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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Low back pain is a symptom with several possible causes. Approximately 80–90% of patients who present with low back pain have nonspecific pain: no specific spinal disorder or referred nonspinal cause adequately explains the symptoms. The intervertebral disc, facet joints, sacroiliac joint, vertebral endplates, and lumbar soft tissues are plausible sources, but routine assessment usually cannot identify a single pain-generating structure.[1][2][3]

Causes

Etiologic categories

Low back pain is commonly grouped as nonspecific pain, pain associated with radiculopathy or spinal stenosis, or pain due to another specific spinal or nonspinal cause.[4][1] Lumbar radiculopathy and symptomatic lumbar spinal stenosis together account for approximately 5–10% of initial primary care presentations for low back pain. Disc herniation can cause radicular symptoms, but a disc abnormality alone does not establish the source of axial low back pain.[3]

Mechanical sources and structural lesions

Source or lesion Clinical context and limits of attribution
Lumbar muscles, fascia, and ligaments Lumbar strain or sprain is a presumptive explanation for some episodes after exertion or abrupt movement. There is no validated reference standard for confirming an individual soft-tissue source.[5][2]
Intervertebral disc Discogenic axial pain is distinct from radicular pain due to disc herniation. In selected patients with persistent low back pain, MRI findings such as disc degeneration, a high-intensity zone, an annular fissure, or Modic type 1 or 2 changes increased the likelihood of a disc source relative to the study reference standard. None of these findings establishes the cause of pain on its own.[6]
Facet (zygapophyseal) joints Facet joints are a plausible source of axial pain. Facet osteoarthritis can coexist with low back pain without establishing that the joint is symptomatic.[5][2]
Sacroiliac joint Reported contexts include trauma, pregnancy, older age, leg-length discrepancy, and prior lumbar or lumbosacral fusion. Inflammatory sacroiliitis is a separate cause and can occur in axial spondyloarthritis.[5][1] A multispecialty consensus guideline estimates that the sacroiliac joint complex is the pain source in 15–30% of patients with chronic, nonradicular low back pain predominantly below L5 (Grade B; moderate certainty). In selected patients with pain after lumbar or lumbosacral fusion, estimates range from 33% to 59% (Grade C; low certainty), based largely on small studies using diagnostic injections.[7] In a separate retrospective cohort, new sacroiliac joint pain occurred in 5.8% after single-segment fusion and 22.5% after fusion of four or more segments.[8]
Vertebral endplate The endplate is a proposed source of vertebrogenic pain. In a systematic review of 31 studies, 15 found a positive association between Modic changes and low back pain and one found a negative association. Only one study had low risk of bias. Associations varied with disc level and disc degeneration. A Modic change alone does not establish the cause of an individual's symptoms.[9]
Spondylolysis and isthmic spondylolisthesis A stress injury or defect of the pars interarticularis is the most frequently identified diagnosis in adolescent athletes presenting with low back pain, particularly in sports involving repetitive lumbar flexion and extension with rotation. Progression to spondylolisthesis is uncommon.[10] Reported prevalence is 4–8% in children overall and as high as 50% in selected groups of athletes presenting with back pain.[11]
Radiographic lumbar spondylolisthesis The Wakayama Spine Study found a prevalence of 15.8% using a slip threshold of ≥5%. Spondylolisthesis was associated with symptomatic lumbar stenosis (odds ratio [OR], 2.07; 95% confidence interval [CI], 1.20–3.44), but not with low back pain.[12] The second ROAD survey found a prevalence of 17.4% using a slip threshold of ≥3 mm and reported a fully adjusted association with low back pain (OR, 1.36; 95% CI, 1.03–1.80). The different radiographic definitions may contribute to the differing findings. Neither estimate was restricted to degenerative slips.[13] In a US Framingham CT substudy of 188 adults, 11.5% had lumbar spondylolysis. The study found no significant association between low back pain and spondylolysis, isthmic spondylolisthesis, or degenerative spondylolisthesis.[14] A separate meta-analysis found a weaker association with low back pain in community samples (OR, 1.12; 95% CI, 1.03–1.23) than in occupational samples (OR, 2.21; 95% CI, 1.44–3.39). A slip alone does not establish the cause of pain.[15]
Degenerative (de novo) lumbar scoliosis De novo scoliosis develops after skeletal maturity and most often affects the lumbar spine. One review reported a prevalence of approximately 6% in adults older than 50.[16] A meta-analysis of five studies in adults aged 41–94, using a Cobb angle of ≥10°, estimated a prevalence of 37.6% (95% CI, 18.7–61.8%). Differences in study populations and definitions limit direct comparison. A curve alone does not establish the source of pain.[17]
Vertebral compression fracture A symptomatic fracture is a specific structural cause of back pain. More than two-thirds of patients with osteoporotic vertebral compression fractures are asymptomatic and diagnosed incidentally. Only about one-fourth to one-third of radiographic vertebral fractures are diagnosed clinically; pain is more likely with more severe or multiple fractures. A fracture on imaging does not by itself explain current symptoms.[18][19]

