Elastase-Treated Auricular Cartilage: Feasibility as a Substitute for Native Tarsus

Reconstruction of upper eyelid defects is challenging due to paucity of fungible local tissue and a lack of adequate tarsal substitutes. Cartilage is too stiff to be directly implanted in the posterior lamella due to the risk of corneal damage with blinking. Since elastin is a key structural element in elastic cartilage, we hypothesized that elastase treatment of cartilage may reduce cartilage’s stiffness sufficiently to make it a feasible posterior eyelid lamella substitute.

Porcine auricular cartilage was treated with elastase or buffer control. Histopathology, electron microscopy, and mechanical testing were performed. Young’s modulus was calculated using the Hertzian method for mechanical indentation testing at baseline, 2, and 24 hours. Group 1 (buffer control auricular cartilage), Group 2 (elastase-treated auricular cartilage), and Group 3 (native tarsus) were compared.

Grossly, elastase treatment increased cartilage flexibility, and microscopically increased chondrocyte lacunae and decreased the density of the interterritorial matrix, relative to controls. Electron microscopy revealed elastin fiber degradation with empty channels preplacing elastin fibers. At 2 hours, cartilage stiffness showed minimal differences between Groups 1 and 2 for both instantaneous modulus (1.34 vs. 1.37 MPa; p = 0.92) and equilibrium modulus (0.31 vs. 0.36 MPa; p = 0.71). By 24 hours, the equilibrium modulus of elastase-treated cartilage (0.055 MPa) resembled native tarsus (0.016 MPa; p = 0.76).

Grossly, elastase treatment increased cartilage flexibility and, microscopically, increased chondrocyte lacunae and decreased the density of the interterritorial matrix, relative to controls.