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E.B. Papas, A. Petznick, F. Stapleton, Q. Garrett; Involvement of Matrixmetalloproteinase–9 (MMP–9) and Tissue Inhibitor of Matrixmetalloproteinase–1 (TIMP–1) During Orthokeratology . Invest. Ophthalmol. Vis. Sci. 2006;47(13):117.
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Despite the increase in the popularity of orthokeratology, the mechanisms by which corneal flattening occur are poorly understood. We hypothesise that upon initial wear of orthokeratology lenses, the mechanical stress may induce corneal epithelial cells to release MMP–9 and a disturbance of the tightly regulated ratio between MMP–9 to its inhibitor, TIMP–1, might lead to central corneal flattening. This study was to investigate the involvement of MMP–9 and TIMP–1 during orthokeratology
In the randomised and controlled clinical trial study, five subjects wore orthokeratology (Ortho–K) lens in one eye leaving the fellow eye as a control for the time periods of 1, 3, 7 and 15 hours. At the end of lens wear, the tears were collected for the measurement of MMP–9 or TIMP–1 expression using ELISA. The activity of MMP–9 was determined using gelatin zymography. Corneal topography was measured to confirm corneal flattening
Orthor–K lens wear caused significant corneal flattening (p<0.01). A greater amount of MMP–9 and greater amount of MMP–9 activity were found in the tears of lens wearing eyes than control eyes. Furthermore, both the amount and the activity of MMP–9 in the tears increased with the length of lens wear. There was no difference in TIMP–1 expression between lens wearing or control eyes, and no difference in TIMP–1 expression regardless of lens wear duration.
A trend toward increasing MMP–9 expression during orthokeratology lens wear was found, suggesting that epithelial cell migration from the central cornea to the mid–periphery mediated by MMP–9 activity may be one of the mechanisms for orthokeratology
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