Jump to:



Lumbar spondylosis (LS) is a radiographic diagnosis that refers to degenerative changes of the discs, vertebral bodies and paired zygapophysial joints (z-joints) of the lumbar spineand may be associated with low back pain (LBP).  does not rely on clinical findings.1,2,3


Though the etiology of lumbar spondylosis remains unclear, many have characterized it as an osteoarthritis of the spine.  It is likely the result of cumulative stress combined with repetitive microtrauma, leading to an imbalance in the synthesis and degeneration of the cartilage, and, combined with increased stress placed on the bones and ligaments, leads to osteophyte creation and calcification, respectively.1,3

Epidemiology including risk factors and primary prevention

The prevalence of radiographic spondylosis increases with age4,5. It is present only in a small percentage of the population in the first few decades of life, but is common by the age of 65. In those with LBP, the prevalence ranges from 7% to 75%, depending on the diagnostic criteria (6). Despite its frequency in patients with LBP, there is no validated correlation between radiographic presence of LS and presence of LBP.

Risk Factors

Age is the greatest risk factor, but other possibilities include, disc dessication, previous injury, joint overload from malalignment and/or abnormal z-joint orientation, and genetic predisposition.2 Studies evaluating the role of BMI, level of activity and gender on incidence and severity of LS do not show a clear correlation.5,7


Some investigators believe that LS is due to a “degenerative cascade.” that is initiated by intervertebral disc desiccation.8 Annulus and nucleus collagen cross-linking and inability to hold water results in stiffening of the cartilage and capsular structures, leading to an altered range of motion which restricts Z joint mobility. In the lumbar spine, the z-joints have a posterolateral orientation to resist axial rotation and translation, resulting in increased reactive osseous changes with earlier and more advanced degenerative changes in these regions.  This is particularly true in the anteromedial portion of the joints and most frequently at the L4/L5 and L5/S1 levels, likely because of their proximity to a fused sacrum. 1,3

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

Although variable, most of patients experience a benign clinical course. Studies have shown the following:

  • radiologic spondylosis directly increases with age, irrespective of pain.9
  • spondylosis was shown to be equally present in those with and without LBP.2
  • no correlation between the magnitude of z-joint arthropathy and the severity of pain.6

Thus, progression is variable and unpredictable, and therefore difficult to study, but seems to be most closely linked to aging.

Specific secondary or associated conditions and complications

Z-joint hypertrophy, because of osteophyte formation combined with ligament redundancy from the disc desiccation, may collectively lead to spinal canal and/or intervertebral foramen narrowing. The increase in translation forces from disc desiccation, combined with the z-joints’ decreased ability to resist these factors, may also result in spinal instabilities, specifically spondylolisthesis. Increased synovial production can lead to synovial cysts formation which often causes radiculopathy. All of these changes can result in referred pain, central or lateral stenosis, radiculopathy, and/or, in severe, but rare, cases, cauda equina syndrome.  Disuse secondary to pain-limited spine motion can also lead to erector spinae and multifidi atrophy.



As mentioned previously, LS is a radiographic finding that does not rely on clinical symptoms for diagnosis.  However, in some patients with acute or gradual onset of LBP, LS is present and could potentially be a cause of the pain.  Pain may refer unilaterally or bilaterally to the buttock, hip, groin, and thigh regions; although, typically, it does not extend past the knee.6,10 The pain tends to worsen with extension, rotation, and standing; it is better with lying and L-spine flexion.10 By definition, lumbar spondylosis exhibits no neurologic deficits; however, because of its association with conditions that can affect the neurologic function of the lower limbs, it is imperative to ask about weakness, balance, gait, and bowel/bladder function.

There are several validated outcome measures for grading functional limitations, including the following: McGill Low Back Pain Scale, Oswestry Disability Index, and the Medical Outcomes Study 36-Item Short-Form Health Survey.11  These should typically be administered at every office visit for following the patient’s progression.

