Sclerochoroidal Calcification (SCC)

Sclerochoroidal calcification means tiny to small lumps or plaques of calcium salts have settled inside the white wall of the eye (the sclera). With time, this calcium can press on the brown blood-rich layer under the retina (the choroid) and make the overlying tissue look a little raised or a little thinner. On a routine eye exam, these spots look pale yellow to white, often with gentle hills and bumps, and most people never feel anything from them. Doctors usually find them by accident during a dilated eye exam in older adults. In most patients, the spots stay quiet and do not reduce sight, and the main job is simply to make the right diagnosis and to check the body’s calcium- and phosphate-related blood tests to look for any treatable imbalance. EyeWikiPubMed

Sclerochoroidal calcification is a rare eye condition where tiny deposits of calcium build up in the tough white coat of the eye (the sclera) and sometimes near the layer under the retina called the choroid. These deposits usually look like flat or slightly raised, pale yellow patches when an eye doctor looks into the back of the eye. Most people do not feel pain. Many people have no symptoms and find it by chance during a routine eye exam. The condition is usually stable and benign. In plain terms, SCC is “calcium spots” in the wall of the eye that usually do not hurt and often do not harm vision. Doctors still pay close attention because SCC can sometimes be linked to imbalances in the body’s calcium and phosphate levels or kidney and parathyroid problems. Very rarely, new abnormal blood vessels can grow near these areas and threaten vision; those can be treated. EyeWikiPMCPubMed

SCC is uncommon. It appears most often in older adults, slightly more in women, and it is often seen in the outer upper part of the back of the eye, and about half of patients have it in both eyes. Many patients have no abnormal blood mineral levels (idiopathic cases), but some patients have body conditions that shift calcium or phosphate levels and make calcium settle in tissues. PubMed

What is happening inside the eye

In SCC, calcium starts in the sclera and may extend toward the choroid. Modern OCT scans that look deep (enhanced-depth imaging) show the bright, hard calcium is mainly inside the sclera, with the choroid thinned or gently pushed. This is why SCC is considered a scleral (not primarily choroidal) problem. On OCT the inner surface can look like four “mountain-like” shapes (flat, rolling, rocky-rolling, or table-mountain). PubMedLippincott Journals

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Types

A) Types by cause (pathologic mechanism)

1. Idiopathic: no clear body-wide problem; blood calcium and phosphate are normal. This is the most common category.

2. Dystrophic: calcium settles in tissue that has been injured or inflamed locally.

3. Metastatic: calcium settles in normal tissue because the blood chemistry is off (for example, high calcium, high phosphate, or hormone problems that shift these levels). EyeWikiPMC

B) Types by shape on OCT (appearance-based)

1. Flat type: a low, smooth mound inside the sclera.

2. Rolling type: a gentle wave-like mound.

3. Rocky-rolling type: a bumpy, uneven mound (often considered the “classic” pattern).

4. Table-mountain type: a broad, flat-topped mound.
   These patterns come from the enhanced-depth OCT view and help doctors recognize SCC quickly. Lippincott Journals

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Causes

SCC can be idiopathic (no cause found) or secondary to conditions that change calcium-phosphate balance or cause local tissue damage. Below are 20 causes and associations described in the literature; each short note explains the logic in simple words:

1. Idiopathic (age-related) — the most common: calcium settles with aging even when blood tests are normal. EyeWiki

2. Primary hyperparathyroidism (often from a parathyroid adenoma) — too much parathyroid hormone (PTH) raises blood calcium and can drive calcium into tissues, including the eye wall. PubMed

3. Secondary hyperparathyroidism from chronic kidney disease (CKD) — poor kidney function disrupts calcium-phosphate balance and PTH rises; calcium can deposit in the eye. PMC

4. Tertiary hyperparathyroidism — long-standing secondary disease can turn autonomous; calcium stays high and calcification can occur. (Mechanism within the metastatic pathway.) PMC

5. Pseudohypoparathyroidism / Albright’s hereditary osteodystrophy — PTH action is faulty; calcium-phosphate handling is abnormal and ocular calcifications have been reported. EyeWiki

6. Gitelman syndrome — a renal tubular salt-loss disorder; low magnesium and other shifts promote calcium pyrophosphate deposition in joints and sometimes the eye. PMC

