Alkali Burn-Induced Keratitis Model

Model Description

Corneal alkali burns induce progressive ocular damage through dual physicochemical mechanisms:

1. Immediate tissue necrosis: NaOH-mediated epithelial dissolution and stromal collagen degradation

2. Chronic pathology: Inflammatory cell infiltration, neovascularization, and corneal ulceration

 Our model replicates key clinical features of severe keratitis:

• Corneal opacity (≥Grade 3 on Fantes scale)
• Neovascular invasion (>5 vessels/quadrant at Day 21)
• Epithelial defect persistence (fluorescein staining ≥4mm²)

 Clinical Relevance:
✓ Mimics human chemical burns (workplace/domestic accidents)
✓ Supports therapeutic testing: Anti-angiogenics, anti-inflammatories, and corneal repair agents

Applications

• Anti-inflammatory drug efficacy evaluation (corticosteroids, NSAIDs)
• Corneal neovascularization inhibition studies
• Stem cell therapy validation for epithelial regeneration
• Collagen cross-linking protocol optimization

Modeling Protocol —— NaOH-Induced Corneal Burn

1. Pre-op Preparation:

• Anesthetize rabbits (ketamine 35 mg/kg + xylazine 5 mg/kg)
• Confirm corneal integrity via slit-lamp exam

2. Burn Induction:

• Apply 1% NaOH-saturated filter paper (5mm diameter) to central cornea for 30 seconds
• Rinse with 200mL saline (pH 7.4)

3. Post-op Care:

• Levofloxacin eye drops TID ×3 weeks
• Weekly clinical scoring: Opacity/neovascularization/fluorescein retention

Validation & Testing

Data

(1) Corneal opacity: The corneal opacity score is the sum of the burn spot score and the opacity score outside the burn spot. Under a slit lamp microscope, observe and score the corneal opacity of the animals except those in the negative control group.

Fluorescein sodium staining image of corneal alkaline burn

(2) Histopathological Analysis

Histopathological images of rabbit corneal tissue at 8, 15, and 22 days after corneal alkaline burn modeling