Pathophysiology of Work-Related Musculoskeletal Disorders





CRITICAL POINTS


Risk Factors for Development of Musculoskeletal Disorders





  • Workplace Factors




    • Repetition



    • Force



    • Awkward, extreme, or fixed postures



    • Cold temperatures



    • Vibration



    • Job-related psychosocial factors




  • Nonworkplace Factors




    • History of injury or disease affecting musculoskeletal tissue(s) (comorbidities)



    • Nonwork activities and lifestyle factors



    • Non-job-related psychosocial factors



    • Advanced age



    • Female gender (industry-specific)



    • Obesity




Pathophysiology of Musculoskeletal Disorders





  • Forceful or repetitive tasks can lead to tissue injury, tissue reorganization, or central nervous system (CNS) reorganization. Any of these pathways can lead to chronic disability if causal factors are perpetuated or if appropriate interventions are not implemented.



  • Repeated microtrauma to previously injured tissues prevents normal healing and reconstitution of structure and physiology.



  • There is an exposure-response relationship between ergonomic factors (e.g., force and repetition) and the severity of musculoskeletal disorders (MSDs), with higher levels of exposure leading to greater pathology.



  • Tissue injury or reorganization can occur in multiple tissues, including muscle, tendon, loose connective tissue, peripheral nerve, and bone.



  • Tissue injury elicits an inflammatory response, which may be acute or chronic (or both) or systemic. Systemic inflammation can cause widespread symptoms.



  • Tissue reorganization is typically pathophysiologic (e.g., degenerative changes, fibrosis) in animal models and human studies of MSD. Compromised tissues have reduced tolerance for exposure to repetitive or forceful tasks and are more vulnerable to reinjury, thus perpetuating a cycle of injury, pain, and disability.



  • Awareness of the pathophysiologic processes involved with MSDs can facilitate development of effective intervention and prevention strategies.





Musculoskeletal Disorders


This chapter reviews current knowledge about the pathophysiologic mechanisms of work-related MSDs. It is important for the clinician to appreciate the pathophysiology of MSDs in order to develop effective interventions and prevention tactics. The U.S. Department of Labor defines MSDs as injuries or disorders of muscles, nerves, tendons, joints, cartilage, or spinal disks associated with exposure to risk factors in the workplace. Examples of MSDs include sprains, strains, tears, back pain, soreness, carpal tunnel syndrome, and musculoskeletal or connective tissue diseases. Upper extremity diagnoses commonly associated with MSDs include tendinopathies, nerve compression or entrapment syndromes, vascular disorders, muscular disorders, joint disorders, and regional complaints of pain that cannot be attributed to a specific clinical diagnosis. MSDs account for a significant proportion of work injuries and workers’ compensation claims in Western industrialized nations (see Chapter 140 ). The economic toll of MSDs is staggering. Direct and indirect costs for work-related injuries were estimated to be $54 billion annually for reported cases.


Documentation of the phenomenon of repetitive motion injury dates back to 1713, when “writer’s cramp” symptoms among scribes and notaries were reported by Ramazzini in his book titled De Morbis Artificum . Ramazzini wrote, “The maladies that affect the clerks arise from three causes: first, constant sitting; secondly, incessant movement of the hand and always in the same direction; and thirdly, the strain on the mind … the incessant driving of the pen over paper causes intense fatigue of the hand and the whole arm because of the continuous … strain on the muscles and tendons.”


Contemporary reviews of epidemiologic research found evidence that MSDs of the hand and wrist have been associated with performance of repetitive and forceful tasks; performance of tasks in awkward, extreme, or fixed postures; in cold temperatures; and with vibration. The National Research Council and Institute of Medicine review of studies related to MSDs supported the association between both physical and psychosocial workplace exposures and upper extremity MSDs.