7. Bartter syndrome — another renal tubular disorder with metabolic alkalosis; reported with SCC. PubMed

8. Chronic kidney disease (as a group) — beyond secondary hyperparathyroidism, CKD alters vitamin D activation and mineral metabolism broadly, favoring calcification. PMC

9. Vitamin D intoxication (hypervitaminosis D) — too much vitamin D raises calcium absorption and can seed calcium in tissues. PMC

10. Hyperphosphatemia — high phosphate teams with calcium and encourages mineral deposition in normal tissue. PMC

11. Hypophosphatemia — phosphate imbalance (even low phosphate in some contexts) is listed among risk factors, reflecting complex mineral handling in systemic disease. EyeWiki

12. Hypomagnesemia — low magnesium reduces the solubility of calcium pyrophosphate and can foster crystal deposition. PMC

13. Chondrocalcinosis / calcium pyrophosphate disease (pseudogout) — body-wide tendency to deposit calcium pyrophosphate crystals sometimes coexists with SCC. PMC

14. Sarcoidosis — granulomas can raise active vitamin D, leading to high calcium and metastatic calcification. EyeWiki

15. Parathyroid adenoma (specific cause of primary hyperparathyroidism) — the classic surgical cause behind high PTH and high calcium. PubMed

16. Parathyroid carcinoma (rare) — a malignant source of very high PTH and calcium; severe mineral imbalance can drive metastatic tissue calcification. (Mechanistic extension of the hyperparathyroid pathway.) PubMed

17. Destructive bone disease (e.g., myeloma or bone metastases) — bone breakdown releases minerals; systemic mineral load contributes to metastatic calcification. PMC

18. Diuretic-related metabolic imbalance — long-term diuretic use can shift electrolytes (including magnesium and potassium) and acid–base balance; SCC has been linked in reports of such imbalances. EyeWiki

19. Pseudohypoparathyroidism variants and related endocrine syndromes — broader defects in PTH signaling and mineral handling are reported with SCC. EyeWiki

20. Dystrophic ocular injury/inflammation — when local tissue is damaged (for example, longstanding degeneration), calcium can precipitate in that spot even if blood tests are normal. (This explains the “dystrophic” SCC pathway.) PMC

Key idea: most patients are asymptomatic and many are idiopathic, but because SCC can be a clue to a hidden mineral disorder, doctors usually order a focused blood/urine work-up at first diagnosis. EyeWiki

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Symptoms

Most people with SCC notice no symptom at all. When symptoms occur, they usually come from lesion location (near the macula) or from uncommon complications like choroidal neovascularization (new fragile vessels). Here is a simple list of what someone might notice:

1. No symptoms (very common; SCC is often found by chance). EyeWiki

2. Mild blurry vision if a lesion sits close to the macula. EyeWiki

3. Wavy or crooked lines (metamorphopsia) when reading lines on a page if the macula is involved.

4. A small dim or gray spot near the center (a paracentral scotoma) if the overlying layers thin.

5. Reduced contrast (things look washed out in low light).

6. Glare sensitivity (bright lights feel harsher).

7. Slower recovery after bright light (photostress feels longer).

8. Color looks slightly dull (mild desaturation) if the macula is affected.

9. Trouble with fine print if central retina is disturbed.

10. Visual fatigue after close work because the signal feels less crisp.

11. Depth perception feels off if one eye sees a little blur.

12. Peripheral “patch” of dim vision if a large peripheral plaque presses the choroid.

13. A sudden drop in vision (rare) if a secondary membrane bleeds or leaks. EyeWiki

14. A rare shift toward more farsighted vision (hyperopic shift) has been reported in isolated cases. PMC

15. No pain, no redness (SCC itself is not an inflammatory disease), which helps to separate it from painful conditions like scleritis. EyeWiki

In the largest long-term series, no patient needed eye treatment for SCC itself; the main concern is screening for an underlying mineral disorder and watching for rare macular complications. PubMed

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Diagnostic tests

A) Physical Exam

1. Visual acuity (distance and near)
   This basic test tells how sharp the eye sees a high-contrast chart. In SCC most patients read normally. A drop suggests the lesion is near the macula or there is another cause. Tracking acuity over time helps confirm stability.

