Assessment of the Association Between In Vivo Corneal Biomechanical Changes After Corneal Cross-linking and Depth of Demarcation Line

2019 ◽  
Vol 35 (3) ◽  
pp. 202-206 ◽  
Author(s):  
Riccardo Vinciguerra ◽  
Argyrios Tzamalis ◽  
Vito Romano ◽  
Esmaeil M. Arbabi ◽  
Mark Batterbury ◽  
...  
Keyword(s):  
Cross Linking ◽  
Demarcation Line ◽  
Biomechanical Changes

In Vivo Early Corneal Biomechanical Changes After Corneal Cross-linking in Patients With Progressive Keratoconus

2017 ◽  
Vol 33 (12) ◽  
pp. 840-846 ◽  
Author(s):  
Riccardo Vinciguerra ◽  
Vito Romano ◽  
Esmaeil M. Arbabi ◽  
Matthias Brunner ◽  
Colin E. Willoughby ◽  
...  
Keyword(s):  
Cross Linking ◽  
Biomechanical Changes

scholarly journals Biomechanical Changes After In Vivo Collagen Cross-Linking With Rose Bengal–Green Light and Riboflavin-UVA

2017 ◽  
Vol 58 (3) ◽  
pp. 1612 ◽  
Author(s):  
Nandor Bekesi ◽  
Patricia Gallego-Muñoz ◽  
Lucía Ibarés-Frías ◽  
Pablo Perez-Merino ◽  
M. Carmen Martinez-Garcia ◽  
...  
Keyword(s):  
Rose Bengal ◽  
Green Light ◽  
Cross Linking ◽  
Biomechanical Changes ◽  
Collagen Cross Linking

New Scheimpflug Dynamic In Vivo Curve Analyses to Characterize Biomechanical Changes of the Cornea After Cross-linking for Progressive Keratoconus

2016 ◽  
Vol 32 (1) ◽  
pp. 34-39 ◽  
Author(s):  
Johannes Steinberg ◽  
Andreas Frings ◽  
Aiham Mousli ◽  
Maria K. Casagrande ◽  
Vasyl Druchkiv ◽  
...  
Keyword(s):  
Cross Linking ◽  
Biomechanical Changes

scholarly journals Reevaluating the Effectiveness of Corneal Collagen Cross-linking and Its True Biomechanical Effect in Human Eyes

2017 ◽  
Vol 6 (1) ◽  
pp. 34-41
Author(s):  
Damien Gatinel
Keyword(s):  
Diagnostic Tools ◽  
Cross Linking ◽  
Corneal Rigidity ◽  
Biomechanical Changes ◽  
Biomechanical Effect ◽  
Human Eyes ◽  
Collagen Cross Linking ◽  
Corneal Collagen

ABSTRACT The induction of cross-links in corneal tissue appears to be a promising technique to increase its stiffness and this has been the basis of treatment of keratoconus (KC) and corneal ectatic disease. However, there exists a striking discrepancy between the reported biomechanical effects of corneal collagen cross-linking (CXL) in vitro compared to in vivo, and this has not received much attention in the literature. Despite the documentation of an increase in corneal stiffness in vitro by many investigators, reports that provide evidence of measurable and consistent biomechanical changes in corneal rigidity in vivo after CXL are lacking. Indeed, the absence of documented in vivo biomechanical improvement in CXL-treated corneas is a conundrum, which needs to be further explored. To explain this discrepancy, it has been postulated that biomechanical changes induced by CXL are too subtle to be measured by currently available diagnostic tools or have characteristics not discernible by these technologies. However, the dynamic bidirectional applanation device (Ocular Response Analyzer) and dynamic Scheimpflug analyzer instruments (Corvis ST) have demonstrated the ability to quantify even subtle biomechanical differences in untreated KC corneas of different ectatic degree, and document the reduction in corneal hysteresis (CH) and corneal resistance factor (CRF) in situations where the corneal stiffness is reduced, such as after laser in situ keratomileusis and surface ablation procedures. It has also been possible to demonstrate an altered CH and CRF in patients with diabetes, smoking habit, glaucoma, Fuchs’ dystrophy, and corneal edema. It is puzzling that these diagnostic tools could document subtle biomechanical changes in these situations, yet fail to measure the purported changes induced by CXL on corneas with progressive KC. This failure to document significant and consistent biomechanical changes in corneal rigidity could suggest that CXL does not induce a simple reversal of the particular biomechanical deficits that characterize KC, or make the cornea significantly more resistant to bending forces as has been widely postulated. The absence of measurable biomechanical change in living KC corneas after CXL could be a consequence of biomechanical strengthening which is insignificant compared to the marked weakening caused by preexisting alteration of the collagen structure, disorganization of collagen fiber intertwining, and compromised structural–mechanical homogeneity that are hallmarks of keratoconic disease, especially in corneas with progressive KC. The changes in the cornea induced by CXL that have been described in vivo may instead be driven by a wound healing process in response to the removal of the corneal epithelial layer and subsequent exposure to riboflavin and ultraviolet-A (UVA). This paper will present evidence that sustains this hypothesis. How to cite this article Gatinel D. Reevaluating the Effect­iveness of Corneal Collagen Cross-linking and Its True Biomechanical Effect in Human Eyes. Int J Kerat Ect Cor Dis 2017;6(1):34-41.

