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Increased tendon calcification and a bone mineralization protein in musculoskeletal tissues with repetitive reaching task.

Authors
Barr-AE; Hobbs-HK; Amin-M; Safadi-FF; Barbe-MF
Source
Temple Univ J Orthop Surg Sports Med 2008 Mar; 3:105-106
NIOSHTIC No.
20041719
Abstract
Work-related musculoskeletal disorders (WMSDs) arise from repeated performance of tasks at submaximal levels of physical exertion that eventually lead to tissue damage due, perhaps, to insufficient recovery of tissues between bouts of performance. Our laboratory has developed a rat model of repetitive and forceful reaching and grasping. Our results indicate that performance of a high rate, low force (HRLF) task regimen results in injury, inflammation and fibrosis in bone, muscles, tendons, nerves and associated loose connective tissues. Osteoactivin (OA) is a recently identified factor that plays a role in bone mineralization and possibly in wound healing and inflammation. Enhanced expression of this protein would suggest that repetitive and/or forceful tasks lead to accelerated bone remodeling and tendon matrix changes, which would further our understanding of the etiology of MSDs. The purpose of this current study was to examine the production of OA in musculoskeletal tissues and tendon calcification following performance of these repetitive and/or forceful tasks for up to 12 weeks. Methods: Young adult, female Sprague-Dawley rats were used. Experimental rats were trained in one of two repetitive tasks. These tasks consisted of reaching forward to pull a lever at a rate of 4 reaches/min at either 15% of maximum grip strength (HRLF) for 2 hours/day in 30 min sessions, 3 days/week for up to 12 weeks. Results were compared to control rats, which are considered week 0 in this study. Following euthanasia using Nembutal (120 mg/kg body weight), rats were perfused intracardially with 4% paraformaldehyde. Musculoskeletal tissues were harvested. Soft tissues were dissected out and frozen sectioned en bloc into 15 micrometer longitudinal sections, while bones were paraffin embedded and cut into 5 micrometer sections, before mounting on coated slides. Tissue sections on slides were analyzed for the presence of calcium salts using von Kossa staining. Sections with tendons were stained in 3% silver nitrate solution for 1.5 hours under intense light, rinsed in distilled water, 5% sodium thiosulfate for 2 minutes, and counterstained with nuclear red. For localization of OA, sections were blocked for endogenous peroxidase, washed, permeabilized with 0.05% Pepsin solution in 0.01N HCL, washed and blocked for nonspecific binding with 10% goat serum for 20 minutes. Primary antibody raised against the c-terminal sequence of osteoactivin was diluted 1:100 with PBS and incubated on slides overnight at room temperature. After washing, sections were incubated with appropriate secondary antibody conjugated to HRP, and visualized using DAB with or without cobalt (black versus brown, respectively). Percent area with OA immunoreactivity was quantifi ed using the Osteo II Bioquant program using methods described previously. Two-way ANOVA (p
Keywords
Musculoskeletal-system; Musculoskeletal-system-disorders; Work-environment; Repetitive-work; Force; Physical-reactions; Physical-capacity; Tissue-culture; Animals; Laboratory-animals; Fibrosis; Bone-structure; Muscles; Nerve-tissue; Nerve-function; Proteins; Etiology; Cumulative-trauma; Cumulative-trauma-disorders
Publication Date
20080301
Document Type
Abstract
Funding Type
Cooperative Agreement
Fiscal Year
2008
NTIS Accession No.
NTIS Price
Identifying No.
Cooperative-Agreement-Number-U01-OH-008599
Source Name
Temple University Journal of Orthopaedic Surgery & Sports Medicine
State
PA
Performing Organization
Temple University, Philadelphia, Pennsylvania
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