2. Pupil exam for an RAPD (relative afferent pupillary defect)
   The swinging-flashlight test checks the optic nerve and macula pathway. SCC rarely causes an RAPD; a normal result supports the idea that SCC is a quiet incidental finding.

3. Intraocular pressure (IOP) by tonometry
   Eye pressure is checked because many older adults also have glaucoma risk. SCC does not raise eye pressure by itself, so a normal IOP fits the typical story.

4. Dilated fundus examination with indirect ophthalmoscopy
   This is the key bedside test. The doctor sees pale yellow to white, flat or slightly raised plaques typically in the superotemporal outer retina, sometimes in both eyes. Recognizing this pattern helps avoid mistaking SCC for a tumor. EyeWikiPubMed

B) “Manual” office tests

5. Pinhole test
   Looking through a pinhole reduces blur from refraction. If acuity improves fully, vision loss is not from macular damage. In SCC, pinhole usually shows normal potential vision.

6. Amsler grid
   A simple check for wavy lines or missing spots near the center. Most SCC patients have a normal grid unless a lesion or a rare membrane affects the macula.

7. Photostress recovery time
   Shine a bright light briefly, then time how long it takes to read again. Prolonged recovery suggests macular stress. Most SCC lesions are away from the macula, so recovery is normal.

C) Laboratory / Pathological tests

8. Serum calcium
   High calcium favors metastatic calcification and should prompt a parathyroid and kidney evaluation. EyeWiki

9. Parathyroid hormone (PTH)
   High PTH with high or normal calcium suggests primary or secondary hyperparathyroidism and points to the parathyroid glands or kidney disease. PMC

10. Serum phosphate
    Phosphate partners with calcium; a high level, especially with kidney disease, supports a metabolic cause. PMC

11. Serum magnesium
    Low magnesium reduces calcium pyrophosphate solubility and is linked to SCC in tubulopathies like Gitelman; correcting it may help the systemic tendency to calcify. PMC

12. Kidney panel (creatinine, eGFR, metabolic panel)
    Kidney function drives vitamin-D activation and mineral balance; chronic kidney disease is a common association with SCC. PMC

13. Urine calcium (spot or 24-hour) and blood pH
    These help sort hyperparathyroidism and tubular disorders (e.g., Bartter/Gitelman) that shift calcium and acid–base balance. EyeWiki

D) Electrodiagnostic tests

14. Electroretinography (ERG; full-field or multifocal)
    If vision is reduced and the exam is unclear, ERG tests retinal function electrically. In ordinary SCC, ERG is usually normal; an abnormal ERG pushes the doctor to look for another retinal disease. (Used selectively, not routine.)

E) Imaging tests

15. Optical coherence tomography (OCT) with enhanced-depth imaging (EDI-OCT)
    This is the most helpful scan. It shows that the bright, hard deposit sits within the sclera and often compresses or thins the choroid above it. The inner surface shape looks like “flat,” “rolling,” “rocky-rolling,” or “table-mountain.” These patterns are highly characteristic. PubMedLippincott Journals

16. B-scan ultrasonography
    The plaque shows as a bright (hyperechoic) solid lesion with a dark “shadow” behind it because sound waves cannot pass through the calcium easily. This acoustic shadow helps separate SCC from soft tumors. EyeWiki

17. Fundus autofluorescence (FAF)
    The calcified area tends to show mixed hyper- and hypo-autofluorescence, reflecting changes in the overlying retinal pigment epithelium. FAF maps these changes over time. PMC

18. Fluorescein angiography (FA)
    On FA, SCC typically shows early hyperfluorescent dots within the lesion and a window defect from RPE thinning; late phases stay bright. This signature helps confirm a benign plaque rather than a tumor. PMC

19. Indocyanine green angiography (ICGA)
    ICGA can outline choroidal circulation around the plaque and may show chorioretinal shunt vessels in some cases; it is helpful when the view is unclear or when membranes are suspected. PMC

20. Orbital CT (thin-slice)
    CT is excellent at detecting calcium. A calcified plaque at the scleral level supports SCC and helps separate it from non-calcified masses. CT is not always needed but is very specific when used. PMC

Non-pharmacological treatments (Therapies & “other” measures)

Below are practical, evidence-informed steps. Most are about monitoring the eyes and optimizing whole-body calcium/phosphate balance. Each item lists what it is (Description), why it matters (Purpose), and how it helps (Mechanism).

