Lattice corneal dystrophy is an inherited eye disease. “Inherited” means it is passed down in families through genes. It affects the cornea, the clear front window of the eye. In LCD, tiny protein clumps called amyloid build up inside the cornea, mainly in the stromal layer (the middle layer). These clumps form thin, branching lines that look like a lattice (a net). Over time, the cornea becomes less clear, which can make vision blurry.
Key features in simple terms:
- Amyloid: A misfolded protein that forms waxy, glass‑like deposits. In LCD it settles in the cornea.
- Lattice lines: Fine, criss‑cross, branching streaks you can see with a special microscope at the clinic.
- Progressive: Changes slowly worsen over years.
- Both eyes: Usually affects both eyes.
- Family pattern: Often autosomal dominant, meaning a parent with LCD has a 50% chance to pass it to a child.
Why does it happen? The main reason is a gene change (mutation). The most common gene in classic LCD is TGFBI. A different gene called GSN (gelsolin) causes a special form called Type II that also affects the body (a systemic amyloidosis). The gene change leads to abnormal proteins that collect as amyloid inside the cornea.
How the Healthy Cornea Works
Cornea: The clear front window of the eye. It bends (focuses) light to help you see clearly.
Layers: From front to back: epithelium (skin of the cornea), Bowman’s layer, stroma (thick middle), Descemet’s membrane, and endothelium (pump cells that keep cornea clear). LCD mainly involves the stroma and can irritate the epithelium, causing painful “erosions.”
Recurrent corneal erosion: Small areas where the surface skin (epithelium) loosens or peels. This hurts, especially on waking, and causes tearing and light sensitivity.
Lattice pattern: The amyloid lines are thin, shiny, and branching, forming a net‑like or lattice pattern in the front stroma. Early on, there may also be small dots under the surface. As deposits grow and merge, the central cornea can look hazy, lowering vision.
Types of Lattice Corneal Dystrophy (LCD)
The word “type” can mean different things: which gene is involved, how it looks in the cornea, or how early/severe it is. Below are the main, plain‑language categories you may hear about in clinics and textbooks.
1) Classic (TGFBI‑related) LCD – often called Type I
- Gene: TGFBI (previously called BIGH3). The well‑known mutation is R124C, but many others exist.
- Pattern: Thin lattice lines in the anterior stroma, sometimes with tiny white dots and haze.
- Onset: Often childhood to early adulthood; slowly progresses.
- Systemic disease: None (limited to the cornea).
2) Gelsolin amyloidosis – “Lattice Type II” or Meretoja syndrome
- Gene: GSN (gelsolin).
- Pattern: Lattice lines may be delicate, radial, or more peripheral; corneal changes can be milder than Type I.
- Systemic disease: Yes. Amyloid in nerves and skin (e.g., facial nerve weakness, loose skin), sometimes other organs. Eye findings are part of a body‑wide condition.
3) Late‑onset / asymmetric LCD variant (TGFBI)
- Gene: TGFBI but different mutation (for example, changes outside the R124C hotspot).
- Pattern: May start later in life, sometimes uneven between the two eyes.
- Note: The IC3D classification recognizes many TGFBI variants with amyloid and lattice‑like lines.
4) Severe early‑onset variant (historically “Type IIIA”)
- Pattern: More dense lattice and haze, earlier vision problems, and more frequent erosions.
- Gene: Often TGFBI variants other than R124C.
5) Post‑surgical / recurrent LCD after corneal transplant
- Meaning: Even after a corneal graft, the dystrophy can recur in the donor cornea over time because the underlying gene remains the same in the patient’s cells (especially in the surface layer and limbus that repopulate the graft).
6) “Pseudo‑lattice” look‑alikes (not true LCD)
- Meaning: Other problems can mimic the lattice pattern (e.g., old infectious scars, trauma, or other dystrophies). These are not LCD but can look similar on quick exam. Special tests help tell them apart.
Bottom line on types: Doctors now often describe LCD by the gene and the exact mutation (for example, “LCD‑R124C”). This helps with family counseling and with predicting the pattern and age of onset.
