A Comparison Of Fatigue Failure Responses Of Old Versus Middle-Aged Lumbar Motion Segments In Simulated Flexed Lifting
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A Comparison Of Fatigue Failure Responses Of Old Versus Middle-Aged Lumbar Motion Segments In Simulated Flexed Lifting

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    Study Design. Survival analysis techniques were used to compare the fatigue failure responses of elderly motion segments to a middle-aged sample. Objectives. To compare fatigue life of a middle-aged sample of lumbosacral motion segments to a previously tested elderly cohort. An additional objective was to evaluate the influence of bone mineral content on cycles to failure. Summary of Background Data. A previous investiga¬tion evaluated fatigue failure responses of 36 elderly lumbosacral motion segments (average age, 81 ± 8 years) subjected to spinal loads estimated when lifting a 9-kg load in 3 torso flexion angles (0°, 22.5°, and 45°). Results demonstrated rapid fatigue failure with increased torso flexion; however, a key limitation of this study was the old age of the specimens. Methods. Each lumbosacral spine was dissected into 3 motion segments (L1-L2, L3-L4, and L5-S1). Motion segments within each spine were randomly assigned to a spinal loading condition corresponding to lifting 9 kg in 3 torso flexion angles (0°, 22.5°, or 45°). Motion segments were statically loaded and allowed to creep for 15 minutes, then cyclically loaded at 0.33 Hz. Fatigue life was taken as the number of cycles to failure (10 mm displacement after creep loading). Results. Compared with the older sample of spines, the middle-aged sample exhibited increased fatigue life (cycles to failure) in all the torso flexion conditions. Increased fatigue life of the middle-aged specimens was associated with the increased bone mineral content (BMC) in younger motion segments (mean ± SD, 30.7 11.1 g per motion segment vs. 27.8 ± 9.4 g). Increasing bone mineral content had a protective influence with each additional gram increasing survival times by approximately 12%. Conclusion. Younger motion segments survive considerably longer when exposed to similar spine loading conditions that simulate repetitive lifting in neutral and flexed torso postures, primarily associated with the increased bone mineral content possessed by younger motion segments. Cycles to failure of young specimens at 22.5° flexion were similar to that of older specimens at 0° flexion, and survivorship of young specimens at 45° flexion was similar to the older cohort at 22.5°. Key words: biomechanics, low back disorders, fatigue failure, age, motion segments, vertebral endplate fractures, torso flexion, lifting, bone mass. Low back disorders (LBDs) are a major cause of both short- and long-term occupational disability in the United States, and it is clear that workers in certain occupations are more susceptible to LBD.2-5 Specifically, epidemiologic studies have shown that jobs involving heavy physical demands such as construction,2,3 mining,2,4 and farming,5 engender increased risk of back pain. These occupations are thought to experience high LBD rates as a result of their extreme postural and manual lifting demands. Studies have shown that jobs involving significant lifting 6-9 and jobs that involve frequent bending10-12 are associated with increased LBD risk. Workers in the mining industry, in particular, often have to lift heavy materials in restricted workspaces that compel torso flexion. An understanding of the impact of repeated loading of the spine in flexion on fatigue failure of spinal tissues is thus a critical issue for our research agency, which is concerned with reducing the pain and disability associated with LBD in the mining industry. It is well accepted that loads experienced by the spine during manual lifting tasks are sufficient to cause fractures in the endplates of lumbar vertebrae, particularly on repeated loading. 13-15 Endplate fractures may not be painful in and of themselves 16; however, evidence suggests that the process of internal disc disruption and disc degeneration may be initiated via endplate fractures. 16,17 It has been shown that endplate damage will alter the distribution of stress in the disc, resulting in buckling of the lamellas of the internal
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