1. Comprehensive medical evaluation and labs
   Description: Work with your clinician to check calcium, phosphate, magnesium, vitamin D, and PTH; consider kidney function tests.
   Purpose: Find underlying causes that may drive calcification.
   Mechanism: Correcting systemic imbalances (e.g., hyperparathyroidism, CKD-related mineral disorders) can stabilize disease. PubMedBROWN EMERGENCY MEDICINE BLOG

2. Regular dilated eye exams
   Description: Follow a schedule your ophthalmologist sets.
   Purpose: Watch for stability vs. complications like CNV.
   Mechanism: Early detection of CNV allows timely anti-VEGF treatment. PubMed

3. Optical coherence tomography (OCT) monitoring
   Description: Painless scan of the retina and choroid.
   Purpose: Track subtle fluid, swelling, or neovascular changes.
   Mechanism: OCT reveals leakage or CNV activity before vision drops. PMC

4. Fundus photography
   Description: Color photos of the retina over time.
   Purpose: Simple visual record to compare size/shape of plaques.
   Mechanism: Detects change patterns suggesting complications. PMC

5. Ultrasound B-scan or CT (if needed)
   Description: Imaging to confirm calcification.
   Purpose: Distinguish SCC from tumors or choroidal osteoma.
   Mechanism: Calcified lesions are highly reflective (ultrasound) or radiopaque (CT). BROWN EMERGENCY MEDICINE BLOG

6. Medication review
   Description: Go over calcium, vitamin D, thiazide diuretics, and phosphate-containing antacids/supplements.
   Purpose: Avoid over-supplementation or drugs that worsen hypercalcemia.
   Mechanism: Thiazides raise serum calcium; excess vitamin D or calcium can increase calcification risk. PubMed

7. Kidney-friendly nutrition plan (if CKD)
   Description: Dietitian-guided phosphate and sodium moderation, adequate—but not excessive—protein and calcium.
   Purpose: Control CKD-mineral bone disorder.
   Mechanism: Lowering dietary phosphate and balancing minerals reduces pathologic calcification drivers. PubMed

8. Hydration
   Description: Maintain adequate fluid intake unless restricted.
   Purpose: Supports kidney handling of calcium and phosphate.
   Mechanism: Better renal excretion of calcium/phosphate when appropriate.

9. Sunlight and vitamin D moderation
   Description: Sensible sun exposure; avoid high-dose unsupervised vitamin D.
   Purpose: Prevent hypervitaminosis D and hypercalcemia.
   Mechanism: Excess vitamin D raises calcium absorption. Canadian Journal of Ophthalmology

10. Magnesium repletion when low
    Description: Treat magnesium deficiency if present.
    Purpose: Hypomagnesemia can worsen calcium-phosphate issues.
    Mechanism: Magnesium affects PTH secretion and calcium handling; certain tubular disorders (e.g., Gitelman) need attention. Jefferson Digital Commons

11. Blood pressure, glucose, and lipid control
    Description: Manage cardiovascular risks.
    Purpose: Support overall retinal and choroidal health.
    Mechanism: Healthier small vessels may reduce secondary complications.

12. Smoking cessation
    Description: Quit smoking with counseling and aids.
    Purpose: Improve ocular and systemic vascular health.
    Mechanism: Reduces oxidative and vascular stress on the retina.

13. Amsler grid self-monitoring
    Description: Weekly home test to notice wavy or missing lines.
    Purpose: Early warning of central vision changes (possible CNV).
    Mechanism: Detects metamorphopsia or scotoma early for prompt care.

14. Protective eyewear for high-risk activities
    Description: Wear safety glasses for sports/DIY.
    Purpose: Avoid trauma that could complicate retinal status.
    Mechanism: Less risk of hemorrhage or retinal damage.

