Evaluating changes in LSCD - Ophthalmology Times Europe

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Evaluating changes in LSCD


Ophthalmology Times Europe
Volume 8, Issue 2

According to Dr Sophie Deng (Jules Stein Eye Institute, University of California, USA), non-invasive imaging could be useful in the identification and monitoring of early stage limbal stem cell deficieny (LSCD) as cellular changes can be detected. This was highlighted as a potential approach during her research on the characterization of the disease.1

Investigating cellular changes

"LSCD is a disease caused by the loss of limbal stem cells. It is important to investigate the cellular changes in the cornea and limbus where these cells are located to understand the pathogenesis of this disease," said Dr Deng. To evaluate the cellular changes in the corneal epithelium and surrounding cells within patients suffering from LSCD, Dr Deng and colleagues examined 27 eyes of 20 patients with in vivo laser scanning confocal microscopy. Healthy eyes were used as control.



"We classified the LSCD patients, after examining them with a slitlamp, into three groups comprising early, intermediate and late disease stages," explained Dr Deng. Then imaging of the central cornea and four limbal locations was performed and the morphologic characteristics of the corneal epithelium were also investigated.

Dr Deng added, "As LSCD is a disease of the stem cells, it is not surprising that the less differentiated cells, in this case the basal cells in the cornea, are affected and the limbal stem cells are presumed to be located at the basal layer in the limbus." To examine the affect LSCD has on these cells, Dr Deng and her team calculated the densities of the basal epithelial cells and subbasal nerves in the central cornea, and looked at whether there was a potential correlation between a decrease in both of these densities in relation to LSCD.

Interesting findings

It was found that there was a significant reduction in both the basal epithelial cell and subbasal nerve densities in the early and intermediate stage patients when compared with the control group. However, in the late stage group of patients, Dr Deng and colleagues found that the normal basal epithelial cell morphology was completely lost and subbasal nerves were missing.

"As we had expected, the basal cells were effected as a result of the decreased limbal stem cells, however, we did not realize that there would be a reduction in the nerve density," revealed Dr Deng. "This is a very interesting finding as it may change our current understanding of LSCD. Neurotrophic factors might be important in the pathogenesis of limbal stem cell deficiency (LSCD)."

A correlation between these decreases was also found, which although suspected was still surprising as a result of the effect LSCD had on the subbasal nerves, noted Dr Deng.

These cellular changes that were identified by non-invasive imaging could help with understanding and monitoring of LSCD. Dr Deng explained that by identifying a change in cell morphology and cell density, a change in the normal haemostasis of the stem cells can be indicated. "When the normal extracellular matrix structure in the limbus is altered compare to the normal control, this indicates a change/damage in the stem cell niche, therefore, the stem cells are probably affected or damaged," she said.

"We still need to continue the study and further delineate the changes. However, these findings could be used to identify early LSCD and to classify the disease in a non-invasive manner. This method could be used to monitor the treatment outcome in the future," Dr Deng concluded.

Special contributor

Dr Sophie Deng is an assistant professor at the Jules Stein Eye Institute, University of California, Los Angeles, California, USA. She specialized in cornea and external eye diseases and devotes half of her time on patient care and the other half on clinical and translational research. She may be reached by E-mail:

Dr Deng has no financial interests in the subject matter.

Reference

1. S.X. Deng et al., Arch. Ophthalmol., Published online 12 December 2011. doi:10.1001/archophthalmol.2011.378.

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