Musculoskeletal Disorders. Sean Gallagher
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Mary F. Barbe
Temple University, Philadelphia, PA, USA
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To Dad and Mom, who set a high bar; to Nancie for her constant love and support; and to Drew and Brendon for being wonderful and thoughtful sons.
Sean Gallagher
To my parents, who taught me how to dream; to Hugh, the love of my life, for his continued aid and support; and to Susan, my twin and other half of my soul, for always being my best friend, companion, and muse.
Mary F. Barbe
Preface
During the course of my [SG’s] doctoral work with Dr. William S. Marras, I became familiar with the work of researchers such as Adams, Cyron, Hutton, and Brinckmann who had performed ex vivo studies examining the effects of repeated stress on fatigue failure of spinal motion segments (Adams & Hutton, 1985; Brinckmann, Biggemann, & Hilweg, 1988; Cyron & Hutton, 1978). When the time came to select a dissertation topic, the option of performing an ex vivo fatigue failure study on spines at different levels of forward flexion was offered and I accepted the opportunity. The results of our research showed once again that spines subjected to repeated stress exhibited a classic fatigue failure response, and that the relationship is also affected by the degree of flexion of the motion segments adopted (Gallagher et al., 2007).
This research added to the existing body of evidence that cadaveric spinal motion segments fail in accordance with the mechanism of fatigue failure. However, though ex vivo fatigue failure data (on various musculoskeletal tissues) had been accumulating for some time, the implications of this mechanism regarding tissue damage were generally neither reflected in the development of musculoskeletal risk assessment tools nor in epidemiological studies examining musculoskeletal disorder risk factors. It is not entirely clear why this is the case, but it is the author's belief that researchers were reluctant to assume that this process would work in a similar manner in the setting of a complex biological system. This is understandable as no real evidence existed at that time that such a process was actually taking place in vivo.
One day in 2011, I had just finished giving a fatigue‐based presentation to some of my NIOSH colleagues in Pittsburgh and was walking out of the conference room door when I suddenly realized that the S–N curve (which governs the fatigue failure response of materials) would predict a specific pattern of interaction between the risk factors of force and repetition and that the interaction predicted would look exactly like the interaction observed in the classic studies by Silverstein et al. for carpal tunnel syndrome and by Armstrong et al. for hand‐wrist tendinitis (Armstrong, Fine, Goldstein, Lifshitz, & Silverstein, 1987; Silverstein, Fine, & Armstrong, 1987).
This result strongly suggested that a fatigue failure process might indeed be occurring in vivo. This finding piqued my curiosity and I then performed (with my NIOSH collaborator John Heberger) a systematic review of epidemiology studies in the ergonomics literature that had tested for a force‐repetition interaction. The goal was to examine whether studies that had tested the interaction found a pattern indicative of a fatigue failure process (like the aforementioned studies). Results of this review showed only twelve studies in the literature that reported results of a statistical test for the interaction of force and repetition (or which provided data by which such an interaction could be examined). Of these, ten provided data indicative of the predicted pattern, one that tested for such an interaction consisted only high force tasks (where the test for interaction was meaningless), and in the other, the relationship was not present (Gallagher & Heberger, 2013). Overall, the results of this systematic review provided compelling evidence that many musculoskeletal disorder (MSD) outcomes exhibited a pattern of force and repetition that would suggest that a fatigue failure process might be an important etiological factor. This appeared to be the case across a wide range of disorders and joints.
Concurrent with the development of this paper, I met Mary Barbe, whose novel rat model provided additional support that fatigue failure of musculoskeletal tissues occurs in vivo. Her research demonstrated that damage to tendons, bone, and cartilage all followed the fatigue failure predicted force‐repetition pattern (Barbe et al., 2013). The same was true for many cytokines, whose expression appears to be tied to the amount of damage occurring in musculoskeletal tissues (Barr, Barbe, & Clark, 2004). Since that time, we have continued to collaborate on numerous papers and projects.
In 2018, I asked Mary if she would be willing to collaborate on