15. Weight-bearing exercise (as your doctor allows)
    Description: Regular walking/resistance training.
    Purpose: Supports bone health and systemic calcium balance.
    Mechanism: Exercise influences bone turnover and insulin sensitivity.

16. Limit ultra-processed foods with phosphate additives
    Description: Read labels; many colas and processed meats add phosphates.
    Purpose: Lower phosphate load, especially in CKD.
    Mechanism: Fewer additives → better phosphate balance. PubMed

17. Educate family and caregivers
    Description: Share the benign nature of SCC, need for labs, and warning signs.
    Purpose: Reduce anxiety and promote timely care.
    Mechanism: Informed support improves adherence.

18. Tailored calcium intake
    Description: Do not self-restrict or overload calcium; follow clinician advice.
    Purpose: Too little harms bones; too much may fuel hypercalcemia.
    Mechanism: Balance prevents compensatory PTH rises or excess calcium load. PubMed

19. Treat underlying endocrine disorders
    Description: If hyperparathyroidism is present, follow specialist treatment (medical or surgical).
    Purpose: Fix the driver of abnormal mineral metabolism.
    Mechanism: Normalizing PTH/calcium can stabilize SCC. PubMed

20. Scheduled follow-up plan
    Description: Agree on visit intervals (e.g., every 6–12 months, sooner if symptoms).
    Purpose: Ensure steady monitoring for life changes.
    Mechanism: Systematic surveillance catches complications early. PubMed

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Drug treatments

Important: Many people with SCC need no eye-specific drug. Medicines are used for (A) treating complications like CNV or (B) correcting an underlying systemic cause of mineral imbalance. Doses below are typical starting points for adults; they must be individualized by your clinicians.

1. Intravitreal anti-VEGF (bevacizumab 1.25 mg/0.05 mL; ranibizumab 0.5 mg; aflibercept 2 mg)
   When/Time: Given in the eye in a clinic procedure, often monthly at first, then “as needed.”
   Purpose: Treat CNV if it develops near SCC, to protect central vision.
   Mechanism: Blocks VEGF to stop leaky abnormal vessels.
   Side effects: Temporary irritation; rare infection (endophthalmitis), increased eye pressure; systemic risk is very low but discussed individually. PMCPubMed

2. Verteporfin photodynamic therapy (PDT)
   When/Time: IV drug (6 mg/m²) followed by laser activation to the retina; sometimes used if CNV is not ideal for anti-VEGF alone.
   Purpose: Seal abnormal vessels with less collateral retinal damage.
   Mechanism: Light-activated drug closes neovascular tissue.
   Side effects: Photosensitivity for 48 hours; transient vision changes. Cureus

3. Focal laser photocoagulation (for extrafoveal CNV)
   When/Time: Single or staged laser sessions away from the fovea.
   Purpose: Destroy small CNV far from the center of vision.
   Mechanism: Thermal closure of abnormal vessels.
   Side effects: Permanent blind spot at the laser site; not used near the fovea. ResearchGate

4. Cinacalcet (calcimimetic; e.g., 30 mg twice daily and titrate)
   When/Time: For primary or secondary hyperparathyroidism, per endocrinology/renal guidance.
   Purpose: Lower PTH and serum calcium when surgery isn’t an option or as bridge therapy.
   Mechanism: Activates calcium-sensing receptor → decreases PTH release.
   Side effects: Nausea, hypocalcemia (requires monitoring). PubMed

5. Alendronate (bisphosphonate; 70 mg weekly) or Zoledronic acid (4 mg IV infusion)
   When/Time: For hypercalcemia due to high bone turnover or malignancy context, guided by specialists.
   Purpose: Lower high calcium; stabilize bone.
   Mechanism: Inhibit osteoclasts to reduce bone resorption.
   Side effects: Esophagitis (oral), flu-like symptoms (IV), rare osteonecrosis of the jaw; monitor renal function. PubMed

6. Denosumab (RANKL inhibitor; 120 mg SC monthly in hypercalcemia of malignancy)
   When/Time: For refractory hypercalcemia when bisphosphonates are unsuitable.
   Purpose: Lower serum calcium.
   Mechanism: Blocks RANKL to suppress osteoclast activity.
   Side effects: Hypocalcemia (especially in CKD), musculoskeletal pain; jaw osteonecrosis risk—dental clearance advised. PubMed