Causes and Contributors
Important truth: The real cause of LCD is a gene mutation. Most other things listed below do not cause LCD by themselves; they can trigger symptoms, worsen discomfort, or speed up haze in someone who already has the gene change. We list them clearly so you can see what is causal vs. what is a trigger.
Primary genetic causes
- TGFBI mutation (classic LCD / Type I): The most common cause. Produces abnormal TGFBI protein that forms amyloid in the cornea.
- GSN (gelsolin) mutation (Type II): Causes systemic amyloidosis with corneal lattice changes as part of a body‑wide condition.
- Other TGFBI variants (non‑R124C): Many variants also make amyloid lattice but differ in age of onset and severity.
- Autosomal dominant inheritance: One changed gene from one parent can be enough to have the disease.
- De novo mutation: A new gene change that starts in a child even if parents do not have LCD.
Non‑causal contributors and symptom triggers
- Aging in gene carriers: Amyloid tends to build up over time, so signs and symptoms increase with age.
- Minor eye trauma / rubbing: Can trigger erosions and increase discomfort.
- Dry eye disease: A poor tear film makes the corneal surface fragile, worsening erosions and blurry moments.
- Blepharitis / eyelid margin inflammation: Increases surface irritation and tear instability, agitating symptoms.
- Contact lens over‑wear: Can stress the epithelium and provoke erosions.
- Refractive surgery (LASIK/PRK) in TGFBI dystrophies: Can unmask or accelerate deposits and erosions; generally not recommended when LCD or TGFBI dystrophy is known or suspected.
- Corneal surgery trauma (e.g., transplants): LCD can recur in the graft because the underlying gene remains.
- Ultraviolet (UV) light exposure: May irritate the surface; good UV‑blocking eyewear helps protect comfort (does not cause LCD).
- Smoking: May worsen ocular surface health and healing; avoiding it is good for eye comfort.
- Systemic amyloidosis mechanisms (Type II): In gelsolin disease, body‑wide amyloid can also affect the cornea.
- Hormonal shifts (e.g., menopause): Can dry the eye, making erosions more likely.
- Diabetes (if present): May slow healing of corneal surface, increasing erosion risk.
- Meibomian gland dysfunction: Thicker or poor‑quality oils in tears cause unstable tears and irritation.
- Low‑humidity environments (air‑conditioning, wind): Dry air can trigger symptoms in gene carriers.
- Genetic modifiers (natural variation): Other small genetic differences can change how early and how severe LCD appears, even within the same family.
Symptoms and Signs
- Blurry vision: Haze and lines in the cornea scatter light, lowering clarity.
- Recurrent corneal erosions: Sudden sharp pain, often on waking when the lids first move.
- Light sensitivity (photophobia): Bright light hurts or feels harsh during erosions or when haze increases.
- Tearing (watering): The eye makes more tears in response to irritation.
- Foreign‑body sensation: Feels like there is sand or grit in the eye.
- Redness: The eye can look red during erosions or irritation.
- Glare and halos: Lights at night may have streaks or rings.
- Poor night vision: Extra scatter from lattice lines lowers contrast in dim light.
- Fluctuating vision: Vision may be good some days and worse on others, depending on surface smoothness and tear film.
- Decreased contrast sensitivity: Fine shades of gray are harder to tell apart.
- Irregular astigmatism: The corneal shape becomes uneven, making vision hard to correct with regular glasses.
- Contact lens intolerance: Some people cannot comfortably wear contact lenses for long.
- Surface haze / central opacification: The center can become cloudy over time, reducing best‑corrected vision.
- Slow healing after minor scratches: The surface re‑breaks or heals slowly.
- Systemic signs in Type II only: In gelsolin amyloidosis, there can be facial nerve weakness, loose skin, numbness, or other body symptoms (the cornea is one part of a bigger condition).
Note: Many people with classic LCD have good vision for years and only later notice more haze or more frequent erosions. The pattern can differ even within the same family.
How Doctors Diagnose LCD:
History: Doctors ask about family members with similar eye problems, age of onset, painful episodes on waking, and any systemic symptoms (to check for gelsolin amyloidosis).
