Author(s): Thomas Chai, MD, Royce A Copeland, DO, Bernardo E Gonzalez, MD, Sara G Nalli, Ishita Mahajan
Originally published: September 20, 2013 Last updated: May 7, 2026
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Disease/Disorder

Definition

Lumbar spondylosis is a radiographic diagnosis referring to degenerative changes in the discs, vertebral bodies, and paired zygapophysial joints, colloquially referred to as facet joints, of the lumbar spine. The term “degenerative lumbar spondylosis” describes a mixed group of spinal bone diseases related to degeneration of the lumbar motion segment and associated pathologies. Spondylosis is not a clinical diagnosis but a general descriptor for spinal pathology. It may be associated with low back pain (LBP) and is correlated with numerous other spinal pathologies, including spinal stenosis, vertebral instability, degenerative spondylolisthesis (anterior or posterior vertebral displacement), osteoarthritis, and malalignment.

Etiology

Generally speaking, lumbar spondylosis refers broadly to a degenerative syndrome of the spine, rather than a specific singular disease entity. Contributing factors include degenerative, osteoarthritic, mechanical, genetic, and multifactorial influences.1 It is thought to result from cumulative stresses combined with repetitive microtrauma, leading to an imbalance between the synthesis and degeneration of fibrocartilage cartilage.1 These stresses on the vertebrae, intervertebral discs, and ligaments subsequently cause the formation of osteophytes and calcifications, respectively. Osteophytes most commonly occur along the anterolateral aspect of the lumbar vertebral body.1,3 However, rare posterior vertebral osteophytes can cause impingement on the nerve roots or spinal cord.1,3 Lumbar spondylosis can also develop due to new bone formation in areas where the annular ligament (annulus fibrosus) is stressed over time.

Epidemiology including risk factors and primary prevention

The prevalence of radiographic spondylosis increases with age.4,5 While present in only a small percentage of the population in the first few decades of life, spondylosis becomes relatively common by the age of 50.5 The prevalence of spondylosis varies greatly from spondylosis with low back pain (20-30%) versus spondylosis detected on radiographic imaging (70-80%) for individuals older than 50.5,6 The prevalence of spondylosis detected on radiography, severe spondylosis, and spondylosis accompanied by low back pain (LBP), is 76.7%, 38.8%, and 20%respectively.5 Despite its frequency in patients with LBP, there is no validated correlation between the radiographic findings of lumbar spondylosis and the presence of LBP.4-6

Risk factors

Age is the greatest risk factor for lumbar spondylosis, but other identified risk factors include disc desiccation, previous lumbar injury, joint overload from malalignment or abnormal facet joint orientation, and genetic predisposition.2 Studies evaluating the role of body mass index (BMI), level of activity, and gender on the incidence and severity of lumbar spondylosis do not show a clear correlation.5,7

Patho-anatomy/physiology

Some investigators believe that lumbar spondylosis is due to a “degenerative cascade” initiated by intervertebral disc desiccation.4,8 The resulting degenerative changes are thought to be secondary to cumulative stresses on the annular ligaments also known as annular fibrosus, which then form degenerative changes (i.e., marginal osteophytes).10 Failure of collagen cross-linking in the annulus and nucleus, combined with the discs’ inability to retain water, causes a stiffening of the cartilaginous and capsular structures. This restriction of facet joint mobility leads to earlier and more advanced degenerative changes, particularly at the L4-L5 and L5-S1 levels, likely due to their proximity to the fused sacral segments.1,3,6

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

Lumbar spondylosis is not a single disease entity but rather a progressive, age-related “wear and tear” of the various components of the lumbar spine, including the intervertebral discs, facet joints, and supporting ligaments.

The progression generally follows a predictable biochemical and mechanical path, often categorized by the Kirkaldy-Willis Three-Stage Model of spinal degeneration.10

1. Phase of Dysfunction (Early Stage)

This stage typically begins in the 20s or 30s. The primary changes are biochemical and microscopic rather than structural.