Physical examination

A systematic review revealed that most physical exam maneuvers have limited or no diagnostic validity for spondylosis.6 Paraspinal tenderness is the only physical exam maneuver that seems to correlate with z-joint arthropathy, but not with high diagnostic confidence. Although classically felt to diagnose z-joint pain, joint loading with pain on extension and ipsilateral rotation has not been shown to consistently correlate with spondylosis.12,13  Because the pain distribution may overlap with other clinical entities, a comprehensive exam including radiculopathy, hip, and sacroiliac joint provocative maneuvers should be performed routinely. Associated neurologic conditions should be ruled out through thorough strength, sensation, reflexes, gait, and balance testing.

Laboratory studies

Although no laboratory studies are routinely indicated, some, such as C-reactive protein, sedimentation rate, and complete blood count, may be ordered if there is clinical suspicion for a more serious condition, such as malignancy, infection, or rheumatologic disease.


Lumbar spondylosis is visible on multiple imaging modalities, including plain radiographs, magnetic resonance imaging (MRI), and computed tomography (CT) studies.  However, as spondylosis on imaging does not constitute a cause for LBP, imaging is typically ordered to rule out other disorders.13,14,15

Plain radiographs are not sensitive for detecting early z-joint OA or spondylosis, but are highly accessible, and often used. Lateral views are important to study sagittal alignment and the presence of spondylolisthesis. If present, patients should undergo flexion and extension radiographs to rule out instability of the spine.

MRI is generally not needed for diagnosis of spondylosis, but it is useful for evaluating the soft tissues and neural elements within the spine, especially to rule out neuroforaminal stenosis in patients with concomitant leg pain. Large amounts of fluid within the z-joints may represent instability and/or infection, which would warrant further work up and/or treatment, but is beyond the scope of this article.

CT is typically utilized when an MRI is unobtainable or if fracture is suspected.  It can also be helpful in identifying synovial cyst borders with implications for surgical vs percutaneous treatment.

Supplemental assessment tools

Diagnostic Injections

Given the low correlation of radiographic spondylosis with axial low back pain, the only means for an accurate diagnosis of symptomatic lumbar spondylosis secondary to facet arthropathy is to perform controlled diagnostic blocks of the medial branch nerves that innervate the z-joints.16  This assumes that the patient’s pain generator(s) is/are the z-joints and not another spondylotic spine component, such as the disc. Each z-joint has dual innervation from the medial branch of the dorsal ramus of the nerve at the corresponding level and the level above. In order to treat the pain associated with a specific z-joint, both nerves must be targeted.

Several key principles exist for diagnostic medial branch blocks:

  1. Because of the inaccuracy of landmark guidance, all blocks should be performed utilizing image guidance.  Both fluoroscopic and ultrasound guidance have been described in the literature.
  2. False positive blocks occur at a high rate of 17% to 41% in the lumbar spine, thus necessitating a second control block for confirmation of the diagnosis. Ideally, the two injections should be performed with anesthetics of differing duration.  Concordant pain relief (>1h with lidocaine and >3h with bupivacaine hydrochloride), greatly enhances the sensitivity and specificity of the injections.13
  3. The greater the percentage of pain relief a patient obtains with a given injection, the more likely that injection correctly targeted the pain generator. Some clinicians accept 50% pain relief as a diagnostic criterion. An 80% pain relief threshold with comparative medial branch blocks results in more successful outcomes with radiofrequency ablation, a denervation procedure which uses radiofrequency to thermally ablate the medial branch nerves (13, 16).  For more details, please see the lumbar zygapophyseal arthropathy section of Knowledge NOW.


Available or current treatment guidelines

No treatment currently exists for the pathological changes involved in lumbar spondylosis, therefore treatments should be focused on decreasing patient pain and increasing function.  Options include medial branch radiofrequency ablation, in addition to other conservative measures, including weight loss, physical therapy, NSAIDs, Acetominophen, and oral and topical pain medication.18

Medial branch RFA is often performed after a dual block provides substantial temporary pain relief.  Ablated nerves can regenerate, which may result in recurrence of pain; repeat RFA is a treatment option.19, 20, 21, 22, 23

Physical therapy should focus on increasing flexibility of the spine with strengthening of core muscles, including the lumbar paraspinals, despite minimal evidence to support physical therapy for the treatment of LS, and the lack of a proven single exercise program. 24

Surgical intervention is not recommended for axial back pain secondary to lumbar spondylosis without neurologic compromise.