Eye exam: A slit‑lamp microscope lets the doctor see the lattice lines and any haze or surface defects.
Confirmatory tests: Genetic testing can identify changes in TGFBI (classic LCD) or GSN (Type II). Imaging like anterior segment OCT and in vivo confocal microscopy can map the deposits. In rare cases a corneal biopsy is analyzed for amyloid.
A) Physical Exam
1) Visual acuity test: Measures how well you can read letters on a chart. Why it matters: Tracks baseline vision and changes over time.
2) Refraction (glasses test): Finds the best lens power for each eye. Why it matters: Tells how much of the blur is due to focus problems versus corneal haze or irregularity.
3) Penlight and red‑reflex check: A simple light test that looks for clarity of the optical path. Why it matters: A dull or distorted reflex may suggest corneal haze.
4) Slit‑lamp biomicroscopy: A microscope with a bright, thin beam to examine the cornea closely. What it shows: Fine lattice lines, dots, anterior stromal haze, and any surface erosions.
5) Corneal sensation testing (esthesiometry): Lightly touches the cornea to see how sensitive it is. Why it matters: Reduced sensitivity can affect healing and comfort.
B) Manual / Bedside Tests
6) Fluorescein staining: A safe orange dye shows scratches or erosions under blue light. Why it matters: Confirms recurrent erosion episodes and maps where the surface is loose.
7) Tear film break‑up time (TBUT): Measures how quickly tears evaporate or break up. Why it matters: A short TBUT means tear instability, which worsens symptoms.
8) Schirmer test: Small paper strips measure tear production. Why it matters: Low tear volume aggravates irritation and erosions.
9) Rigid contact lens over‑refraction trial: A doctor may briefly place a rigid lens and re‑check vision. Why it matters: If vision improves a lot, it suggests irregular corneal optics from lattice and haze.
C) Lab and Pathological Tests
10) Genetic testing – TGFBI: A blood or saliva test looks for changes in the TGFBI gene. Why it matters: Confirms classic LCD and helps counsel family members.
11) Genetic testing – GSN (gelsolin): Checks for gelsolin gene changes. Why it matters: Confirms Type II and tells the team to screen for systemic issues.
12) Corneal biopsy with amyloid stains: In uncommon, unclear cases, a small sample can be stained with Congo red or Thioflavin T and examined for apple‑green birefringence. Why it matters: Proves amyloid in tough cases.
13) Electron microscopy / proteomic analysis (specialized): Ultra‑detailed look at fibrils and protein makeup. Why it matters: Research‑level detail when diagnosis is uncertain.
D) Electrodiagnostic Tests
14) Visual evoked potential (VEP): Measures electrical signals from the visual pathway after a light pattern is shown. Why it matters: If vision is poor, VEP helps ensure the optic nerve/brain is working normally; LCD mainly affects the cornea.
15) Electroretinogram (ERG): Measures retina function. Why it matters: Helps rule out retinal disease if vision loss seems too severe for the corneal findings alone.
E) Imaging Tests
16) Anterior segment optical coherence tomography (AS‑OCT): A non‑contact scan of corneal layers. What it shows: Hyper‑reflective lines and deposits in the anterior stroma, and the depth of involvement.
17) Corneal topography (Placido): Maps the cornea’s surface curve. Why it matters: Detects irregular astigmatism from lattice lines and haze.
18) Corneal tomography (Scheimpflug / optical): 3‑D map of front and back corneal surfaces and thickness. Why it matters: Quantifies distortion and monitors progression.
19) In vivo confocal microscopy (IVCM): A microscope that images cells and deposits in a living cornea. What it shows: Highly reflective amyloid, sometimes beaded nerves; useful for differential diagnosis and for recurrence after surgery.
20) Specular microscopy: Photographs the endothelial cell layer. Why it matters: LCD is mainly stromal, but this test documents overall corneal health before any surgery.
Non-pharmacological treatments
Each item includes a plain description, purpose, and “how it helps” (mechanism). These are everyday and clinic-based measures without medicines. Many are used together.