7. Calcitonin (e.g., 4 IU/kg SC/IM every 12 hours short-term)
   When/Time: Short-term in acute hypercalcemia while definitive therapy takes effect.
   Purpose: Rapid but transient calcium lowering.
   Mechanism: Inhibits osteoclast action and increases renal calcium excretion.
   Side effects: Nausea, flushing; tachyphylaxis within days. PubMed

8. Sevelamer carbonate (phosphate binder; e.g., 800–1600 mg with meals)
   When/Time: In CKD with hyperphosphatemia per nephrology.
   Purpose: Control high phosphate, a calcification driver.
   Mechanism: Binds phosphate in the gut to reduce absorption.
   Side effects: GI upset; must separate from some meds. PubMed

9. Glucocorticoids (e.g., prednisone 0.5–1 mg/kg/day short course for vitamin D intoxication)
   When/Time: Selected cases of hypervitaminosis D under physician supervision.
   Purpose: Reduce intestinal calcium absorption and vitamin D activation.
   Mechanism: Decreases calcitriol production and inflammation.
   Side effects: Elevated glucose, mood changes, infection risk—short term only. PubMed

10. Loop diuretic (e.g., furosemide) with IV fluids in acute hypercalcemia (hospital setting)
    When/Time: Guided inpatient therapy after rehydration.
    Purpose: Increase urinary calcium excretion.
    Mechanism: Blocks sodium-potassium-chloride in loop of Henle, increasing calciuresis.
    Side effects: Dehydration, electrolyte disturbances; requires monitoring. PubMed

These treatments do not “melt” the eye deposits; they treat complications (like CNV) or fix body-wide mineral problems that may be associated with SCC. Most people only need monitoring. PubMed

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Dietary molecular supplements

Important safety note: No supplement has been proven to remove SCC. These options support general eye or metabolic health and must be tailored—especially if you have kidney disease, clotting disorders, or take anticoagulants. Dosages are typical adult amounts.

1. Lutein (10 mg/day)
   Function: Supports macular pigment and antioxidant defense.
   Mechanism: Filters blue light, quenches free radicals in retina.

2. Zeaxanthin (2 mg/day)
   Function: Works with lutein to protect central retina.
   Mechanism: Antioxidant in the macula.

3. Omega-3 (EPA/DHA ~1 g/day)
   Function: Helps retinal cell membranes; anti-inflammatory.
   Mechanism: Resolvin pathways may calm micro-inflammation; evidence stronger for dry eye/AMD than SCC.

4. Vitamin C (≈500 mg/day)
   Function: Aqueous antioxidant support.
   Mechanism: Scavenges reactive oxygen species.

5. Vitamin E (≈200–400 IU/day)
   Function: Lipid-phase antioxidant.
   Mechanism: Stabilizes photoreceptor outer segment membranes.

6. Zinc (≈25–40 mg elemental/day) with Copper (2 mg/day)
   Function: Enzymatic co-factor for retinal antioxidant enzymes.
   Mechanism: Supports antioxidant enzymes; add copper to avoid deficiency with zinc.

7. Magnesium (200–400 mg/day, if low)
   Function: Supports normal PTH and calcium handling.
   Mechanism: Corrects hypomagnesemia that can disturb mineral balance—important in Gitelman/Bartter contexts. Jefferson Digital Commons

8. Vitamin K2 (MK-7 90–180 mcg/day; avoid if on warfarin unless your doctor adjusts dose)
   Function: Helps direct calcium to bone rather than soft tissues.
   Mechanism: Carboxylates matrix Gla protein; human evidence for ocular calcification is limited—discuss with your clinician.

9. Coenzyme Q10 (100–200 mg/day)
   Function: Mitochondrial antioxidant support.
   Mechanism: Electron transport cofactor; may reduce oxidative stress.

10. Curcumin (500–1000 mg/day with food; watch drug interactions)
    Function: Anti-inflammatory adjunct.
    Mechanism: NF-κB pathway modulation; human ocular calcification data are limited.

