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Mahdy Ranjbar, Annekatrin Pahl, Johannes Rendenbach, Fred Reinholz, Salvatore Grisanti; Development and evaluation of a new laser-assisted experimental model for Fuchs endothelial corneal dystrophy. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):1172.
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Fuchs endothelial corneal dystrophy (FECD) is characterized by progressive loss of corneal endothelial cells (CEC), alterations in the extracellular matrix and loss of vision. Existing disease models focus on the destruction of CEC through the application of toxic agents or genetic modifications. In this study, the possibility of an alternative, non-invasive, laser-assisted disease model for FECD was evaluated.
For the experiments, freshly enucleated porcine eyes were positioned in front of a conventional slit lamp combined with a Nd:YAG-laser. Laser spots were placed into the anterior chamber with varying energy levels and different distances to the corneal endothelium. Corneas were excised using a punch trephine and were then analyzed for laser-mediated lesions by light microscopy and two-photon microscopy.
Aiming the laser at the anterior chamber results in the generation of a gas bubble, which spreads out. If the gas bubble is large enough it can hit the CEC and detach them machanically. Choosing higher laser energy levels and focusing closely behind the CEC resulted in larger areas with no CEC. However, in these cases a ruptured Descemet’s membrane was often observed and the laser damage even affected the corneal stroma. On the other hand, aiming the laser too deep into the anterior chamber or selecting lower energy levels resulted in no detectable laser-mediated effects on CEC. Nevertheless, it is possible to set a margin for the parameters to create lesions of CEC-free Descemet’s membrane without rupturing it.
Using a Nd:YAG-laser it is possible to produce small gas bubbles in the anterior chamber, which damage the corneal endothelium mechanically, leaving areas of bare Descemet’s membrane with no CEC attached. This non-invasive, laser-assisted technique can be used as an alternative experimental model for diseases with loss of CEC like FECD.
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