Education and trigger control
Purpose: Know what LCD is and what worsens it.
How it helps: Understanding that rubbing, dryness, and trauma can trigger erosions helps you avoid flare-ups.Strict “no eye rubbing” rule
Purpose: Reduce micro-trauma.
How it helps: Rubbing loosens the corneal surface; stopping it cuts erosion risk.Regular blinking and the 20-20-20 screen rule
Purpose: Prevent dry spots when using screens.
How it helps: Blinking spreads tears evenly; short breaks reduce tear evaporation and surface friction.Humidify your air and avoid wind
Purpose: Keep the ocular surface moist.
How it helps: Humidity slows evaporation; avoiding fans/AC airflow prevents drying.Moisture chamber glasses / wraparound sunglasses
Purpose: Shield the cornea from wind and light.
How it helps: A protected micro-environment retains tears; tinted lenses reduce glare.Nighttime eye protection (sleep goggles or eye shields)
Purpose: Stop the eyelid from sticking to the cornea overnight.
How it helps: A barrier reduces overnight friction, a common trigger for morning erosions.Warm compresses
Purpose: Improve the oils from eyelid glands (meibomian glands).
How it helps: Better oils stabilize the tear film, reducing dry-eye-related friction.Lid hygiene (gentle cleaning of lid margins)
Purpose: Reduce debris and inflammation at the eyelid edges.
How it helps: Cleaner lids → better tear quality → less surface irritation.Bandage soft contact lens (clinic-placed)
Purpose: Protect the corneal surface during erosions or high-risk periods.
How it helps: Acts like a “skin” over the cornea, reducing pain and allowing healing. Requires close follow-up to avoid infection.Scleral lens / PROSE device
Purpose: Provide a liquid reservoir over the cornea for comfort and vision.
How it helps: The lens vaults over the cornea and holds sterile saline against it, smoothing optical irregularities and preventing friction.Punctal occlusion (temporary plugs)
Purpose: Keep more of your own tears on the eye.
How it helps: Blocking the tear drain raises tear levels, improving lubrication (minor in-office procedure).Therapeutic taping at night (guided by clinician)
Purpose: Keep the eyelid gently closed in people with incomplete lid closure.
How it helps: Prevents exposure drying and morning sticking.Treating allergies and avoiding irritants
Purpose: Stop itch and rubbing cycles.
How it helps: Fewer allergens/irritants → less rubbing → fewer erosions.Protective eyewear for sports or dusty jobs
Purpose: Prevent minor trauma.
How it helps: Goggles block particles and accidental bumps that can start an erosion.Nutritional and hydration habits
Purpose: Support tissue healing (see diet section).
How it helps: Adequate protein, vitamins A & C, omega-3s, and water aid corneal repair.Mind-body pain strategies during erosions
Purpose: Reduce distress and muscle tension.
How it helps: Relaxed facial/eyelid muscles lower friction and perceived pain.Schedule-based lubrication plan
Purpose: Make lubrication a habit (even when asymptomatic).
How it helps: A routine prevents dry spots that kick off erosions.Avoiding desiccating medications/environment when possible
Purpose: Reduce dryness triggers (e.g., smoke, high altitudes).
How it helps: Fewer drying factors → steadier tear film.Dilute hypertonic saline rinses in clinic protocols
Purpose: Draw excess water from swollen corneal surface (used with medical guidance).
How it helps: De-swells the epithelium, helping it adhere better.Regular follow-up and early intervention plan
Purpose: Catch changes early.
How it helps: Seeing your eye doctor regularly allows quick treatment before problems escalate.
Medication options
Doses are typical examples. Your ophthalmologist may adjust them for your eyes. Never self-start steroids or antibiotics without guidance.
Lubricating artificial tears (carboxymethylcellulose, HPMC, hyaluronate)
Class: Ocular lubricants.
Dose/time: 1 drop every 2–4 hours (or as needed); gel at evening; ointment at bedtime.
Purpose: Reduce friction, soothe dryness, support healing.
