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Evaluation and management of ocular injuries following sulfur mustard exposure

TitleEvaluation and management of ocular injuries following sulfur mustard exposure
Publication TypeConference Proceedings
Year of Conference2008
AuthorsAmir A., Dachir S., Gutman H., Givant-Horwitz V., Cohen M., Cohen L., Fishbine E., Sahar R., Turetz J., Kadar T.
Conference NameProceedings of the U.S. Army Medical Defense Bioscience Review
Volume1
Paginationp. 143
Conference LocationHunt Valley, MD
Abstract

Ocular injuries induced by sulfur mustard (SM) are characterized by an acute injury phase, expressed by inflammatiopn of the anterior segment and corneal erosions. A delayed phase follows, starting weeks or years after a spontaneous apparent healing and consisting of epithelial defects and corneal neovascularization (NV). During recent years, we have studied the temporal development of these lesions and have shown, in our rabbit ocular model, that the symptoms of the late-phase injury are typical features of an ocular surface disorder categorized as limbal stem cell deficiency (LSCD) that leads to visual loss. Nevertheless, the pathological mechanism underlying these injuries is still unclear, and therapy is only partially efficient. We recently applied two non-invasive tools, impression cytology (IC) and tear collection, to further investigate in vivo ocular surface changes after SM exposure and to elucidate the role of potential therapy. Through long-term cytological evaluation, we observed progressive pathological changes and squamous metaplasia in the conjunctiva, associated with a reduction in the goblet cell population and leading to mucin deficiency and tear film abnormality, months after the initial exposure. Moreover, IC was found to be useful for the early diagnosis of LSCD through the identification of conjunctival epithelial cells in the cornea before the appearance of typical clinical symptoms. Tear film analysis showed increased matrix metalloproteinase activity, which correlated with the appearance of delayed injury. We propose that the chronic inflammation and prolonged impairment in corneal innervation that we had found previously contribute to the formation of a pathological microenvironment for epithelial stem cells, leading to their death and to a second cascade of events that ends with severe, long-term injuries. Therefore, the results support treatment paradigms previously suggested for SM injuries and the need for ocular surface reconstruction by amniotic membrane and stem cell transplantation.This work is supported in part by the U.S. Army Medical Research and Materiel Command under Contract DAMD 17-03-C-0064.

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