Mainly for infectious/necrotizing cases with tissue loss or for imminent perforation, where debridement and grafting help save the globe in combination with drugs. PMC

8. Could my scleritis be infectious?
   Yes—especially after eye surgery, trauma, or with abscess-like lesions. Cultures and early antimicrobial therapy are critical; steroids only with antimicrobial cover. NCBI

9. How long does treatment last?
   Weeks to months for the acute phase, then slow taper; some patients need maintenance immunomodulators to prevent relapses. WebEye

10. Will I go blind?
    Most patients maintain vision with timely, appropriate care. Risk rises with necrotizing or posterior scleritis and with delayed treatment. Ajo

11. Can diet really help?
    Diet does not replace medicines, but an anti-inflammatory pattern with omega-3s supports resolution biology and overall health during therapy. FASEB Journal

12. Are supplements required?
    No. Some (omega-3s, vitamin D, curcumin) have supportive evidence in ocular/systemic inflammation, but discuss with your doctor for safety and interactions. PMCPubMed

13. Is exercise okay?
    Yes—gentle, regular activity supports mood, sleep, bone health, and steroid safety—avoid contact sports during active scleral thinning.

14. Could scleritis recur?
    Yes. A flare plan, control of the underlying disease, and adherence to maintenance therapy reduce recurrence.

15. Who should manage my care?
    An ophthalmologist (preferably uveitis/scleral disease trained) plus rheumatology or infectious-disease as needed is ideal. NCBI

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 24, 2025.