Mechanism: Add moisture and viscosity → smoother blinking.
Side effects: Temporary blur with gels/ointments; rare allergy.Hypertonic saline 5% drops and 5% ointment
Class: Decongestant osmotic agents.
Dose/time: Drops 4×/day; ointment at bedtime.
Purpose: Reduce corneal epithelial swelling, improve adherence.
Mechanism: Pulls excess water out (osmotic effect).
Side effects: Stinging on instillation.Topical antibiotic (e.g., erythromycin 0.5% ointment or moxifloxacin 0.5% drops)
Class: Antibiotic.
Dose/time: During an erosion: erythromycin at bedtime to 4×/day; or moxifloxacin 3–4×/day for 3–5 days.
Purpose: Prevent infection when the surface is open.
Mechanism: Kills or blocks growth of bacteria.
Side effects: Rare allergy; temporary blur with ointment.Cycloplegic drop (e.g., homatropine 2%)
Class: Anticholinergic.
Dose/time: 2×/day for 1–3 days during severe pain.
Purpose: Pain relief from ciliary spasm.
Mechanism: Temporarily relaxes the focusing muscle and reduces light sensitivity.
Side effects: Blurry near vision, light sensitivity; avoid driving until effects wear off.Oral pain reliever (acetaminophen ± ibuprofen, if appropriate)
Class: Analgesic/NSAID.
Dose/time: Acetaminophen 500 mg every 6–8 h (max per local guidance); ibuprofen 200–400 mg every 6–8 h with food if safe.
Purpose: Control pain during erosions.
Mechanism: Central pain modulation (acetaminophen); inflammation reduction (ibuprofen).
Side effects: NSAIDs can irritate the stomach; ask your doctor if you have kidney, heart, or ulcer history.Topical corticosteroid (e.g., fluorometholone 0.1%)
Class: Corticosteroid anti-inflammatory.
Dose/time: 3–4×/day for 1–2 weeks, then taper.
Purpose: Calm severe surface inflammation that follows erosions.
Mechanism: Suppresses inflammatory signals.
Side effects: Possible eye pressure rise, delayed healing, infection risk with long use—must be monitored.Oral doxycycline
Class: Tetracycline antibiotic with MMP-inhibiting effect.
Dose/time: 50 mg twice daily for 4–8 weeks (doctor-directed).
Purpose: Reduce recurrent erosions by improving epithelial adhesion.
Mechanism: Inhibits matrix metalloproteinases (MMPs) that break epithelial anchors.
Side effects: Sun sensitivity, stomach upset; avoid in pregnancy and children.Topical cyclosporine (e.g., 0.05% or 0.1%)
Class: Immunomodulator.
Dose/time: 2×/day long-term.
Purpose: Improve tear quality and calm surface inflammation in dry-eye-prone LCD patients.
Mechanism: Lowers T-cell–driven inflammation in the tear glands and ocular surface.
Side effects: Initial burning, rare infection; benefits usually take 4–8 weeks.Lifitegrast 5%
Class: LFA-1/ICAM-1 anti-inflammatory for dry eye.
Dose/time: 2×/day.
Purpose: Similar goal as cyclosporine; improves comfort and tear stability.
Mechanism: Blocks inflammatory T-cell adhesion.
Side effects: Temporary irritation, taste disturbance.Autologous serum tears (e.g., 20%)
Class: Biologic tear substitute (patient’s own serum).
Dose/time: Commonly 4–8×/day for persistent epithelial problems.
Purpose: Provide growth factors and vitamins to help stubborn epithelial healing.
Mechanism: Serum contains epithelial growth factors, vitamin A, and other nutrients missing in artificial tears.
Side effects: Preparation/logistics; contamination risk minimized by sterile compounding.
Notes:
Topical NSAID drops (e.g., ketorolac) are generally avoided in erosions because they can delay epithelial healing.
Long-term steroids are avoided unless your ophthalmologist insists for a short, monitored course.
Dietary, molecular, and supportive supplements
(These do not cure LCD. They mainly support the surface and healing, especially if you have dry eye or frequent erosions. Always check with your clinician for interactions and safe doses.)
