of approximately 30% (Andersson, 1999). Sixty percent of those who suffer from acute LBP recover in 6 weeks and up to 80–90% recover within 12 weeks; however, the recovery of the remaining patients with LBP is less certain (Andersson, 1999).
Historical data suggest that in Americans less than 45 years of age, chronic LBP is the commonest cause of disability (Kelsey & White 3rd, 1980; Waddell, 1987). Each year, 3–4% of the US population is temporarily disabled, and 1% of the working‐age population is totally and permanently disabled by LBP (Andersson, 1999; Cunningham & Kelsey, 1984; Mayer & Gatchel, 1988). Difficulty most often begins between 20 and 40 years of age (Casazza, 2012). Men and women are approximately equally affected (“Back Pain Fact Sheet”, NINDS, 2014). LBP is more common among people aged between 40 and 80 years, with the overall number of individuals affected expected to increase as the population ages (Hoy, 2012).
Although common in the general population, there is considerable evidence that LBP risk is exacerbated by the performance of occupational tasks, and account for a significant portion of morbidity in occupational settings. A great deal of evidence suggests that heavy physical work, repetitive lifting, prolonged static work postures, bending and twisting, and exposure to whole‐body vibration likely contribute to the development of LBP (National Institute for Occupational Safety and Health [NIOSH], 1997; National Research Council – Institute of Medicine, 2001). Jobs that are highly demanding, that involve prolonged standing, and that require awkward lifting are among work‐related physical risk factors for LBP (Sterud & Tynes, 2013).
Anatomy/pathology
The lumbar spine is a complex structure composed of several different materials (see Figures 2.1–2.3), many of which have been touted as potential sources of LBP. Some of the potential pain‐generating structures include the intervertebral disk, facet (zygopophyseal) and sacroiliac joints, spinal nerve roots, and the muscles that attach to the bony processes of the vertebra (Chawla, 2018).
Figure 2.1 A motion segment of the lumbar spine.
Duckworth, T. & Blundell, C. M. (2010). Lecture notes: Orthopaedics and fractures, 4th ed., Wiley. ISBN: 978‐1‐405‐13329‐6.
Figure 2.2 Focal damage in the intervertebral disc. Fissures of grade 1 (grade 2 not shown) and circumferential tears are not likely to be symptomatic. However, grade 3 fissures are highly associated with chronic back pain. Cartilage endplate damage is also shown.
Fournier, D.E., Kiser P.K., Shoemaker, J.K., Battié, M.C., & Séguin, C.A. (2020). Vascularization of the human intervertebral disc: a scoping review. JOR Spine, 3(4): e1123. doi: 10.1002/jsp2.1123 / John Wiley & Sons / CC BY‐4.0.
Figure 2.3 Lumbar vertebrae and their facet (zygopophyseal) joints, which are the articulation of superior and inferior processes.
The intervertebral disc has been shown to be a structure capable of causing pain. Kuslich, Ulstrom, and Michael (1991) demonstrated that pain could be elicited by the use of surgical instruments or a low voltage electrical current stimulating the annulus fibrosis of the disc. The process of internal degeneration of the disc has also been implicated in the development of pain (Bogduk, Aprill, & Derby, 2013). Specifically, fissures radiating outward from the nucleus pulposus as the disc degenerates appear to be highly correlated with pain report from patients, especially as these fissures move into the outer third of the disc, where pain fibers are known to exist (Figure 2.2). The action of proinflammatory cytokines has also been implicated in the development of intervertebral disc pain (Zhang, 2016). The slow rate of tissue repair in the poorly perfused intervertebral disc has been suggested as a possible factor in patients experiencing chronic LBP (Chawla, 2018).
Facet joints (Figure 2.3), or more properly zygopophyseal joints, are a small set of joints formed by the superior and inferior articular processes of adjacent vertebrae. These joints are believed, when loaded, to develop wear and tear of the gliding surfaces of the joint, which may lead to arthritis over time (Eisenstein & Parry, 1987; Farfan, 1973). Bending forward and/or side‐to‐side bending is believed to place damaging stress concentrations on the cartilage surface of the joints, leading to degeneration (Farfan, 1973). As the facet joint begins to degenerate, small defects in the joint surfaces appear. As with the disc, the cartilage surfaces of the facet joints have limited blood supply, which impedes the body’s ability to repair the damage. This limited repair capacity makes the facet joint susceptible to degeneration. In fact, degeneration of the facet joints is believed by some to be a result of disc degeneration (Vernon‐Roberts & Pirie, 1977). This is because when a disc degenerates, it loses height. When this occurs, it causes the bone and cartilage of the facet joint (normally separated) to come into contact and grind against each other, causing degeneration of the surfaces. Studies have suggested that up to 45% of patients with back pain demonstrate facet pain and that approximately 15% of chronic LBP cases may be due to facet joint pain (Schwarzer, Aprill, & Bogduk, 1995).
The sacroiliac joint is formed where the sacrum of the spine joins the iliac bone in the pelvis, is innervated by the first four sacral nerves, and is a demonstrated source of LBP (Schwarzer et al., 1995). Data from studies involving nerve‐blocking agents suggest the prevalence of sacroiliac pain to be 2–30% in chronic LBP sufferers (Chawla, 2018).
Pathological mechanisms associated with spinal nerve root pain (or radicular pain) are not well understood. It has been hypothesized that spinal nerve roots may be vulnerable to compression, potentially leading to pain. Some early studies found that nerve roots might exhibit an inflammatory response when exposed to viable nucleus pulposus material from an intervertebral disc (McCarron, Wimpee, Hudkins, & Laros, 1987). However, degenerated nucleus pulposus material appears not to provoke such an inflammatory response (Chawla, 2018). Exposure of spinal nerve roots to the proinflammatory cytokine TNF‐α is another suggested cause, as it would be expected to provoke neuropathic pain in spinal nerves (Klyne, Barbe, & Hodges, 2017; Klyne & Hodges, 2020).
Physical risk factors/activities associated with LBP
Most experts agree that heavy physical work, lifting, prolonged static work postures, frequent bending and twisting, and exposure to vibration may contribute to back injuries. A systematic review of physical work factors performed by the NIOSH found strong evidence of a causal relationship between both lifting/forceful movements and exposure to whole‐body vibration and LBP. Evidence suggesting a causal relationship to LBP was also found for adoption of awkward postures and heavy physical work (NIOSH, 1997). A further systematic review performed by the (National Research Council–Institute of Medicine, 2001) demonstrated that activities such as manual materials handling, frequent twisting and bending, heavy physical load, and exposure to whole‐body vibration demonstrated positive association to risk of low back disorders in the preponderance of studies investigating such factors. These findings have been supported by more recent data on the relationship between LBP and occupational activities, in which tasks such as carrying, lifting heavy weight while in trunk flexion, and adoption