Comparison of Artemis 2 Ultrasound and Visante Optical Coherence Tomography Corneal Thickness Profiles

Purpose: To compare corneal thickness profiles of cross-sections of cornea determined by arc-scanned immersion ultrasound and optical coherence tomography (OCT). Methods: Corneas of 28 eyes from 14 participants were scanned in triplicate using the Artemis 2 high frequency arc-scanned ultrasound system (ArcScan Inc) and the Visante OCT system (Carl Zeiss Meditec). Corneal thickness and reproducibility were compared within 3.5 mm of central cornea in the horizontal plane. Results: Although highly correlated, Visante central and peripheral corneal thickness values were systematically thinner than Artemis 2 values. Within the central 0.5 mm, the difference was approximately 8 μm, but the difference increased with distance from the center. Reproducibility for each instrument was comparable, measuring 4 μm centrally and increasing peripherally. Conclusions: Visante OCT measurements of corneal thickness are thinner than Artemis 2 ultrasound values centrally with an increasing difference with peripheral position. Measurement reproducibility was comparable for the two techniques

Hypocellular scar formation or aberrant fibrosis induced by an intrastromal corneal ring: a case report

INTRODUCTION:Intrastromal corneal rings or segments are approved for the treatment of myopia and astigmatism associated with keratoconus. We describe a clinicopathological case of intrastromal corneal rings. For the first time, the molecular pathological findings of intrastromal corneal rings in the cornea are illustrated.CASE PRESENTATION:A 47-year-old African-American man with a history of keratoconus and failure in using a Rigid Gas Permeable contact lens received an intrastromal corneal ring implant in his left eye. Due to complications, penetrating keratoplasty was performed. The intrastromal corneal ring channels were surrounded by a dense acellular (channel haze) and/or hypocellular (acidophilic densification) collagen scar and slightly edematous keratocytes. Mild macrophage infiltration was found near the inner aspect of the intrastromal corneal rings. Molecular analyses of the microdissected cells surrounding the intrastromal corneal ring channels and central corneal stroma revealed 10 times lower relative expression of IP-10/CXCL10 mRNA and two times higher CCL5 mRNA in the cells surrounding the intrastromal corneal ring, as compared to the central corneal stroma. IP-10/CXCL10 is a fibrotic and angiostatic chemokine produced by macrophages, endothelial cells and fibroblasts.CONCLUSION:An intrastromal corneal ring implant can induce hypocellular scar formation and mild inflammation, which may result from aberrant release of fibrosis-related chemokines.This item is part of the UA Faculty Publications collection. For more information this item or other items in the UA Campus Repository, contact the University of Arizona Libraries at [email protected]

Hypocellular scar formation or aberrant fibrosis induced by an intrastromal corneal ring: a case report

Abstract Introduction Intrastromal corneal rings or segments are approved for the treatment of myopia and astigmatism associated with keratoconus. We describe a clinicopathological case of intrastromal corneal rings. For the first time, the molecular pathological findings of intrastromal corneal rings in the cornea are illustrated. Case presentation A 47-year-old African-American man with a history of keratoconus and failure in using a Rigid Gas Permeable contact lens received an intrastromal corneal ring implant in his left eye. Due to complications, penetrating keratoplasty was performed. The intrastromal corneal ring channels were surrounded by a dense acellular (channel haze) and/or hypocellular (acidophilic densification) collagen scar and slightly edematous keratocytes. Mild macrophage infiltration was found near the inner aspect of the intrastromal corneal rings. Molecular analyses of the microdissected cells surrounding the intrastromal corneal ring channels and central corneal stroma revealed 10 times lower relative expression of IP-10/CXCL10 mRNA and two times higher CCL5 mRNA in the cells surrounding the intrastromal corneal ring, as compared to the central corneal stroma. IP-10/CXCL10 is a fibrotic and angiostatic chemokine produced by macrophages, endothelial cells and fibroblasts. Conclusion An intrastromal corneal ring implant can induce hypocellular scar formation and mild inflammation, which may result from aberrant release of fibrosis-related chemokines.</p

Hypocellular scar formation or aberrant fibrosis induced by an intrastromal corneal ring: a case report

INTRODUCTION: Intrastromal corneal rings or segments are approved for the treatment of myopia and astigmatism associated with keratoconus. We describe a clinicopathological case of intrastromal corneal rings. For the first time, the molecular pathological findings of intrastromal corneal rings in the cornea are illustrated. CASE PRESENTATION: A 47-year-old African-American man with a history of keratoconus and failure in using a Rigid Gas Permeable contact lens received an intrastromal corneal ring implant in his left eye. Due to complications, penetrating keratoplasty was performed. The intrastromal corneal ring channels were surrounded by a dense acellular (channel haze) and/or hypocellular (acidophilic densification) collagen scar and slightly edematous keratocytes. Mild macrophage infiltration was found near the inner aspect of the intrastromal corneal rings. Molecular analyses of the microdissected cells surrounding the intrastromal corneal ring channels and central corneal stroma revealed 10 times lower relative expression of IP-10/CXCL10 mRNA and two times higher CCL5 mRNA in the cells surrounding the intrastromal corneal ring, as compared to the central corneal stroma. IP-10/CXCL10 is a fibrotic and angiostatic chemokine produced by macrophages, endothelial cells and fibroblasts. CONCLUSION: An intrastromal corneal ring implant can induce hypocellular scar formation and mild inflammation, which may result from aberrant release of fibrosis-related chemokines