Regenerative / stem cell drugs

Straight talk: There are no approved immune boosters, regenerative medicines, or stem-cell therapies for SCC. Offering or using such products for this condition outside a regulated clinical trial is not evidence-based and may be dangerous. Below are six items explaining why they’re not recommended and what safer, proven alternatives exist.

1. Autologous or allogeneic stem-cell eye injections
   Not approved for SCC; high risk of infection, inflammation, or retinal detachment.
   Safer alternative: Evidence-based monitoring; treat CNV with anti-VEGF if it occurs. PMC

2. Systemic stem-cell infusions marketed for “eye regeneration”
   No clinical evidence for SCC; potential immune reactions and infection.
   Safer alternative: Address systemic calcium-phosphate drivers (renal, parathyroid). PubMed

3. “Immune-boosting” prescription stimulants (e.g., thymic peptides) for SCC
   No proven benefit; could mislead patients and delay proper care.
   Safer alternative: Vaccinations and healthy lifestyle to reduce general illness burden—not a treatment for SCC lesions.

4. Platelet-rich plasma (PRP) intraocular use
   Not indicated or approved for SCC; carries procedure risks.
   Safer alternative: Guideline-consistent CNV care (anti-VEGF/PDT) when needed. Cureus

5. Topical or systemic growth factors for “calcification reversal”
   No evidence in SCC; theoretical risk of abnormal vessel growth.
   Safer alternative: Evidence-based surveillance with OCT and prompt CNV treatment. PMC

6. Gene therapy for SCC
   No known gene target or trial for SCC.
   Safer alternative: Identify and treat endocrine/renal causes if present; most SCC is simply watched. PubMed

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Procedures / surgeries

SCC itself usually needs no surgery. Procedures are for complications or diagnostic uncertainty.

1. Intravitreal anti-VEGF injections (office procedure)
   Procedure: Eye is numbed; tiny needle injects medicine into the vitreous.
   Why done: Treat CNV threatening central vision.
   Notes: Often effective; requires series of visits. PMC

2. Photodynamic therapy (PDT) with verteporfin
   Procedure: IV infusion followed by a low-energy laser to activate the drug at the CNV site.
   Why done: Alternative or adjunct when anti-VEGF alone is not ideal. Cureus

3. Focal laser photocoagulation (for extrafoveal CNV only)
   Procedure: Brief focal laser spots outside the center of vision.
   Why done: Close small CNV if far from the fovea. ResearchGate

4. Pars plana vitrectomy (rare)
   Procedure: Microsurgery to remove non-clearing blood or scar tissue from the vitreous.
   Why done: If CNV causes a vitreous hemorrhage that does not clear or traction that threatens vision.

5. Biopsy (very rare)
   Procedure: Small tissue sample if imaging cannot rule out tumor.
   Why done: Confirm diagnosis when SCC mimics melanoma or metastasis. Imaging usually avoids this. PMC

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Preventions

These steps do not “prevent” SCC itself in everyone, but they reduce systemic drivers and help catch complications early.

1. Do not self-prescribe high-dose vitamin D or calcium. Get levels checked first. PubMed

2. If you have CKD, follow a kidney-friendly plan to control phosphate and PTH. PubMed

3. Keep regular eye check-ups and OCT when advised. PubMed

4. Know the warning symptoms of CNV (distortion, gray spot, sudden blur) and seek care quickly. PubMed

5. Review all supplements and over-the-counter products with your doctors. BROWN EMERGENCY MEDICINE BLOG

6. Moderate processed foods high in phosphate additives (colas, processed meats). PubMed

7. Treat endocrine issues like hyperparathyroidism promptly. PubMed

8. Stop smoking and control blood pressure, sugar, and cholesterol.

9. Use an Amsler grid weekly if your doctor recommends it.

10. Keep a symptom and medication log to share at visits.

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When to see doctors

• Immediately (urgent same-day or next-day) if you notice new central blur, straight lines looking wavy, a gray/black spot in central vision, or sudden vision drop—possible CNV or bleeding. PubMed

• Soon (within weeks) if you were just told you have SCC and have never had calcium, phosphate, vitamin D, magnesium, PTH, and kidney function checked. These tests help find treatable causes. PubMed

• Routinely for scheduled eye imaging (OCT/photos) and for follow-ups with primary care, nephrology, and endocrinology if mineral imbalances or CKD exist. PubMed

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What to eat and what to avoid

These are general adult suggestions; kidney disease or other conditions may change the plan, so get personalized advice.

