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C. Boote, S. Hayes, R. D. Young, N. Hawksworth, K. M. Meek; A Structural Investigation of Corneal Graft Failure in Suspected Recurrent Keratoconus. Invest. Ophthalmol. Vis. Sci. 2009;50(13):4530.
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In keratoconus, a leading cause of corneal transplant surgery, progressive thinning and steepening of the cornea leads to severe irregular astigmatism. Despite the high success rate of penetrating keratoplasty, recurrence of keratoconus has been reported up to 40 years post-graft. The aetiology of primary and recurrent keratoconus is unclear, and diagnosing recurrences of the disease remains a difficult and contentious issue. Structural changes have been widely observed in primary keratoconus, most notably in the collagenous architecture of the stromal extracellular matrix. Here we investigated collagen fibril size and arrangement in failed corneal graft tissue from a patient with suspected recurrence of keratoconus 13 years after original transplant.
Wide- and small-angle X-ray scattering were used to provide information on average collagen fibril diameter, dominant fibril orientation, and the relative distribution of collagen throughout the stroma from limbus to limbus. Corneal ultrastructure was also examined by transmission electron microscopy. Results were compared to data from normal and primary keratoconus corneas.
In contrast to primary keratoconus, the orientation and distribution of collagen as determined by X-ray diffraction appeared normal throughout most of the failed-graft button. The exception was localised abnormalities in fibril alignment in the infero-nasal quadrant of the button at a distance of 2.5-3.5mm from the centre at the original graft/host junction. Electron micrographs from this region showed evidence of stromal lamellar disruption, with the remainder of the button displaying normal ultrastructure. The average diameter of collagen fibrils in the failed-graft button (34.5nm +/- 0.4) was within the typical range for normal corneas.
The structural abnormalities identified in the failed graft button were not consistent with those that underlie primary keratoconus. It is possible that recurrent keratoconus has a different pathologic mechanism to the primary condition. Mechanical weakness brought about by disruption to normal collagen organisation around the graft-host interface may have a role to play in some incidences of apparent keratoconus recurrence.
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