Omega-3 fatty acids (EPA+DHA)
Dose: ~1,000 mg/day combined EPA+DHA (or as advised).
Function: Improve tear quality.
Mechanism: Anti-inflammatory lipid mediators stabilize meibomian gland oils.Vitamin A (retinol/β-carotene as RAE)
Dose: Adults typically 700–900 mcg RAE/day from diet/supplements.
Function: Maintains healthy corneal epithelium.
Mechanism: Supports mucin and epithelial cell differentiation.Vitamin C (ascorbic acid)
Dose: 500–1,000 mg/day.
Function: Collagen support and wound healing.
Mechanism: Cofactor for collagen cross-linking and antioxidant defense.Vitamin D3
Dose: 1,000–2,000 IU/day (or per blood level guidance).
Function: Immune balance, may help dry eye.
Mechanism: Modulates inflammatory cytokines.Zinc
Dose: 8–11 mg/day; avoid long high doses without copper.
Function: Epithelial repair enzyme cofactor.
Mechanism: Supports DNA synthesis and cell division.Copper
Dose: 1–2 mg/day if supplementing zinc.
Function: Protect against copper deficiency from zinc use.
Mechanism: Cofactor for lysyl oxidase in collagen and elastin maturation.Lutein + Zeaxanthin
Dose: 10 mg lutein + 2 mg zeaxanthin/day.
Function: Ocular surface antioxidant support and glare tolerance.
Mechanism: Concentrated macular carotenoids reduce oxidative stress; some people report less light discomfort.Collagen peptides
Dose: 5–10 g/day.
Function: General tissue repair support.
Mechanism: Provide amino acids for collagen turnover.N-Acetylcysteine (oral)
Dose: 600 mg once or twice daily.
Function: Mucolytic/antioxidant; sometimes used when stringy mucus aggravates symptoms.
Mechanism: Breaks disulfide bonds in mucus; boosts glutathione.Curcumin (turmeric extract, standardized)
Dose: 500–1,000 mg/day with piperine if tolerated.
Function: Systemic anti-inflammatory support.
Mechanism: Down-regulates NF-κB inflammatory pathways.Evening primrose oil / GLA
Dose: 240–320 mg GLA/day.
Function: May help dry eye symptoms in some people.
Mechanism: Converts to anti-inflammatory lipid mediators.Taurine
Dose: 500–1,000 mg/day.
Function: Osmoprotection for epithelial cells (supportive).
Mechanism: Helps cells balance water and ions under stress.Trehalose (oral or eye-drop form if available)
Dose: Oral per product; eye drops as labeled.
Function: Protect proteins and cells from drying stress.
Mechanism: Disaccharide osmoprotection, stabilizes membranes.Proline-rich protein blends or whey isolate
Dose: 20–30 g protein/day from supplements if diet is low.
Function: Provides amino acids for epithelial repair.
Mechanism: Supplies building blocks for collagen and keratin.General hydration
Dose: Aim for adequate daily fluids (e.g., pale-yellow urine goal unless restricted).
Function: Stabilize tears.
Mechanism: Better body hydration → better tear volume.
Reality check: Supplements can support the surface but cannot remove amyloid or stop the genetic process. Use them as adjuncts.
Regenerative / stem-cell–type” therapies
Important: There is no approved drug that reverses amyloid in LCD. The options below either support healing, modulate surface inflammation, or are investigational. Use only under specialist care; some are off-label or clinical-trial only.
Topical cyclosporine (0.05–0.1%) — approved for dry eye; supportive in LCD
Dose: 2×/day.
Function: Immunomodulator that helps tear glands and surface.
Mechanism: T-cell suppression lowers chronic surface inflammation, helping epithelium adhere.Lifitegrast 5% — approved for dry eye; supportive in LCD
Dose: 2×/day.
Function: Anti-inflammatory for ocular surface.
Mechanism: Blocks LFA-1/ICAM-1 interaction; reduces inflammation and discomfort.Autologous serum / platelet-rich plasma (PRP) eye drops — biologic, compounded
Dose: Typically 4–8×/day, protocol-based.