Work in certain industries increases the risk of developing a MSD. In 2006, occupations with the highest number of MSDs were nursing aides, orderlies, attendants; laborers; freight, stock, material movers; and tractor-trailer drivers. A sizable percentage (18%) of MSDs occur in the manufacturing sector. These epidemiologic trends clearly suggest that the task demands associated with certain jobs are related to the incidence of MSDs. In addition, specific ergonomic and job sector risk factors and nonworkplace factors such as individual predisposition and comorbidities (see Critical Points for a list all risk factors) can play a role in the development of MSDs. For example, a sewing machine operator with a history of fibromyalgia, degenerative joint disease, and heavy cigarette smoking is at greater risk for developing an MSD than is an otherwise healthy nonsmoker who performs that same job. The relative contributions of these nonworkplace risk factors are elusive and may vary greatly among individuals. Further study of the role of nonworkplace factors is needed.


The exposure-response relationships between repetitive tasks and MSDs in the upper extremities have not been well defined. Scientific investigation in this area is ongoing. Multiple studies suggest a strong relationship between the development of MSDs and the interactive effects of repetition and force. Silverstein and colleagues reported that prevalence ratios for MSDs were 3.6 for high-repetition/low-force tasks, 4.9 for low-repetition/high-force tasks, and 30.3 for high-repetition/high-force tasks. This suggests that force and repetition have a more than additive effect in increasing the risk for development of MSDs.


A large number of studies using animal models (summarized in Tables 137-1 to 137-4 ) have illustrated the exposure-response relationship among repetitive tasks, tissue injury, and behavioral changes. For example, Barbe and coworkers reported exposure-dependent differences in proinflammatory cytokines/chemokines, macrophages, and grip strength based on exposure to low- or high-repetition reaching in rats. Using the same rat model, other studies from the same lab found declines in motor performance were greater with high-repetition/negligible-force reaching than with low-repetition/negligible-force reaching. Clark and associates found that declines in median nerve conduction velocity and motor performance were greater after exposure to high-force repetitive reaching versus negligible-force repetitive reaching. Compared with Clark and associates’ findings in rats that performed high-repetition/negligible-force reaching, Elliott and colleagues found 17% fewer inflammatory cells in the median nerve and delayed macrophage infiltration into the nerve in rats that performed a low-repetition/negligible-force task. Elliott and colleagues also found fewer TNF-α-positive cells than did Al-Shatti and coworkers, who exposed rats to high-repetition/negligible-force reaching. Nakama and associates found that adverse microstructural changes were greater with a higher rate of repetition in rabbit flexor digitorum profundus tendon. Findings such as these illustrate that the magnitude of exposure is related to the severity of pathophysiologic change.



Table 137-1

Summary of Animal Studies Exploring Soft Tissue Changes in Response to Repetitive Motion













































































































Reference Model/Tissue Exposure Key Findings



  • Rabbit



  • Achilles tendon




  • Electrically induced kicking



  • 2 hr/day



  • 3 days/week



  • 11 weeks

11 weeks: Increased mRNA expression of type III collagen and matrix metalloproteinase
Rat supraspinatus tendon


  • Decline treadmill running



  • 1 hr/day



  • 5 days/week



  • 1–4 weeks

2 and 4 weeks: Up-regulation of multiple cartilage-specific genes; down-regulation of genes normally associated with tendon phenotype



  • Rabbit



  • Achilles tendon




  • Electrically induced kicking



  • 2-hr sessions



  • 3 days/week



  • 5–6 weeks




  • 4 weeks: Irregular tendon thickening



  • 5–6 weeks: Degeneration and matrix reorganization in tendon; paratendon fibrosis, vascularity, inflammatory cells, and edema




  • Rat



  • Forelimb and palm



  • Tendon, connective tissue, and muscle; serum




  • High-rate/negligible-force reaching



  • 2 hr/day



  • 3 days/week



  • 3–8 weeks




  • 3–8 weeks: Increased ED1-IR macrophages in palm



  • 4–8 weeks: Increased ED1-IR macrophages in forearm



  • 6 and 8 weeks: Fraying of tendon fibers and increased ED2-IR macrophages in forearm



