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J. Buehren, L. J. Nagy, G. Yoon, M. DiMagistris, S. M. MacRae, K. R. Huxlin; Biological Correlates of Higher-Order Aberrations (HOAs) After Photorefractive Keratectomy (PRK) in a Cat Model. Invest. Ophthalmol. Vis. Sci. 2008;49(13):2922. doi: https://doi.org/.
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To measure the relative contribution of laser ablation efficiency loss, biomechanics and myofibroblast differentiation to the induction of higher-order aberrations (HOAs) after PRK.
Eight eyes from four adult, domestic short-hair cats were treated with -10D PRK (Technolas217, Bausch & Lomb, 6mm optical zone). A PMMA lens with a curvature similar to that of the feline corneas (r=8.95mm) received an identical excimer ablation. Following PRK, one eye of each cat received 50µg of anti-transforming growth factor (TGF)β antibody (Clone 1D11, R&D Systems) b.i.d. for the first post-operative week in order to inhibit myofibroblast differentiation, while the other (control eye) received vehicle solution alone. Wavefront sensing was performed in the awake-fixating state with a Hartmann-Shack sensor pre-operatively and 2, 4, 8 and 12 weeks postoperatively. The curvature of the PMMA lens was measured using surface profilometry, adjusted for the individual ablation rate of each eye and wavefront changes were computed from curvature changes after ablation. All wave aberrations were reconstructed up to the 10th Zernike order.
The root-mean-square (RMS) of HOAs induced in PMMA over a 6 mm pupil diameter (PD) was 0.401±0.081µm and consisted only of spherical aberrations (SAs). Induced SA RMS in cat eyes did not differ significantly from that in PMMA (difference to PMMA at week 4: -0.122±0.084µm in the treated and -0.055±0.336µm in the control eyes) and there was no significant difference between anti-TGFβ-treated and control eyes. However, on average, the treatment group exhibited 55% less coma and 48% less other HOA (RMS excluding coma and spherical) induction than the control eyes at all time points examined.
The present experiments differentiate, for the first time, the relative contribution of myofibroblast-mediated wound healing from that of laser efficiency loss and corneal biomechanics to the induction of HOA after PRK. Our data suggest that during PRK, SA is induced mainly by loss of laser ablation efficiency and biomechanics rather than by myofibroblast-mediated wound healing. In contrast, myofibroblast differentiation appears to contribute significantly to the induction of coma and other HOAs. Thus, pharmacological modulation of wound-healing using myofibroblast-blocking agents could enhance optical quality after surface ablation.
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