Biomechanics of tearing in planar soft tissues and tissue-derived biomaterials

Tearing has been identified in the trauma and disease of a variety of human planar soft tissues; however, very limited knowledge is available regarding the nature of these failures. A laboratory understanding of the biomechanics associated with out-of-plane tissue tearing in a representative material (bovine pericardium) was undertaken to promote an understanding of related tearing events in vivo and benefit the design of biomedical devices based on these tissues.; Fresh and treated samples of ventral bovine pericardial samples were torn in one of two anatomical directions relative to the anatomy of the heart and according to a scale-down of an ASTM standard for textile tearing. Force/grip separation/time data were collected to produce tearing profiles from which the mode of tissue failure, peak tearing force, and energy required for tearing could be determined to assess tearing resistance. The effects of grip separation rate, anatomical orientation, glutaraldehyde (GLUT) and carbodiimide (EDC) crosslinking, and matrix hydration on tearing behaviour were examined. The effects of a dehydrating solvent environment on GLUT crosslinking were also assessed. Torn samples were examined with scanning electron microscopy (SEM) to ascertain influences of collagen architecture on tear propagation.; The peak tearing force increased markedly with grip separation rate, but was largely independent of anatomical orientation; however, the energy during tearing was significantly higher when samples were torn in the base-to-apex anatomical direction compared to the circumferential direction.; The crossed-lamellar structure of pericardium determines that a tear does not pass through a sample in a uniform direction, but is instead diverted to a direction aligned with the local collagen fibre orientation. SEM micrographs indicated that tissue failure ultimately occurs by delamination---the mechanism with the lowest energy expenditure. This suggests that tearing resistance is most dependent on the resistance of the woven collagen network to separation and bundle pullout. Crosslinking and alterations in the solvent environment did not increase tearing resistance or alter the failure mode. GLUT likely produced crosslinks of insufficient length (even after polymerization or dehydration) to bridge interfibrillar gaps between adjacent lamellae and thereby reinforce the woven tissue structure. EDC crosslinking did not sufficiently crosslink the proteoglycan "glue" to fibres in different collagen layers.; Matrix dehydration in a saturated sucrose solution significantly raised the peak tearing force and energy when compared to fresh and super-hydrated samples. Sucrose dehydration may have produced a more tightly packed collagen architecture that enhanced interfibrillar interactions and imbued a greater tearing resistance by reducing collagen fibre mobility. Since delamination dominates tissue tearing, sucrose dehydration likely heightened interfibrillar interactions between different tissue layers, effectively reinforcing the lamellar structure.