DOI: 10.1097/j.jcrs.0000000000002011 ISSN: 0886-3350

Comparative Analysis of Human and Porcine Corneal Mechanics and Structure after Glycosaminoglycan Degradation

Hamed Hatami-Marbini, Esharuzzaman Emu

Purpose:

To compare biomechanical and microstructural effects of keratan sulfate (KS) glycosaminoglycans (GAGs) in human and porcine cornea.

Setting:

Computational Biomechanical Laboratory, University of Illinois Chicago.

Design:

Experimental in vitro laboratory study.

Methods:

Human and porcine corneal samples were divided into control (untreated), enzyme-treated (enzyme) groups. For enzyme-treated samples, keratanase enzyme II was used to deplete KS GAGs. Uniaxial tensile experiments along with histochemical and transmission electron microscopy (TEM) studies were used to characterize biomechanical and microstructural properties.

Results:

Human corneas were mechanically stronger (P<0.05), with maximum modulus of 14.31±2.87 MPa and stress of 0.55±0.10 MPa; compared to 6.71±1.35 MPa and 0.27±0.04 MPa, respectively for porcine corneas. Following KS GAG removal, samples became significantly softer and weaker (P<0.05), with maximum moduli of 7.49±1.55 MPa and 2.80±0.30 MPa and maximum stresses of 0.33±0.06 MPa and 0.13±0.01 MPa for human and porcine corneas, respectively. Histochemical staining for GAGs showed markedly reduced blue color intensity following the treatment, indicating a substantial decrease in GAG content. TEM images showed significant differences in collagen fibril diameter and interfibrillar spacing between control porcine and human cornea (P<0.05). GAG depletion had an insignificant effect on collagen fibril diameter but caused a significant increase in the interfibrillar spacing in both human and porcine corneas (P<0.05).

Conclusions:

Although human and porcine corneas exhibit distinct tensile properties, alterations in KS GAG content substantially affect their microstructure and structural integrity. A thorough understanding of roles of GAGs could facilitate improved management of visions diseases rooted in GAG defects.

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