Function: Deliver growth factors to stubborn epithelial defects.
Mechanism: Serum/PRP contains epidermal growth factor, vitamin A, and other healing signals.Cenegermin (recombinant nerve growth factor) — approved for neurotrophic keratitis; off-label consideration
Dose: Per label when used (e.g., 6×/day for 8 weeks); only if your doctor believes neurotrophic issues contribute.
Function: Encourages corneal nerve/epithelium healing in nerve-related disease.
Mechanism: NGF supports nerve survival and epithelial trophism.
Note: Not a routine LCD drug; used case-by-case.RGTA (matrix-regenerating agents; availability varies) — investigational/regional
Dose: Per product if available.
Function: Mimic natural matrix to protect growth factors and aid healing.
Mechanism: “Shelters” growth factors in the wound bed so epithelial cells repair more efficiently.Gene-targeted therapies (siRNA/CRISPR for TGFBI) — experimental only
Dose: Not clinically established.
Function: Aim to silence or correct the faulty gene instruction.
Mechanism: Allele-specific knock-down or gene editing to reduce amyloid formation.
Status: Research stage; ask about clinical trials, but do not expect routine availability.
What’s not currently used: Limbal stem-cell transplantation is for limbal stem-cell deficiency, not typical LCD. Bone-marrow or systemic stem-cell therapy does not treat corneal amyloid.
Surgical and procedural options
Phototherapeutic keratectomy (PTK)
What it is: A laser gently polishes/removes the top layers of the cornea to remove superficial amyloid and smooth roughness.
Why it’s done: To reduce erosions and improve clarity when deposits are shallow or when the surface is very irregular.
Reality: Vision often improves, but recurrence can happen over months to years because the underlying gene is unchanged.Superficial keratectomy (manual or diamond-burr)
What it is: A surgeon manually peels/polishes the abnormal surface layers.
Why it’s done: To treat recurrent erosions or remove localized superficial deposits when PTK is not available or not ideal.Deep Anterior Lamellar Keratoplasty (DALK)
What it is: A partial-thickness corneal transplant—the surgeon replaces the front and middle stroma but keeps your own endothelium.
Why it’s done: For deeper opacities that seriously reduce vision while aiming to reduce rejection risk compared with full-thickness transplant.
Reality: Recurrence in the graft can still occur over time.Penetrating Keratoplasty (PK, full-thickness corneal transplant)
What it is: The entire cornea is replaced with a donor cornea.
Why it’s done: When deposits are very deep or widespread, or if other surgeries are unsuitable.
Reality: Good visual restoration is common, but graft rejection and LCD recurrence years later are possible; long follow-up needed.Adjunct procedures for recurrent erosions
Examples: Anterior stromal puncture (tiny, peripheral pricks to “spot-weld” epithelium—avoided in the central visual zone), alcohol delamination, or Bowman’s polishing in selected cases.
Why they’re done: To strengthen epithelial adhesion when erosions keep recurring despite other care.
Prevention strategies
We cannot prevent the gene, but we can prevent erosions, infections, and scarring.
Do not rub your eyes—ever.
Use lubricants on a schedule, not just when it hurts.
Humidify rooms; avoid direct fans/air vents.
Wear wraparound sunglasses outdoors.
Keep lids healthy with warm compresses and gentle cleaning.
Follow a bedtime routine: ointment + shield/goggles if advised.
Treat allergies early to stop itching.
Safety glasses for sports/yard work.
Keep a flare plan (who to call, what to use) agreed with your doctor.
Regular eye exams—don’t wait for severe pain or big vision drops.
When to see a doctor—right away vs routine
Right away (urgent):
Severe eye pain that doesn’t ease with your usual plan.
Sudden vision drop, new haze, or a white spot on the cornea.
Pus-like discharge or significant redness (possible infection).
Light sensitivity with deep, constant ache.
Soon (make an appointment):
More frequent erosions or worsening glare.
Lubricants are not enough anymore.
You want to discuss PTK or transplant timing.