  • 8 weeks: Increased serum IL-1α




  • Rat



  • Forelimb flexor muscle, tendon and loose connective tissue



  • Serum




  • High-repetition/negligible-force or low-repetition/negligible-force reaching



  • 2 hr/day



  • 3 days/week



  • 6–8 weeks




  • Week 6: Increased loose connective tissue macrophages with low repetition



  • Weeks 6 and 8: Increased serum IL-1α, IL-1β, TNF-α, MIP2, MIP3a, and RANTES with high repetition; increased serum MIP2 and MIP3a with low repetition



  • Week 8: Increased tissue IL-1α, IL-1β, TNF-α, and IL-10 with high repetition; increased IL-10 with low repetition




  • Rat



  • Forelimb and palm



  • Tendon and muscle




  • High-rate/negligible-force reaching



  • 2 hr/day



  • 3 days/week



  • 2–9 weeks




  • 3 weeks: Increased heat shock protein-72-IR in lumbricals



  • 4 weeks: Increased heat shock protein-72-IR in forelimb flexor muscles and tendons




  • Rat



  • Supraspinatus tendon




  • Decline treadmill running with or without experimental alteration of tendon



  • 17 min/day



  • 1 hr/day



  • 5 days/week



  • 4–8 weeks




  • 4 and 8 weeks: Increased cellularity, collagen disorganization, and cross-sectional areas with greater increase in altered tendons



  • 8 weeks: Degradation of material properties (tissue modulus, maximum stress)




  • Rat



  • Soleus

Forced lengthening 5 × 10 repetitions


  • 48 hr after exercise: Increased unsulfated chondroitin proteoglycans



  • 72 hr after exercise: decreased chondroitin 6-sulfate; increased concanavalin A and heparin sulfate




  • Rat



  • Tibialis anterior




  • Repeated isometric or eccentric contractions



  • 20×/min



  • 3–15 min




  • Eccentric: Decreased peak isometric torque after 60 contractions; fiber swelling, centralization of nuclei, infiltration of mononuclear cells after 180 contractions



  • Isometric: Decreased peak isometric torque after 60 contractions; fiber swelling after 300 contractions




  • Rat



  • Gastrocnemius muscle–tendon unit

Cast immobilization ×3 weeks followed by treadmill running 3–11 weeks Recovery of tenascin-C after 8 weeks of running; expression of tenascin-C was exposure-dependent



  • Rat



  • Triceps surae




  • Electrically induced eccentric contractions



  • 1-hr sessions



  • 3 days/week



  • 7–11 weeks




  • 5 weeks: Fibrillation and hypervascularization



  • 7 weeks: Hypervascularization, decreased proteoglycans



  • 7–11 weeks: Increased substance P and CGRP, hypervascularization, increased nerve filaments




  • Rabbit



  • Flexor digitorum profundus tendon




  • Electrically induced contraction



  • 60 reps/min



  • 2 hr/day



  • 3 days/week



  • 14 weeks

14 weeks: Increased microstructural changes (tear area, tear density, and mean tear size); increased VEGF, VEGFR-1, and CTGF cell densities



  • Rabbit



  • Flexor digitorum profundus tendon




  • Electrically induced contraction



  • 10 reps/min



  • 2 hr/day



  • 3 days/week

14 weeks: Increased microstructural changes (tear area, tear density, and mean tear size) in outer regions of tendon; less than with higher repetition rate in earlier studies



  • Rat



  • Supraspinatus tendon




  • Decline treadmill running



  • 1 hr/day



  • 5 days/week



  • 3 days–16 weeks




  • 3 days–16 weeks: Increase in vascular endothelial growth factor and von Willebrand factor



  • 3 days and 8 weeks: Increase in 5-lipoxygenase-activating protein



  • 8 weeks: Increase in cyclooxygenase-2




  • Rat



  • Supraspinatus tendon ( n = 36)




  • Decline treadmill running



  • 1 hr/day



  • 5 days/week



  • 4–16 weeks

4, 8, and 16 weeks: Increased cellularity, collagen disorganizaton, increased cross-sectional area, degradation of material properties



