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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).