scholarly journals Chemically-Boosted Corneal Cross-Linking for the Treatment of Keratoconus through a Riboflavin 0.25% Optimized Solution with High Superoxide Anion Release

2021 ◽  
Vol 10 (6) ◽  
pp. 1324
Author(s):  
Cosimo Mazzotta ◽  
Marco Ferrise ◽  
Guido Gabriele ◽  
Paolo Gennaro ◽  
Alessandro Meduri
Keyword(s):  
Superoxide Anion ◽  
Hydroxypropyl Methylcellulose ◽  
Anterior Segment ◽  
Preclinical Study ◽  
Cross Linking ◽  
Specular Microscopy ◽  
The Novel ◽  
Power Setting ◽  
Contralateral Eye

The purpose of this study was to evaluate the effectiveness and safety of a novel buffered riboflavin solution approved for corneal cross-linking (CXL) in progressive keratoconus and secondary corneal ectasia. Following the in vivo preclinical study performed on New Zealand rabbits comparing the novel 0.25% riboflavin solution (Safecross®) containing 1% hydroxypropyl methylcellulose (HPMC) with a 0.25% riboflavin solution containing 0.10% EDTA, accelerated epithelium-off CXL was performed on 10 patients (10 eyes treated, with the contralateral eye used as control) through UV-A at a power setting of 9 mW/cm2 with a total dose of 5.4 J/cm2. Re-epithelialization was evaluated in the postoperative 7 days by fluorescein dye test at biomicroscopy; endothelial cell count and morphology (ECD) were analyzed by specular microscopy at the 1st and 6th month of follow-up and demarcation line depth (DLD) measured by anterior segment optical coherence tomography (AS-OCT) one month after the treatment. We observed complete re-epithelization in all eyes between 72 and 96 h after surgery (88 h on average). ECD and morphology remained unchanged in all eyes. DLD was detected at a mean depth of 362 ± 50 µm, 20% over solutions with equivalent dosage. SafeCross® riboflavin solution chemically-boosted corneal cross-linking seems to optimize CXL oxidative reaction by higher superoxide anion release, improving DLD by a factor of 20%, without adverse events for corneal endothelium.

Cross-linking of fibrinogen by factor XIII zymogen is not apparent in vivo

2003 ◽  
Vol 89 (05) ◽  
pp. 943-944 ◽  
Author(s):  
Patricia DiBello ◽  
John Shainoff
Keyword(s):  
Factor Xiii ◽  
Cross Linking

scholarly journals Signaling via β2 Integrins Triggers Neutrophil-Dependent Alteration in Endothelial Barrier Function

2000 ◽  
Vol 191 (11) ◽  
pp. 1829-1840 ◽  
Author(s):  
Narinder Gautam ◽  
Heiko Herwald ◽  
Per Hedqvist ◽  
Lennart Lindbom
Keyword(s):  
Protein S ◽  
Endothelial Barrier ◽  
Cheek Pouch ◽  
Cross Linking ◽  
Endothelial Lining ◽  
Hamster Cheek Pouch ◽  
Cationic Protein ◽  
Edema Formation ◽  
Β2 Integrins

Activation of polymorphonuclear leukocytes (PMNs) and adhesion to the endothelial lining is a major cause of edema formation. Although known to be dependent on the function of β2 integrins (CD11/CD18), the precise mechanisms by which adherent PMNs may impair endothelial barrier capacity remain unclear. Here, the role of transmembrane signaling by β2 integrins in PMN-induced alterations in tight junctional permeability of cultured endothelial cell (EC) monolayers was investigated. PMN activation, in the absence of proinflammatory stimuli, was accomplished through antibody cross-linking of CD11b/CD18, mimicking adhesion-dependent receptor engagement. CD18 cross-linking in PMNs added to the EC monolayer provoked a prompt increase in EC permeability that coincided with a rise in EC cytosolic free Ca2+ and rearrangement of actin filaments, events similar to those evoked by chemoattractant PMN activation. Cell-free supernatant obtained after CD18 cross-linking in suspended PMNs triggered an EC response indistinguishable from that induced by direct PMN activation, and caused clear-cut venular plasma leakage when added to the hamster cheek pouch in vivo preparation. The PMN-evoked EC response was specific to β2 integrin engagement inasmuch as antibody cross-linking of l-selectin or CD44 was without effect on EC function. Our data demonstrate a causal link between outside-in signaling by β2 integrins and the capacity of PMNs to induce alterations in vascular permeability, and suggest a paracrine mechanism that involves PMN-derived cationic protein(s) in the cellular crosstalk between PMNs and ECs.

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