  • Rat



  • Supraspinatus tendon




  • Decline treadmill running with or without extrinsic compression



  • 1 hr/day



  • 5 days/week



  • 4–16 weeks

4, 8, and 16 weeks: Increased cellularity, collagen disorganization, increased cross-sectional area, degradation of material properties



  • Rat



  • Soleus muscle




  • Slow or fast forced lengthening



  • 3×/week



  • 4–6 weeks




  • Slow stretch: Increased muscle mass, myofiber area, collagen struts



  • Fast stretch: Increased muscle mass; decreased myofiber area; myofiber splitting and increased type A fibers; fibrosis




  • Rat



  • Soleus muscle




  • Forced lengthening



  • 50 strains/day



  • 5×/week



  • 6 weeks

Hypervascularity: Decreased muscle mass and myofiber area; increased noncontractile tissue and collagen content



  • Rat



  • Supraspinatus tendon




  • Decline treadmill running



  • 1 hr/day



  • 5 days/week



  • 4 weeks

4 weeks: Increased mRNA expression of inducible and endothelial nitric oxide synthase



  • Monkey



  • Digit flexor tendon




  • Repetitive reaching/grasping



  • 1.5 hr/day



  • 24 weeks

One of three animals with increased tenocytes density, disorganized collagen, and large areas of pink-stained glycosaminoglycans

CGRP, calcitonin gene-related peptide; CTGF, connective tissue growth factor; ED1-IR, infiltrating immunoreactive macrophages; ED2-IR, resident immunoreactive macrophages; IL-1α, interleukin-1α; IL-1β, interleukin-1β; IL-10, interleukin-10; MIP2, macrophage inflammatory protein 2; MIP3a, macrophage inflammatory protein 3; mRNA, messenger RNA; RANTES, Normal T-cell Expressed and Secreted; TNF-α, tumor necrosis factor-α; VEGF, vascular endothelial growth factor; VEGFR-1, vascular endothelial growth factor receptor 1.


Table 137-3

Summary of Animal Studies Exploring Peripheral Nerve Changes in Response to Repetitive Motion or Compression












































Reference Model/Tissue Exposure Key Findings



  • Rat



  • Median nerve




  • High-repetition/negligible-force reaching and grasping



  • 2 hr/day



  • 3 days/week



  • 3–8 weeks




  • Week 3: Increased IL-6



  • Week 5: Increased IL-6, IL-1α, IL-1β, TNF-α, and IL-10



  • (All returned to control levels by week 8)




  • Rat



  • Median nerve




  • High-repetition/negligible-force repetitive reaching and grasping



  • 2 hr/day



  • 3 days/week



  • 3–12 weeks




  • 4 weeks: Motor degradation



  • 5–6 weeks: Increased ED1+ macrophages



  • 8 weeks: Increased collagen (fibrosis)



  • 9–12 weeks: Decline in nerve conduction velocity



  • 12 weeks: Increased connective tissue growth factor; degraded myelin basic protein




  • Rat



  • Median nerve




  • High-repetition/high-force repetitive reaching and grasping



  • 2 hr/day



  • 3 days/week



  • 12 weeks




  • Declines in motor performance over 12 weeks



  • 12 weeks: Increased ED1+ macrophages; increased type I collagen and connective tissue growth factor; declines in grip strength and nerve conduction velocity, increase in sensory threshold




  • Rat



  • Median nerve



  • Spinal cord




  • Low-repetition/negligible-force reaching and grasping



  • 2 hr/day



  • 3 days/week



  • 12 weeks




  • Week 8: Increased substance P and neurokinin-1 in spinal cord dorsal horn



  • Week 12: Increased ED1+ macrophages and TNF-α in distal nerve and increased neurokinin-1 in spinal cord dorsal horn




  • Rat



  • Sciatic nerve




  • Silastic tubing-induced compression



  • 1–6 months

Demyelination and degeneration/regeneration; hypervascularity; intraneural fibrosis, decreased nerve conduction velocity