  • Intervertebral Discs: Small circumferential and radial tears (annular tears) develop in the outer ring of the disc. The nucleus pulposus begins to lose its ability to retain water (desiccation).
  • Facet Joints: Synovitis (inflammation of the joint lining) may occur, leading to localized back pain.
  • Symptoms: Intermittent, non-specific low back pain, often aggravated by certain movements. Physical exams may show localized tenderness or minor muscle guarding.

2. Phase of Instability (Intermediate Stage)

Usually seen in middle age (40s to 60s), this phase is characterized by a loss of structural integrity.

  • Disc Height Loss: As the disc continues to dehydrate, it loses height, which increases the mechanical load on the posterior elements (facet joints).
  • Segmental Laxity: The ligaments and the disc can no longer hold the vertebrae in a tight, stable alignment. This can lead to spondylolisthesis (one vertebra slipping over another).
  • Facet Changes: The cartilage in the facet joints begins to erode, similar to osteoarthritis in the hip or knee.
  • Symptoms: More frequent and severe episodes of “giving way” or “catching” in the back. Pain is often worse with standing or extension (leaning back).

3. Phase of Stabilization (Late Stage)

In older age (60s+), the body attempts to heal the instability by “growing” more bone to stiffen the segment.

  • Osteophyte Formation: Bone spurs (osteophytes) develop around the disc spaces and facet joints to increase surface area and stabilize the joint.
  • Hypertrophy: The ligamentum flavum thickens, and facet joints enlarge (hypertrophy).
  • Spinal Stenosis: While the spine becomes “stable” (less mobile), the trade-off is a narrowing of the spinal canal or the neural foramina where nerves exit.
  • Symptoms: Back pain may actually decrease as the segment becomes “fused” by bone spurs. However, new symptoms of neurogenic claudication (leg pain/heaviness when walking) or radiculopathy (sciatica) may emerge due to the narrowing of the nerve spaces.

The trajectory of lumbar spondylosis is universal but variable.

  • Universality: Radiographic evidence (radiographs/magnetic resonance imaging) of spondylosis is present in nearly all individuals over age 70.10
  • Long-term Outlook: Most patients experience a waxing and waning course. While the structural changes are irreversible and progressive, the functional impairment can often be managed or improved through physical therapy and activity modification.

Specific secondary or associated conditions and complications

Lumbar spondylosis serves as the structural precursor to several distinct clinical complications, primarily categorized by mechanical instability and neurological compression. The most common complication from lumbar spondylosis is facet hypertrophy leading to cartilage erosion and joint hypertrophy, causing localized axial pain often called lumbar facet syndrome.9,10 Another condition associated with lumbar spondylosis is called spondylolisthesis, which occurs when segmental instability allows one vertebra to slip forward, frequently at the L4-L5 level.10 These structural changes, combined with ligamentous thickening, facet hypertrophy, and disc bulging can decrease the spinal canal space, leading to spinal stenosis, which can manifest as neurogenic claudication and leg heaviness during ambulation. Furthermore, when this degenerative process narrows the neural foramina, it may result in radiculopathy, characterized by dermatomal pain and sensory-motor deficits due to direct nerve root compression. Lastly, atrophy of the erector spinae and multifidus muscles secondary to pain-limited spinal motion can also manifest.

Essentials of Assessment

History

As previously noted, lumbar spondylosis is defined by specific radiographic findings that do not rely on clinical symptoms for diagnosis. However, in patients presenting with acute, subacute, or chronic LBP, these radiological changes can serve as clues for potential pain generators. Patients typically report axial lumbosacral pain, which may involve nociceptive input from the intervertebral discs, nerve roots, facet joints, sacroiliac joints, and overlying myofascial structures. This pain may be referred unilaterally, bilaterally, or to the contralateral buttock, hip, groin, and thigh; notably, it typically does not extend distal to the knee.6,10 Symptoms are also frequently exacerbated by spinal extension and rotation.10 While lumbar spondylosis is not inherently associated with neurological deficits, related conditions such as spinal stenosis, spondylolisthesis, and lumbar disc herniations often are. Consequently, clinicians must screen for weakness, gait and balance disturbances, and changes in bowel or bladder function during assessment. In order to objectively monitor patient progression, validated outcome measures—including the Oswestry Disability Index (ODI), the McGill Low Back Pain Scale, and the SF-36—may be administered.11

