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

Xiaoguang Cao12, Roxana Ursea3, Defen Shen1, Hema L Ramkumar14 and Chi-Chao Chan1*

Author Affiliations

1 Immunopathology Section, Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD, USA

2 Department of Ophthalmology, People's Hospital, Peking University, Beijing, China

3 Department of Ophthalmology & Visual Science, University of Arizona, AZ, USA

4 Howard Hughes Medical Institute, Chevy Chase, MD, USA

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Journal of Medical Case Reports 2011, 5:398  doi:10.1186/1752-1947-5-398

Published: 19 August 2011



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.


An intrastromal corneal ring implant can induce hypocellular scar formation and mild inflammation, which may result from aberrant release of fibrosis-related chemokines.