Corneal collagen cross-linking (CXL) for keratoconus uses riboflavin (vitamin B2) with ultraviolet-A light. The mechanism by which it halts keratoconus progression is:

• A Ablation of irregular ectatic stroma to restore a spherical surface
• B Inhibition of corneal MMPs to prevent proteolytic degradation
• C Formation of new covalent bonds between collagen fibrils, increasing corneal stiffness ✓
• D Induction of epithelial hyperplasia to fill the ectatic depression

Explanation

Riboflavin absorbs UVA and acts as a photosensitiser to generate reactive oxygen species (singlet oxygen), which catalyse the formation of covalent bonds (cross-links) between collagen fibril amino groups via pyridinium cross-links. This biomechanical stiffening of the anterior corneal stroma resists further ectasia. The Dresden protocol uses 370 nm UVA at 3 mW/cm² for 30 minutes (total 5.4 J/cm²). Ablation is the excimer laser approach; MMP inhibition is not the primary mechanism; epithelial hyperplasia is a separate corneal wound-healing phenomenon.

Reference: Khurana Comprehensive Ophthalmology, 7th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.