Corneal collagen cross-linking (CXL) with riboflavin and UVA light is the treatment of choice for progressive keratoconus. The primary mechanism by which CXL halts progression is:
- A Increasing corneal anterior curvature to reduce ectasia
- B Stimulating keratocyte proliferation to regenerate lost stromal collagen
- C Creating new covalent bonds (pyridinium cross-links) between collagen fibrils, increasing corneal stiffness by 4–5 times ✓
- D Depositing riboflavin in the stroma to block UV-induced proteolysis
Explanation
CXL works by riboflavin (vitamin B2) acting as a photosensitizer that, when activated by 365 nm UVA light, generates reactive oxygen species (singlet oxygen). These reactive species induce covalent cross-links (pyridinium cross-links) between lysine groups of adjacent collagen fibrils in the corneal stroma — measurably increasing stromal stiffness by approximately 4–5 times. This biomechanical strengthening halts ectasia progression. Standard CXL requires epithelial removal (epi-off) for adequate riboflavin penetration; transepithelial (epi-on) CXL uses modified riboflavin formulations but is generally considered less effective.
Reference: Khurana Comprehensive Ophthalmology, 7th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.