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 facet joint arthropathy, but not with high diagnostic confidence. Although classically felt to diagnose facet joint pain, joint loading with pain on extension and ipsilateral rotation has not been shown to correlate with spondylosis consistently.12 The pain distribution of lumbar spondylosis may overlap with other clinical entities. A comprehensive physical exam that includes evaluation of radiculopathy, including dural tension signs, as well as hip and sacroiliac joint provocative maneuvers, which can help guide clinical decision making. Neurologic deficits associated with lumbar nerve root compression should be evaluated using muscle strength, sensation, reflexes, gait, and balance testing. Discogenic pain can be exacerbated when the patient is asked to repeatedly bend forward or with seated lumbosacral flexion and concurrent hip flexion.

Laboratory studies

Although laboratory studies are not routinely indicated, C-reactive protein, sedimentation rate, and a complete blood count may be ordered if there is clinical suspicion of malignancy, infection, or rheumatologic disease.

Imaging

Lumbar spondylosis is visible on multiple imaging modalities, including plain radiographs, magnetic resonance imaging (MRI), and computed tomography (CT). 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 facet joint arthropathy or spondylosis, yet they are often obtained. Lateral views are important for sagittal alignment and for assessing spondylolisthesis. If present, patients should undergo flexion and extension radiographs to rule out segmental instability, which may necessitate earlier surgical consultation.

MRI is generally not needed but is useful for evaluating soft tissues and neural elements within the spine, especially to rule out neuroforaminal stenosis in patients with concomitant leg pain. The presence of small amounts of fluid or synovial cysts within the facet joints may be physiologic or may represent instability and/or infection within the lumbar spine and therefore would warrant further workup and/or treatment.

CT is typically used when an MRI is unavailable, when a fracture is suspected, or for the assessment of pseudoarthrosis.

Supplemental assessment tools

Diagnostic Injections

Given the low correlation between radiographic spondylosis and axial low back pain, the only means of accurately diagnosing symptomatic lumbar spondylosis secondary to facet arthropathy is controlled diagnostic blocks of the medial branch nerves that innervate the facet joints.16 This suggests that the patient’s pain generator(s) are the facet joints and not the intervertebral discs. Each facet joint has dual innervation from the medial branch of the dorsal ramus of the spinal nerve at the corresponding level and the level above. To treat the pain associated with a specific facet joint, both nerves must be targeted.

Several key principles exist for diagnostic medial branch blocks

  • Because landmark guidance is inaccurate, all blocks should be performed using image guidance. Both fluoroscopic and ultrasound guidance have been described in the literature.30
  • False-positive blocks occur at a high rate of 17% to 41% in the lumbar spine, necessitating a second control block for confirmation of the diagnosis.31     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.32
  • The greater the percentage of pain relief a patient obtains with a given injection, the more likely that injection is correctly targeted at the pain generator. An 80% pain relief threshold with comparative medial branch blocks results in more successful outcomes with radiofrequency ablation, a denervation procedure that uses radiofrequency to ablate the medial branch nerves thermally.16 For more details, please see the Lumbar Zygapophyseal Joint Arthropathy section of PM&R KnowledgeNOW.

Rehabilitation Management and Treatments

Available or current treatment guidelines

Management of lumbar spondylosis without myelopathy or radiculopathy is initially conservative, focusing on pain reduction, functional improvement, and activity maintenance. Current management guidelines emphasize on non-pharmacologic treatment options as a first-line approach that typically involves patient education, activity maintenance, acupuncture, mindfulness-based stress reduction, and exercise-based rehabilitation.18 Nonpharmacologic interventions are prioritized because they are associated with fewer harms than pharmacologic options. For patients with inadequate response to nonpharmacological therapy, current management guidelines recommend pharmacologic treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) as first-line therapy for analgesia.19 Other first line treatment options include topical creams (NSAIDs) and lidocaine patches given their low risk profile although studies are inconclusive regarding their efficacy for the treatment of chronic low back pain.19 Secondary treatment options include duloxetine (weak recommendation, moderate-quality evidence).19 Studies have shown one additional patient will experience at least 30% pain reduction with duloxetine compared with patients who receive placebo (number needed to treated = 9; CI 6 to 16).19 Tricycle antidepressants, gabapentinoids, and nonbenzodiazepine muscle relaxants have been shown in large studies that these agents do not improve pain or function in chronic low back pain compared to placebo.19 In regard to oral corticosteroids, there may be slight improvement in disability in acute back pain with radicular symptoms compared to placebo but not recommended for the treatment of chronic low back pain given the potential harmful systemic effects on the body.19 The use of opioid pain medications has been shown to improve pain and function in chronic low back pain, but long-term risks are high with substantially consequences and should only be considered after failure of all treatment options, potential benefits outweigh risks, and patient-clinician sharded decision making. If initiated, individuals should start with low-potency opioids such as tramadol and be carefully monitored.19