Coordination of care

As with all spine conditions, treatment should ideally be guided by the coordinated approach of a multidisciplinary team, including, but not limited to, a physician and physical therapist.  Other potential team members include a pain psychologist for patients having difficulty coping with chronic pain secondary to this condition, as well as a nutritionist for education and assistance with weight loss, among others.

Patient & family education

Patients should be educated that LS typically responds well to treatment, but education should be provided regarding warning signs for disease progression into secondary neurologic conditions, such as myelopathy and bowel and bladder changes.  Patients should be informed that spondylosis on imaging doesn’t necessarily correspond with pain. Patients should be encouraged to lose weight and increase physical activity.  Patients should be educated on diagnostic blocks to rule in/out LS related LBP.

Practical Application

Physicians should have a low threshold for ruling out other serious conditions that also commonly present as LBP. As age increases, so does the incidence of lumbar facet pain, resulting in a higher positive predictive value of diagnostic medial branch blocks, resulting in a higher likelihood of positive results and subsequent pain relief with RFA.  After successful treatment of pain, patients should be encouraged to engage in daily therapeutic spine exercises to maximize function and hopefully prevent relapse of pain.

Emerging/unique Interventions

Nerve growth factor (NGF) has been linked with persistent pain. This pathway is being targeted with is anti-NGF for patients with chronic low back pain.  Although it has little evidence supporting its efficacy, there is has been shown to be a slight improvement in pain and functional outcomes for patients treated with anti-NGF vs placebo.25

New techniques and methods are also being developed to enhance RFA lesion size while preserving safety. Limited literature exists on their efficacy, but two such technologies are water-cooled RFA and multi-tined needles.26, 27, 28 These will hopefully enhance success rates and minimize technical failures. Studies are also currently underway on biologics to alter disease progression.

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

Physicians should have a low threshold for ruling out other serious conditions that also commonly present as LBP in this age group. If injections are required and successful because of a failure of other treatments, patients should be encouragd to engage in daily therapuetic spine exercises to maximize function and hopefully prevent relapse of pain.


Cutting edge concepts and practice

New techniques and methods to enhance RFA lesion size while preserving safety are being developed. Limited literature exists on their efficacy, but 2 such technolgies are water-cooled RFA and Nimbus needles. These will hopefully enhance success rates and minimize technical failures. Studies are also currently underway on biologics to alter disease progression.


Gaps in the evidence-based knowledge

Current literature suggests significant limitations in the diagnostic value of patient history, physical exam, and imaging for LS.  Next steps in research should focus upon individual characteristics of history, physical examination, laboratory values, and/or imaging that may help predict a successful response to a particular treatment.  This requires more studies be done on all aspects of evaluation and treatment, especially on patients with block-proven LS.


