Abstract

Over the past 20 years, corneal cross-linking (CXL) has been used by surgeons to halt the progression of keratoconus (KC). This chapter reviews the literature regarding the indications, mechanism of action of CXL, the role of each of its components, the strong biological reaction, and their effects on cell interaction, proteins involved, wound healing, and combinations. CXL surgery involves a photochemical response in which ultraviolet light at a given wavelength and riboflavin participate. The combination of irradiation with ultraviolet A light and riboflavin leads to an intense process of apoptosis of keratocytes in the anterior stroma. Differences in light irradiation, as well as the importance of riboflavin and its vehicle, were also detailed. The primary clinical indications for corneal CXL include progressive KC in adults and corneal ectasia after corneal refractive surgery. More recently, indications have expanded to include pediatric KC, with treatment offered at the time of diagnosis in this group. The surgery creates additional chemical bonds between the amino terminals of the collagen side chains and the proteoglycans of the extracellular matrix. A photosensitization reaction catalyzed by riboflavin classically involves the production of singlet oxygen. Microstructure studies show changes in the size of the fibril and potentially in the interfibrillar space; the most significant changes related to the stiffening effect of CXL occur in the anterior third of the cornea, and short irradiation times, especially less than 5 minutes, may not have the same biological effect. Many studies have suggested that CXL is safe and effective in the standard and accelerated protocols that have been used by surgeons. After the initial depletion of anterior keratocytes, keratocyte density seems to return to average 6–12 months after surgery when corneas are examined with the confocal microscope.

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