You’re considering biologic drops or immunomodulators.
Routine:
Even if stable, plan regular follow-ups (your doctor will set the interval).
What to eat and what to avoid
Helpful to eat regularly:
Fatty fish (salmon, sardine) or fish-oil for omega-3s.
Leafy greens (spinach, kale) for lutein/zeaxanthin.
Orange/yellow veg (carrots, pumpkin) for vitamin A precursors.
Citrus and berries for vitamin C.
Lean proteins (eggs, legumes, poultry, tofu) for repair.
Nuts and seeds (flax, chia, walnut) for healthy fats.
Whole grains to support overall nutrition.
Water throughout the day—stay well hydrated.
Zinc sources (seafood, beans) in moderation.
Dairy or fortified alternatives for vitamin D and calcium (or as per your nutrition plan).
Best to limit/avoid:
Smoking and vape (drying, slows healing).
Excess alcohol (dehydrates).
Very spicy/salty foods late at night if they worsen dryness or wake-time irritation.
Highly processed snacks that displace nutrient-dense options.
Anything that triggers acid reflux at night (can worsen sleep and dryness).
(Diet doesn’t remove amyloid, but it can support comfort and healing.)
Living day to day with LCD (quick routine you can adopt)
Morning: Lubricating drop, sunglasses outdoors, don’t rub.
Day: Blink breaks every 20 minutes, water bottle on desk, drops before symptoms start.
Evening: Warm compress + lid hygiene, gel drop if needed.
Bedtime: Hypertonic ointment and/or shield/goggles per plan.
Flare kit: Lubricants, your doctor’s rescue drops, emergency contact.
FAQs
1) Can lattice corneal dystrophy be cured?
Not yet. It is a genetic condition. We can manage symptoms, treat erosions, and clear deposits with PTK or transplant, but recurrence can happen later.
2) Will I go blind?
Most people do not go completely blind. Vision can be blurred by deposits and scarring but is often improved with surface care and timely surgery.
3) Why do erosions happen in the morning?
At night, the cornea can stick to the eyelid. The first blink pulls on a fragile surface, causing it to lift. Night ointment and shields reduce this.
4) Are contacts bad for me?
Bandage or scleral lenses placed/managed by your eye team can be very helpful. Regular cosmetic contacts need careful hygiene and may not suit everyone with erosions.
5) Will artificial tears alone fix it?
They soothe and prevent friction, which helps a lot, but they don’t remove deposits. They are a core part of long-term care.
6) Do steroids help?
Short doctor-supervised courses can calm inflammation after erosions, but long use has risks like eye pressure rise. Never self-start.
7) What is PTK and how long does it last?
A laser smooths the cornea and removes shallow deposits. Many people enjoy months to years of better comfort/vision. Recurrence varies.
8) What’s the difference between DALK and PK?
DALK replaces the front layers and keeps your own endothelium (lower rejection risk). PK replaces the whole cornea (used for very deep disease) but has higher rejection risk.
9) Can special vitamins cure LCD?
No vitamin or supplement cures LCD. Some nutrients support healing and tear quality.
10) Does stress affect my eyes?
Stress can increase pain perception and sleep issues, which may worsen morning erosions. Good sleep routines help.
11) Is LCD the same as gelsolin amyloidosis?
There’s a systemic form (sometimes called type II/Meretoja) related to gelsolin that affects skin and nerves too. The classic LCD is usually TGFBI-related and mainly corneal. Your doctor can clarify which type you have.
12) Will I definitely need a transplant?
Not everyone. Many manage for years with drops, lenses, and sometimes PTK. Transplant is for advanced clarity loss.
13) Does surgery stop recurrences?
Surgery removes deposits in the treated tissue. Because the cells still make amyloid, deposits can return—often after years, not weeks.
14) Can children be tested?
Families can discuss genetic counseling and testing. Decisions depend on age, symptoms, and local policies.
15) What should my follow-up look like?
Your eye doctor will set a schedule. As a guide: every 6–12 months when stable; sooner after procedures or if symptoms change.
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 10, 2025.
