Today's Hot Topic: Corneal Reshaping
BY MARJORIE J. RAH, OD, PHD
It is becoming increasingly apparent that the
science (and the art) of contact lens corneal reshaping is a hot topic. But one particular issue -- the question of the mechanism of action of the
corneal reshaping procedure -- still seems to challenge us.
In the November 1998 issue of Optometry and Vision Science, Helen Swarbrick and colleagues reported significant central
neal flattening after one day of lens wear.
Figure 1. Photo depicting the affects of fluid forces on the corneal epithelium.
Photo provided with permission from Paragon Vision Sciences, Inc.
The authors attributed this flattening to central epithelial thinning and to midperipheral corneal thickening at approximately 2.5mm from the central cornea as measured by optical
pachymetry. They concluded that "the initial corneal response to orthokeratology may be explained by redistribution of corneal tissue rather than by overall bending of the cornea," perhaps resulting from post-lens fluid forces (Figure 1).
These data were supported by an ARVO 2002 poster by Mita et al, which showed thinning of the central corneal epithelium in histological sections of rabbit
orthokeratology. Similarly, Nguyen et al also reported a decrease in central corneal epithelial thickness along with an increase in stromal thickness, measured by confocal microscopy and Orbscan
topography, in their ARVO 2002 poster.
A Matter of Migration?
Many people describe this shift in epithelial thickness as epithelial migration; however, a speaker at a recent meeting relayed the conflicting opinion of an astute optometry student who has a background in microbiology.
The student had pointed out that the tight junctions adhering corneal epithelial cells to one another are quite strong and intricately interconnected. In order for the connections to break and a cell to shift in position, each adjacent cell would have to undergo a similar process. Therefore, epithelial migration is unlikely in this model.
Closing In on the Answer
This brings up the question of whether it is perhaps compression of the epithelium at work after all or perhaps the answer lies in the
stroma. Just when we thought we knew that the mechanism responsible for treatment was epithelial migration,
Alharbi, Swarbrick and LaHood presented an intriguing poster on changes in stromal thickness at the ARVO 2003 meeting. When compared to eyes wearing traditional GP contact lens designs and eyes with no contact lens wear, overnight wear of reverse geometry contact lenses actually appeared to suppress central stromal edema. At the same time, normal overnight levels of stromal edema were noted in the midperipheral and peripheral cornea.
Although it appears that we are closing in on the answer, some questions are still unanswered at present. I look forward to seeing the next round of posters and papers at the upcoming meetings. Perhaps they will shed light on the issue.
Dr. Rah is an assistant professor at the New England College of Optometry where she works primarily in the Cornea and Contact Lens Service in patient care, teaching and
Contact Lens Spectrum, Issue: September 2003