1. Eat: Colorful vegetables and fruits each day for antioxidants (spinach, kale, oranges, berries).

2. Eat: Lean protein in reasonable portions; if CKD, follow your renal dietitian’s protein targets.

3. Eat: Foods naturally rich in lutein/zeaxanthin (dark leafy greens, corn, eggs).

4. Eat: Healthy fats (olive oil, fish like salmon/sardines) for omega-3s.

5. Eat: Whole grains and legumes as tolerated.

6. Avoid: High-phosphate processed foods and cola drinks with phosphate additives (especially in CKD). PubMed

7. Avoid: Unsupervised high-dose vitamin D or calcium supplements. PubMed

8. Avoid: Smoking and excessive alcohol; they harm vascular health.

9. Avoid: Diet fads that severely restrict nutrients needed for bone and eye health.

10. Customize: If you have CKD or endocrine disease, ask for a written meal plan that fits your labs.

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Frequently Asked Questions

1) Is SCC cancer?
No. SCC is a benign deposition of calcium in the eye wall. It is not a tumor and not a cancer. Doctors check carefully because the spots can look like tumors, but imaging and the overall pattern usually make the diagnosis clear. PMC

2) Will SCC make me blind?
Most people never lose meaningful vision from SCC itself. Rarely, abnormal vessels (CNV) can form and threaten central vision, but this can often be treated successfully with anti-VEGF injections. PubMed+1

3) How is SCC diagnosed?
Your doctor examines your retina and uses imaging such as OCT, ultrasound, fundus photos, and sometimes CT to confirm calcification and rule out look-alikes like choroidal osteoma, melanoma, or metastasis. PMCBROWN EMERGENCY MEDICINE BLOG

4) Why do I need blood tests if the problem is in my eye?
Because SCC can be linked to body-wide mineral problems (calcium, phosphate, magnesium, vitamin D, and parathyroid hormone). Finding and treating those conditions protects your overall health and may help stabilize the eye findings. PubMed

5) Is SCC the same as choroidal osteoma?
No. Osteoma is a bone-like tumor in the choroid, more often in younger adults, often near the optic nerve or macula, and can threaten vision more than SCC. SCC tends to occur in older adults, often in the mid-periphery, and usually stays stable. EyeWiki

6) Do the calcium spots go away?
They usually stay. The goal is to watch them and treat any associated systemic issue—and to treat CNV promptly if it develops. PubMed

7) Do I need injections even if I feel fine?
No. Injections are only for complications like CNV. Many people with SCC never need any eye procedure at all. PMC

8) Can lifestyle help?
Yes—mainly by keeping calcium-phosphate balance healthy if you have kidney or endocrine problems and by reducing processed foods high in phosphate additives. Don’t self-dose high vitamin D or calcium. PubMed

9) Is SCC hereditary?
Most cases are idiopathic (no clear cause) or related to systemic conditions rather than simple inheritance. Family screening is usually not needed unless there is a shared systemic disease. EyeWiki

10) Could my supplements be a problem?
They can be if they contain high-dose vitamin D or calcium or if they interact with your conditions or medicines. Share all supplements with your doctors. PubMed

11) What symptoms should I watch for?
New central blur, straight lines appearing wavy, or a gray spot in your central vision—possible CNV. Seek care quickly. PubMed

12) How often should I follow up?
Your ophthalmologist will tailor it, often every 6–12 months when stable, sooner if there are changes. Systemic follow-up depends on your labs and diagnoses. PubMed

13) Can SCC be confused with dangerous conditions?
Yes, including melanoma or metastasis. That is why eye imaging and sometimes additional tests are important early on. PMC

14) I have chronic kidney disease. Does that change care?
Yes. CKD can raise phosphate and PTH, which can promote soft-tissue calcification. Your care team may use phosphate binders, diet changes, and other therapies. Eye monitoring remains the same. PubMed

15) What is the long-term outlook?
Generally good. Most cases remain stable for years. The key is to treat any underlying systemic condition and to watch for the rare development of CNV, which is treatable. PubMed

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.