The pathophysiology of mechanical LBP remains complex and multifaceted. Multiple anatomic structures and elements of the lumber spine (eg, bones, ligaments, tendons, disks, muscle) are all suspected to have a role. Many of these components of the lumber spine have sensory innervation that can generate nociceptive signals representing responses to tissue-damaging stimuli. Other causes could be neuropathic (eg, sciatica). Most chronic LBP cases most likely involve mixed nociceptive and neuropathic etiologies.
Biomechanically, the movements of the lumbar spine consist of the cumulative motions of the vertebrae, with 80-90% of the lumbar flexion/extension occurring at the L4-L5 and L5-S1 intervertebral disks. The lumbar spine position most at risk for producing LBP is forward flexion (bent forward), rotation (trunk twisted), and attempting to lift a heavy object with out-stretched hands. Axial loading of short duration is resisted by annular collagen fibers in the disk. Axial loading of a longer duration creates pressure to the annulus fibrosis and increased pressure to the endplates. If the annulus and endplate are intact, the loading forces can be adequately resisted. However, compressive muscular forces may combine with the loading forces to increase intradiscal pressure that exceeds the strength of the annular fibers.
Repetitive, compressive loading of the disks in flexion (eg, lifting) puts the disks at risk for an annular tear and internal disk disruption. Likewise, torsional forces on the disks can produce shear forces that may induce annular tears. (Degenerative disk forces are demonstrated in the image below.)
In lumbar flexion, the highest strains are recorded within the interspinous and supraspinous ligaments, followed by the intracapsular ligaments and the ligamentum flavum. In lumbar extension, the anterior longitudinal ligament experiences the highest strain. Lateral bending produces the highest strains in the ligaments contralateral to the direction of bending. Rotation generates the highest strains in the capsular ligaments.
Research since the late 20th century suggests that chemical causes may play a role in the production of mechanical LBP. Components of the nucleus pulposus, most notably the enzyme phospholipase A2 (PLA2), have been identified in surgically removed herniated disk material. This PLA2 may act directly on neural tissue, or it may orchestrate a complex inflammatory response that manifests as LBP.
Mechanical low back pain (LBP) exists in every culture and country. Estimates by numerous investigators indicate that at some point in their lives, 80% of all human beings experience LBP. Mechanical LBP becomes more prevalent in countries with higher per capita income
No published information suggests that race is a factor in the prevalence of mechanical low back pain.
Age has been shown to be associated more consistently with mechanical low back pain (LBP) than with sex. the prevalence of disk degeneration increases with age, but degenerated disks are not necessarily painful.
LBP secondary to degenerative disk disease affects men and women equally.
In a systematic study review, Chen et al investigated whether a sedentary lifestyle (which the authors defined as including sitting for prolonged periods at work and during leisure time) is a risk factor for LBP. Examining journal articles published between 1998 and 2006, they identified 8 high-quality reports (6 prospective cohort and 2 case-control studies). While 1 of the cohort studies reported a link between sitting at work and the development of LBP, the other investigations did not find a significant connection between a sedentary lifestyle and LBP. Chen and coauthors concluded that a sedentary lifestyle alone does not lead to LBP.
Deyo and Tsui-Wu reported that 33.2% of patients with LBP reported symptoms for less than 1 month, 33% reported pain for 1-5 months, and 32.7% reported pain for longer than 6 months. Most patients had low levels of back pain, with 20% rating their pain at 4 or greater on a scale of 0-10 (where 0 indicates no pain), 13% rated their pain as 5 or greater, and 8% reporting pain of 6 or greater.
Von Korff and colleagues reported that 15-20% of primary care patients with LBP had moderate-to-severe limitations in activity during a 1-year follow-up after their initial episode resolved. Recurrence rates of 60-85% have been reported in the first 2 years after an acute episode of LBP