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document the temporal relationship between exposure and effect. Due to the different levels of development of these models and the methods used to evaluate tissue damage, the depth of knowledge of the mechanism of injury varies from tissue to tissue.

In vertebral bone, strength diminishes and damage is irreversible with each trabecular fracture. However, the role of the smaller microcracks in the pathophysiology of bone damage is uncertain; they may be a harbinger of fractures, or they may be repaired. In humans, vertebral microfractures are not visible using current imaging methods (e.g., X-ray, CT, MRI), which contributes to the known poor correlation between images of the spine and low back pain. Both disc and vertebra demonstrate fatigue failure, but vertebral endplates fail before the disc in response to repeated loading. Cumulative spinal loading affects disc pressure and water content, and these factors, in turn, influence cell viability and function. In vivo loading of sufficient magnitude can cause altered cell metabolism and cell death following a dose-response relationship.

In vivo animal models that expose tendons to repeated loading demonstrate an inflammatory response with fibrosis in the peritenon. The process may be mediated by an initial release of inflammatory mediators and microtrauma. In the central tendon, degenerative changes are observed with edema, collagen disorganization, and fibrosis. Although the initial steps may include microtrauma, they are not well characterized.

In muscle, prolonged fatigue damage can occur with single or cyclical loads. Eccentric loading is more damaging than concentric loading. Repeated eccentric loading can produce a persistent force decrement with structural damage to the sarcomeres (Z-line streaming, fiber necrosis, and inflammation). A threshold or endurance limit for injury has not been identified. The mechanical fatigue injury mechanism may be complemented by physiological mechanisms (e.g., intramuscular pressure, Cinderella hypothesis).

In the peripheral nerve, compression causes edema accumulation, elevated endoneural pressure, vascular disruption, fibrosis, demyelination, and axon injury. The steps linking the initial effects to demyelination and permanent nerve damage are uncertain. Compression of the nerve for a sufficient duration also leads to chronic pain. Exposure to vibration causes a similar process of edema formation followed by demyelination and axon degradation. Although the relationship between nerve injury and compression follows a dose-response model, the critical pressure and duration relationships for chronic nerve compression have not been determined. For the spinal nerve roots, adjacent tissue compression may release cytokines that stimulate pain transmission.

Age can influence the mechanical and biological properties of bone, disc, muscle, and nerve. Increasing age leads to increased degenerative

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