Limits of source attribution

In a systematic review of 62 diagnostic-accuracy studies in persistent low back pain, 45 were conducted in tertiary care and none in primary care. Median estimates were 46% for discogenic pain, 42% for facet joint pain, and 53% for sacroiliac joint pain. These estimates came from different sets of studies and should not be added together or applied to unselected primary care patients.[6] Disc, facet, and sacroiliac sources can coexist. In one specialty cohort, discogenic pain was more common among younger patients, while facet and sacroiliac joint pain were more common among older patients.[5][20]

Degenerative findings are common in people without pain. In a systematic review of asymptomatic individuals, estimated disc degeneration increased from 37% at age 20 to 96% at age 80. An imaging finding alone is insufficient to attribute pain to a structure.[21][3]

Serious spinal and nonspinal causes

Serious spinal pathology and nonspinal referred pain are separate considerations when evaluating presumed mechanical low back pain. A systematic review estimated serious spinal pathology in 0.8% of primary care presentations, 2.1% in emergency care, 4.6% in secondary care, and 6.9% in tertiary care.[22] Specific diagnoses, red flags, and workup are covered in Differentiating back pain from other diseases.

References

  1. ↑ 1.0 1.1 1.2 Chiarotto A, Koes BW (2022). "Nonspecific low back pain". New England Journal of Medicine. 386 (18): 1732–1740. doi:10.1056/NEJMcp2032396. PMID 35507483 Check |pmid= value (help).
  2. ↑ 2.0 2.1 2.2 Maher C, Underwood M, Buchbinder R (2017). "Non-specific low back pain". The Lancet. 389 (10070): 736–747. doi:10.1016/S0140-6736(16)30970-9. PMID 27745712.
  3. ↑ 3.0 3.1 3.2 Cashin AG, Chou R, Weimer MB, McAuley JH (2026). "Low back pain: a review". JAMA. 336 (2): 144–158. doi:10.1001/jama.2026.9631. PMID 42295944 Check |pmid= value (help).
  4. ↑ Expert Panel on Neurological Imaging; Hutchins TA, Peckham M; et al. (2021). "ACR Appropriateness Criteria® Low Back Pain: 2021 Update". Journal of the American College of Radiology. 18 (11S): S361–S379. doi:10.1016/j.jacr.2021.08.002. PMID 34794594 Check |pmid= value (help).
  5. ↑ 5.0 5.1 5.2 5.3 Knezevic NN, Candido KD, Vlaeyen JWS, Van Zundert J, Cohen SP (2021). "Low back pain". The Lancet. 398 (10294): 78–92. doi:10.1016/S0140-6736(21)00733-9. PMID 34115979 Check |pmid= value (help).
  6. ↑ 6.0 6.1 Han CS, Hancock MJ, Sharma S; et al. (2023). "Low back pain of disc, sacroiliac joint, or facet joint origin: a diagnostic accuracy systematic review". EClinicalMedicine. 59: 101960. doi:10.1016/j.eclinm.2023.101960. PMID 37096189 Check |pmid= value (help).
  7. ↑ McCormick ZL, Hurley RW, Anitescu M; et al. (2025). "Consensus practice guidelines on sacroiliac joint complex pain from a multispecialty, international working group". Pain Medicine. 26 (12): 817–917. doi:10.1093/pm/pnaf129. PMID 41318933 Check |pmid= value (help).
  8. ↑ Unoki E, Abe E, Murai H, Kobayashi T, Abe T (2016). "Fusion of multiple segments can increase the incidence of sacroiliac joint pain after lumbar or lumbosacral fusion". Spine. 41 (12): 999–1005. doi:10.1097/BRS.0000000000001409. PMID 26689576.