  1. Middleton K, Fish D. Curr Rev Musculoskeletal Med (2009) 2:94–104. Lumbar spondylosis: clinical presentation and treatment approaches.
  2. Bogduk N. Degenerative joint disease of the spine. Radiol Clin North Am. 2012;50:613-628.
  3. Schneck CD. The anatomy of lumbar spondylosis. Clin Orthop. Relat Res. 1985;193:20–36.
  4. Brinjikji W, et al. AJNR Am J Neuroradiol. Author manuscript; available in PMC 2015 June 13. Systematic Literature Review of Imaging Features of Spinal Degeneration in Asymptomatic Populations. Department of Radiology (W.B., P.H.L., J.T.W., D.F.K.), Mayo Clinic, Rochester
  5. Zukowski LA, et al. J. Anat. (2012) 220, pp57–66. The influence of sex, age and BMI on the degeneration of the lumbar spine.
  6. Kalichman L, et al. Facet joint osteoarthritis and low back pain in the community-based population. Spine. 2008;33:2560-2565.
  7. O’Neill TW, et al. The distribution, determinants, and clinical correlates of vertebral osteophytosis: a population based survey. J Rheumatol. 1999;26:842–8.
  8. Kirkaldy-Willis W, Bernard T. Managing low back pain. New York: Churchill Livingstone; 1983.
  9. Lawrence JS, Bremner JM, Bier F. Osteo-arthrosis. Prevalence in the population and relationship between symptoms and x-ray changes. Ann Rheum Dis. 1966;25:1-24.
  10. Eisenstein SM, Parry CR. The lumbar facet arthrosis syndrome. Clinical presentation and articular surface changes. J Bone Joint Surg Br. 1987;69:3-7.
  11. Wittink, Harriët PT, MS, PhD, et al. Clinical Journal of Pain: May/June 2004 – Volume 20 – Issue 3 – pp 133-142. Comparison of the Redundancy, Reliability, and Responsiveness to Change Among SF-36, Oswestry Disability Index, and Multidimensional Pain Inventory
  12. Datta S, Lee M, Falco FJ, et al. Systematic assessment of diagnostic accuracy and therapeutic utility of lumbar facet joint interventions. Pain Physician. 2009;12:437-460.
  13. Bogduk N, Dreyfuss P, Govind J. A narrative review of lumbar medial branch neurotomy for the treatment of back pain. Pain Med. 2009;10:1035-1045.
  14. Boden SD, Davis DO, Dina TS, et al. Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects: a prospective investigation. J Bone Joint Surg. 1990;72:403–8.
  15. Wiesel SW, Tsourmas N, Feffer HL, et al. A study of computer-assisted tomography. The incidence of positive CAT scans in an asymptomatic group of patients. Spine. 1984;9:549.
  16. Macvicar J, Borowczyk JM, Macvicar AM, et al. Lumbar medial branch radiofrequency neurotomy in New Zealand. Pain Med. In press.
  17. Wu T et al. Arch Phys Med Rehabil. 2016 Sep;97(9):1558-1563. Effectiveness of Ultrasound-Guided Versus Fluoroscopy or Computed Tomography Scanning Guidance in Lumbar Facet Joint Injections in Adults With Facet Joint Syndrome: A Meta-Analysis of Controlled Trials.
  18. Carette S, et al. A controlled trial of corticosteroids injections into facet joints for chronic low back pain. N Engl J Med. 1991;325:1002-1007.
  19. Slipman CW, et al. A critical review of the evidence for the use of zygapophysial injections and radiofrequency denervation in the treatment of low back pain. Spine J. 2003;3:310-316.
  20. van Kleef M, et al. Randomized trial of radiofrequency lumbar facet denervation for chronic low back pain. Spine. 1999;24:1937-1942.
  21. Nath S, Nath CA, Pettersson K. Percutaneous lumbar zygapophysial (Facet) joint neurotomy using radiofrequency current, in the management of chronic low back pain: a randomized double-blind trial. Spine. 2008;33:1291-1297.
  22. Dreyfuss P, Halbrook B, Pauza K, et al. Efficacy and validity of radiofrequency neurotomy for chronic lumbar zygapophysial joint pain. Spine. 2000;25:1270-1277.
  23. Schofferman J, Kine G. Effectivness of repeated radiofrequeny neurotomy for lumbar facet pain. Spine. 2004;29:2471-2473.
  24. Braddom, R L, et al. Physical Medicine and Rehabilitation (Fourth Edition). 2011. Philadelphia, PA. Saunders/Elsevier
  25. Leite VFBuehler AM, et al. Anti-nerve growth factor in the treatment of low back pain and radiculopathy: a systematic review and a meta-analysis. Pain Physician. 2014 Jan-Feb;17(1):E45-60.
  26. Bajaj PS1, et al. PMR. 2015 Oct;7(10):1095-101. doi: 10.1016/j.pmrj.2015.09.001. Cooled Versus Conventional Thermal Radiofrequency Neurotomy for the Treatment of Lumbar Facet-Mediated Pain.
  27. Stryker Inc. Venom Cannula. https://strykerivs.com/conditions/facet-joint-pain#
  28. Nimbus Concepts.  http://www.nimbusconcepts.com/the-product.html

Original Version of the Topic

D.J. Kennedy, MD, Renata Jarosz, MD, Ryan Demirjian, MD. Lumbar spondylosis without myelopathy. 09/20/2013.

Author Disclosure

Ameet Nagpal, MD
Nothing to Disclose

Alan Swearingen, MD
Nothing to Disclose