Corneal collagen crosslinking (CXL) for keratoconus works through which primary mechanism?
- A Creating new collagen fibrils to replace degraded stroma
- B Ablating the abnormal cone and reshaping the cornea with excimer laser
- C Injecting synthetic polymer to support the stromal architecture
- D Riboflavin (vitamin B2) absorbs UVA radiation and generates reactive oxygen species, forming new covalent crosslinks between collagen fibers to increase corneal biomechanical rigidity ✓
Explanation
In corneal CXL (Dresden protocol), riboflavin (0.1%) is instilled after epithelial removal (epi-off) to saturate the stroma, then UVA light (365 nm, 3 mW/cm²) is applied for 30 minutes. Riboflavin acts as a photosensitizer, absorbing UVA and generating singlet oxygen and free radicals that form new intra- and inter-fibrillar covalent (crosslink) bonds between collagen molecules. This increases corneal stiffness by ~300% in experimental models, halting keratoconus progression. Accelerated CXL protocols (higher irradiance, shorter time) achieve the same total fluence (5.4 J/cm²).
Reference: Khurana Comprehensive Ophthalmology, 7th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.