  9. ↑ Herlin C, Kjaer P, Espeland A; et al. (2018). "Modic changes—Their associations with low back pain and activity limitation: A systematic literature review and meta-analysis". PLOS One. 13 (8): e0200677. doi:10.1371/journal.pone.0200677. PMID 30067777.
  10. ↑ Putukian M, Leclere LE, Herring SA; et al. (2026). "The adolescent athlete and the team physician: A consensus statement. 2025 update". Medicine & Science in Sports & Exercise. 58 (2): 371–402. doi:10.1249/MSS.0000000000003863. PMID 41529152 Check |pmid= value (help).
  11. ↑ Lamb M, Brenner JS (2020). "Back pain in children and adolescents". Pediatrics in Review. 41 (11): 557–569. doi:10.1542/pir.2019-0051. PMID 33139409 Check |pmid= value (help).
  12. ↑ Ishimoto Y, Yoshimura N, Muraki S; et al. (2017). "Association of lumbar spondylolisthesis with low back pain and symptomatic lumbar spinal stenosis in a population-based cohort: The Wakayama Spine Study". Spine. 42 (11): E666–E671. doi:10.1097/BRS.0000000000001960. PMID 27779607.
  13. ↑ Arita S, Ishimoto Y, Hashizume H; et al. (2025). "Age-related prevalence of radiographic lumbar spondylolisthesis and its associations with low back pain, walking speed, and muscle index: findings from the second survey of the ROAD study". European Spine Journal. 34 (4): 1359–1365. doi:10.1007/s00586-025-08751-x. PMID 40042642 Check |pmid= value (help).
  14. ↑ Kalichman L, Kim DH, Li L, Guermazi A, Berkin V, Hunter DJ (2009). "Spondylolysis and spondylolisthesis: prevalence and association with low back pain in the adult community-based population". Spine. 34 (2): 199–205. doi:10.1097/BRS.0b013e31818edcfd. PMID 19139672.
  15. ↑ Raastad J, Reiman M, Coeytaux R, Ledbetter L, Goode AP (2015). "The association between lumbar spine radiographic features and low back pain: a systematic review and meta-analysis". Seminars in Arthritis and Rheumatism. 44 (5): 571–585. doi:10.1016/j.semarthrit.2014.10.006. PMID 25684125.
  16. ↑ Diebo BG, Shah NV, Boachie-Adjei O; et al. (2019). "Adult spinal deformity". The Lancet. 394 (10193): 160–172. doi:10.1016/S0140-6736(19)31125-0. PMID 31305254.
  17. ↑ McAviney J, Roberts C, Sullivan B; et al. (2020). "The prevalence of adult de novo scoliosis: A systematic review and meta-analysis". European Spine Journal. 29 (12): 2960–2969. doi:10.1007/s00586-020-06453-0. PMID 32440771 Check |pmid= value (help).
  18. ↑ McCarthy J, Davis A (2016). "Diagnosis and management of vertebral compression fractures". American Family Physician. 94 (1): 44–50. PMID 27386723.
  19. ↑ Ensrud KE, Schousboe JT (2011). "Vertebral fractures". New England Journal of Medicine. 364 (17): 1634–1642. doi:10.1056/NEJMcp1009697. PMID 21524214.
  20. ↑ DePalma MJ, Ketchum JM, Saullo T (2011). "What is the source of chronic low back pain and does age play a role?". Pain Medicine. 12 (2): 224–233. doi:10.1111/j.1526-4637.2010.01045.x. PMID 21266006.
  21. ↑ Brinjikji W, Luetmer PH, Comstock B; et al. (2015). "Systematic literature review of imaging features of spinal degeneration in asymptomatic populations". AJNR American Journal of Neuroradiology. 36 (4): 811–816. doi:10.3174/ajnr.A4173. PMID 25430861.
  22. ↑ Reginato LS, Machado GC, Maher CG; et al. (2026). "Prevalence of serious spinal pathologies and nonspinal conditions in low back pain: a systematic review and meta-analysis". Pain Medicine. 27 (1): 43–52. doi:10.1093/pm/pnaf078. PMID 40581763 Check |pmid= value (help).