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S. X. Deng, K. D. Sejpal, A. J. Aldave, Q. Tang, F. Yu; Evaluation of Structural Changes in Limbal Stem Cell Deficiency Using in vivo Confocal Microscopy. Invest. Ophthalmol. Vis. Sci. 2010;51(13):2501.
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© ARVO (1962-2015); The Authors (2016-present)
To describe the cellular changes in limbal stem cell deficiency (LSCD) using in vivo confocal microscopy (ICM).
This is a prospective comparative case control study. Patients with LSCD and healthy control subjects underwent ICM (Heidelberg Retina Tomograph-3 Rostock Cornea Module) of the central cornea and the limbus. Patients were categorized into four groups based on clinical presentations: the presence of stippling fluorescein late staining without other abnormalities was classified as early stage; persistent vortex keratopathy and late staining as intermediate stage; persistent vortex keratopathy with recurrent epithelial defect as late stage; complete conjunctivalization and vascularization of the entire cornea as end stage. The epithelial layer and subepithelial nerve plexus were analyzed.
Twenty-one eyes with LSCD and 6 normal eyes were included. The most common causes of LSCD were multiple prior surgeries followed by drug toxicity. There were 8 eyes at early, 10 eyes at intermediate, 2 eyes at late and 1 eye at end stage of LSCD. At early stage, prominent and hyper-reflective nuclei were observed in the superficial and wing layers in the central corneas. Starting at the intermediate stage, basal epithelial cells became affected and the cell density decreased. The central corneal basal cell density (cells/mm2) in the control subjects, early and intermediate stages of LSCD were 10901+1188, 10674+3499 and 7236+1788, respectively. The basal cells were absent in the late and end stages and the Bowman’s membrane became undetectable. Subepithelial nerve density also decreased and the nerve fibers became increasingly tortuous. The central corneal nerve density (nerve/frame) in the control subjects, early and intermediate stages of LSCD were 13+5, 12+8 and 5+3, respectively. Intraepithelial vascularization and inflammatory cells infiltration were observed at the late and the end stages. Similar changes were seen in the limbus. Palisades of Vogt and limbal crypts were absent and the normal underlying stromal architecture was altered. Limbal changes were seen in areas where corneal epithelium had not demonstrated clinical and structural abnormalities.
ICM is able to detect abnormalities of the epithelium, stroma and subepithelial nerve plexus in the cornea and limbus at all stages of LSCD. Changes in the limbus appear to occur prior to the onset of corneal pathology. Identification of these changes may help in early detection and monitoring the progression of LSCD.
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