Purchase this article with an account.
T. Kadar, L. Cohen, S. Dachir, M. Cohen, E. Fishbine, R. Sahar, J. Turetz, A. Rozner, A. Solomon, A. Amir; Partial Limbal Stem Cell Deficiency Following Sulfur Mustard Exposure in Rabbits - The Potential Use of Amniotic Membrane Transplantation. Invest. Ophthalmol. Vis. Sci. 2007;48(13):398.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Ocular injuries induced by sulfur mustard (SM) are characterized by acute corneal erosions, anterior segment inflammation and delayed Partial Limbal Stem Cell Deficiency (PLSCD) appearing in 50-70% of the exposed eyes, expressed by chronic inflammation, neovascularization (NV), persistent epithelial defects and impairment in corneal innervation. The aim of the present study was to further elucidate the pathological mechanism of SM- induced delayed keratopathy in our rabbit model and to test the potential use of amniotic membrane transplantation (AMT) for treatment of the impaired ocular surface in SM corneas.
All experiments were performed according to ARVO resolution on the Use of Animals in Research. Rabbit eyes were exposed to SM vapor. Slit-lamp examination and pachymetry were carried out once a week. AMT was conducted in corneas displaying delayed injuries by placing a single layer of human AM over the cornea following superficial keratectomy. A soft bandage contact lens as applied over the AM and a tarsorrhaphy was performed. Topical chloramphenicol ointment was applied for 3 days. The rabbits were sacrificed 2-3 weeks after AMT and corneas were processed for histology.
Focal limbal damage was observed in corneas displaying the typical delayed injuries. This was expressed by stromal inflammatory infiltrate invading into limbal epithelium, destroyed epithelium including stem cells (SC) and presence of goblet cells in corneal epithelium. AM treated corneas exhibited reduced edema and NV, smooth surface and clear stroma, compared to the severe edema, progressive NV and epithelial defects observed in the untreated controls. Thus, AMT attenuated the manifestations of limbal deficiency and improved both epithelial migration and adherence. Yet, the abnormal corneal epithelial phenotype was still seen 3 weeks after transplantation.
A continuing cell death was observed in limbal epithelium following SM exposure, associated with focal inflammatory response. It is suggested that stromal inflammation in the limbus of SM exposed corneas conferred impaired microenvironment to epithelial SC, thus leading to their loss and to a second cascade of pathological events. AMT reduced the ongoing inflammation and facilitated epithelial healing. Further studies are needed to assess the long-term effects of the AM and to determine whether AM alone is sufficient for therapy of PLSCD following SM exposure.
This PDF is available to Subscribers Only