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358                             Handbook of Properties of Textile and Technical Fibres

         fibroblast necrosis (Provenzano et al., 2002a,b), and altered collagen fiber orientation.
         At the macroscopic level collagen fiber failure in tendon has a distinct morphological
         character.
            Statistical analyses indicate that the onset of subfiber failure occurs at a strain of
         about 5% in a ligament that is below the threshold for structural damage (Provenzano
         et al., 2002a,b). Cellular damage induced by ligament sprains occurs at strains signif-
         icantly below failure strains (Provenzano et al., 2002a,b). Subfiber failure appears to be
         associated with altered collagen fiber rotation during tissue extension. While tissue
         remodeling and synthesis of collagen types I and III can occur at subfailure strains
         through fibroblast mediated processes, the pre-subfailure strengths of ligaments are
         never regained and permanent joint laxity occurs (Provenzano et al., 2002a,b,
         2005). Subfiber failure is first observed in thin diameter collagen fibrils followed by
         failure of the larger diameter collagen fibrils (Yahia et al., 1990). Ker (2008) has
         reviewed the macroscopic fracture mechanics of tendon. When a tendon is notched
         laterally and loaded in tension longitudinally, the crack opens up and the tip becomes
         curved. Since the ratio of the shear modulus to that of the tensile modulus of tendon is
                 3
         about 10 , the crack propagates longitudinally and leads to a mode of failure called
         “interdigitation.” This failure surface is characterized by the presence of numerous
         collagen fibrils that one by one tear at different lengths and morphologically look
         like series of fingers projecting across the failed tendon ends. Ker et al. (2000) reported
         a correlation between stress-in-life (physiological operating stress levels) and resis-
         tance to fatigue damage leading to the conclusion that all tendons are equally likely
         to experience damage independent of their normal operating stresses. Ker (Ker,
         2008; Ker et al., 2000) further hypothesized that damage of tendon during normal
         loading acts to trigger tendon repair processes and that tendon damage and failure
         are limited by the weakness of the attached muscle.



         11.9   Nondestructive methods for studying mechanical
                behavior of collagen fibers and tissues

         The ability to monitor the mechanical properties of collagen and ECMs in vivo is an
         important measurement needed for early diagnosis of disease and the ability to follow
         disease progression. The ability of physicians to “palpate” changes in the properties of
         tissues associated with tumors and calcification suggests that there are major changes
         in the structure and properties of collagen and ECMs during disease processes. It is
         essential that clinicians be able to assess the changes at the collagen fibril and fiber
         levels of structure to accurately diagnose and treat diseases such as cancer. Several
         new methods have been developed to try and discern these changes early in the disease
         process. It is essential that these methods be validated so that the properties measured
         have some meaning.
            There are several fairly new methods that have been evaluated in the literature to
         study the mechanical properties of tissues in vivo such as magnetic resonance elastog-
         raphy (MRE), ultrasound elastography (UE), optical coherence tomography (OCT),
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