A model for wrist and elbow musculoskeletal disorders.
Rempel-D; King-K; Nakama-L; Abrahamsson-S
NIOSH 2006 Sep; :1-130
The prevention of work-related tendionopathies, a group of common and debilitating disorders associated with hand intensive work, is hampered by the limitations of epidemiologic studies to clearly identify specific and generalizable risk factors, especially biomechanical risk factors. The purpose of this research was to use a rabbit model to investigate the effects of long-term, repetitive, digit loading on structural and cellular changes of degeneration on the tendon at the epicondyle. The goals were to study the pathophysiologic mechanisms of tendon damage and to determine the relative contribu1ions of various biomechanical characteristics of loading, such as repetition rate and applied force to injury. An in vivo rabbit model was developed to expose the tendon to repetitive loading for 2 hours per day, 3 days per week for 12 weeks (80 cumulative hours). Three combinations of peak forces (High: 0.42N; Low: 0.14N) and repetition rates (High: 60 reps/min; Low: 10 reps/min) were selected: High Force/High Repetition (HFHR), High Force/Low Repetition (HFLR) and Low Force/High Repetition (LFHR). At the end of the exposure period, changes to tendon microstructure and biology were measured. Microtears were quantified using photomicroscopy and image analysis methods. Biological changes were measured by immunohistochemical staining of cells for growth factors associated with angiogenesis and matrix repair (VEGF, VEGFR-1 and CTGF). Microtears were increased under HFHR loading. There were moderate increases with HFLR loading and no changes associated with LFHR loading. Dose-response relationships were observed for both force and repetition with tear measures being affected more by peak force than repetition rate. Cell densities of VEGF, VEGFR-1 and CTGF staining cells were increased under HFHR loading. No changes were found under the other loading conditions. VEGF staining cell density correlated to microtears (tear density) regardless of the loading pattern. VEGFR-1 cell density, the main receptor for VEGF, was associated to tear density only under HFHR loading. This is the first study to systematically document the relationship between repetitive loading of the upper extremity and the formation of microtears in tendon. Microtears have been hypothesized as being a mediator or the initial route of damage in tendon/leading ultimately to chronic tendinosis, but the evidence has been missing until now. The results of this study provide evidence at the basic science level for a relationship between repetitive loading of the upper extremity and injury to tendons. As the tendon experiences repetitive loading, microtears may accumulate causing a cellular response, such as an up-regulation of VEGFR-1. This suggests a pathway for inflammatory and angiogenic mediators further downstream in tendon degeneration. The study also provides evidence that during repetitive loading, the peak force of the load contributes more to microtear damage to the tendon than the repetition rate. These findings suggest that in order to decrease risk of tendon related injuries among workers due to hand intensive tasks, greater benefit may be obtained by reducing the peak hand loads than by reducing repetition rates.
Musculoskeletal-system-disorders; Epidemiology; Arm-injuries; Back-injuries; Hand-injuries; Models; Injuries; Repetitive-work; Animals; Animal-studies; Ergonomics; Cumulative-trauma; Cumulative-trauma-disorders; Laboratory-animals; Muscles; Repetitive-work; Carpal-tunnel-syndrome; Neurological-system; Neuromotor-activity; Neuropathology; Neurotransmitters; Biomechanical-modeling; Biomechanics
David Rempel, Ergonomics Program, Division of Occupational and Environmental Medicine, University of California, San Francisco, 1301 South 46th Street, Building 163, Richmond, CA 94804
Final Grant Report
Disease and Injury: Musculoskeletal Disorders of the Upper Extremities
National Institute for Occupational Safety and Health
University of California - San Francisco