  • Primate



  • Median nerve

4–12 months Demyelination; decreased neural tissue in fascicles; intraneural fibrosis



  • Primate



  • Median nerve




  • Moderate-force repetitive reaching



  • 8 hr/day



  • 5 days/week



  • 3–4 months

Declines in nerve conduction velocity in three of four working hands; enlargement of nerves; recovery of NCV after termination of task exposure

ED1+, immunoreactive macrophages; IL-1α, interleukin-1α; IL-1β, interleukin-1β; IL-6, interleukin 6; IL-10, interleukin-10; NCV, nerve conduction velocity; TNF-α, tumor necrosis factor-α.


Table 137-4

Summary of Animal Studies Exploring the Effects of Repetitive Motion on Behavior



























































Reference(s) Model Exposure Key Findings
Rat


  • High-repetition/negligible-force reaching and grasping



  • 2 hr/day



  • 3 days/week



  • 3–11 weeks




  • Decline in reach rate at weeks 5 and 6; decline in task duration at week 5; increased “scooping” and “raking” behavior at week 5 (observed in all animals by week 7–8)



  • “Scooping” behavior returned to baseline during this period; all animals demonstrated “raking” by week 11; decrease in reach rate in weeks 9–11




  • Rat



  • Forelimb flexor muscle, tendon and loose connective tissue



  • Serum




  • High-repetition/negligible-force or low-repetition/negligible-force reaching and grasping



  • 2 hr/day



  • 3 days/week



  • 6–8 weeks

Decreased grip strength at weeks 6 and 8 in the high-repetition group, and at week 6 in the low-repetition group
Monkey


  • Opening/closing of hand



  • 1–2 hr/day



  • 12–25 weeks




  • Difficulty removing hand from handpiece (1 animal at 5 weeks and 1 at 8 weeks)



  • Difficulty with grip contact (both animals) late in training period



  • Reduced grip accuracy in 1 animal late in training period

Monkey


  • Repetitive closure of handpiece



  • 300–400 trials/day



  • 20 weeks




  • Decreased grip force at weeks 5 and 8



  • 60% decline in task performance speed and decreased food retrieval efficiency in 1 of 2 animals

Rat


  • Low-repetition and low-force reaching and grasping



  • 2 hr/day



  • 3 days/week



  • 12 weeks

Increased movement reversals at week 8; trend for reduced task duration at week 12
Rat


  • High- or low-repetition/negligible-force reaching and grasping



  • 2 hr/day



  • 3 days/week



  • 6–9 weeks

Decline in reach rate at weeks 6 and 9; increased number of reach reversals and total reach time at week 9 in both high- and low-repetition groups
Rat


  • Low-repetition/negligible-force; high-repetition/negligible-force; high-repetition/high-force reaching and grasping



  • 2 hr/day



  • 3 days/week



  • 6 weeks




  • Reach rate declined in both high-repetition groups at week 6



  • Task duration declined at week 3 in both high-repetition groups, and persisted at week 6 in the high-repetition/high-force group



  • Movement reversals, reach time, and grasp time increased in the high-repetition/high-force group at week 6

Rat


  • Electrically induced eccentric contractions



  • 1-hr sessions



  • 3 days/week



  • 7–11 weeks

Adverse gait changes in 2 rats at 3 and 4 weeks; limping in 1 rat at 3 weeks
Primate


  • Moderate-force repetitive reaching



  • 8 hr/day



  • 5 days/week



  • 3–4 months

Declines in attempts and successes in 2 of 4 animals; decline in successful trials per day in 2 of 4 animals around the time of diagnosis of carpal tunnel syndrome
Monkey


  • Repetitive reaching/grasping



  • 1.5 hr/day



  • 24 weeks

Difficulty gripping and reduced ability to flex digits in 1 animal at 5 weeks and the other animal at 24 weeks

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Apr 21, 2019 | Posted by in PHYSICAL MEDICINE & REHABILITATION | Comments Off on Pathophysiology of Work-Related Musculoskeletal Disorders
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