Corneal collagen crosslinking (CXL) with riboflavin and UV-A light halts keratoconus progression primarily through which mechanism?

• A Stimulating keratocyte proliferation to fill ectatic areas
• B Removing degraded proteoglycans and restoring normal stromal architecture
• C Riboflavin deposition in Bowman layer, mechanically stabilising the surface
• D Introducing additional covalent bonds between collagen fibrils, increasing stromal stiffness ✓

Explanation

UV-A irradiation (365 nm) activates riboflavin (vitamin B2) to produce reactive oxygen species that form new covalent (crosslinks) bonds between amino groups of collagen fibrils. This significantly increases corneal stiffness (biomechanical strength), halting ectatic progression. The corneal stroma does not regenerate or fill ectatic areas — keratocyte density actually transiently decreases after CXL due to UV damage. Riboflavin deposition per se is not a mechanical barrier mechanism.

Reference: Khurana Comprehensive Ophthalmology, 7th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.