In selected patients with persistent symptoms or suspected facet mediated pain, interventional procedures such as medial branch blocks or radiofrequency ablations may be considered depending on clinical findings or underlying cause.20 Surgical intervention is not recommended for axial low back pain from lumbar spondylosis in the absence of neurologic compromise, infection or spinal instability.21

Coordination of care

Management should ideally be guided by an interdisciplinary approach, including, but not limited to physicians and physical therapists, as well as pain psychologists, who may help address psychosocial contributors to chronic pain secondary to lumbar spondylosis.

Patient & family education

Patients should be educated that lumbar spondylosis-related symptoms typically respond well to treatment; however, they should be made aware of warning signs consistent with neurologic involvement. Patients should seek immediate medical attention if they develop myelopathy and/or changes in bowel and bladder. Patients should be informed that spondylosis on imaging does not necessarily correspond with pain and that a diagnostic block may be used to rule in/out lumbar spondylosis-related low back pain.

Providers should work with their patients to develop an individualized treatment plan, while continuing to emphasize maintenance of normal activities, exercise, and avoiding movements that exacerbate symptoms. Guidance regarding stretching, strengthening exercises, posture, and ergonomic modifications may help reduce mechanical stress on the lumbar spine and support long-term symptom management.

Practical application

In clinical practice, rehabilitation programs for lumbar spondylosis focus on improving spinal stability, flexibility, and tolerance for functional activities. Although various exercise strategies have been studied, no single supervised exercise program has been identified as superior. Multiple forms of exercise, including lumbar stabilization programs that strengthen abdominal, lumbar, and hip musculature while improving flexibility, may reduce pain and restore function.19

Degenerative findings on imaging should be interpreted in the context of clinical symptoms rather than used as the sole basis for treatment decisions, as such findings are common in asymptomatic individuals.22 Only after conservative management has failed and facet-mediated pain is suspected should a diagnostic medial branch blocks be used to identify appropriate candidates for radiofrequency ablation.

Emerging/unique interventions

There’s been an emergence of interventions for lumbar pain secondary to degenerative changes, focusing on biologic therapies and minimally invasive procedures. Regenerative medicine approaches including platelet-rich plasma (PRP), bone-marrow aspirate concentrate (BMAC), and mesenchymal stem-cell (MSC) therapies have gained interest for their potential anti-inflammatory and reparatory effects within spinal structures when conventional therapies fail.29 Current guidelines report level III (fair) evidence with moderate consensus-based recommendations for intradiscal PRP and BMAC injections, as well as PRP for epidural injections, while PRP and MSC therapies for facet joint injections have moderate consensus-based recommendations but remain supported by Level IV (limited) evidence.23,29

In addition to biologic therapies, minimally invasive procedural innovations continue to expand within pain management. Basivertebral nerve ablation has emerged as a treatment option for vertebrogenic back pain associated with Modic endplate changes and has demonstrated durable improvements in pain and function in selected patients.24

Further, for when surgical intervention is warranted, advances in minimally invasive and endoscopic techniques have enabled targeted decompression and disc procedures with smaller incisions, reduced soft tissue disruption, and faster recovery compared with traditional open approaches.25

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

Physicians should maintain a low threshold to rule out serious conditions that may also present as low back pain. The incidence of lumbar facet pain increases with age, resulting in a higher positive predictive value of diagnostic medial branch blocks and improvement of pain following radiofrequency ablation.  After successful treatment of pain with a radiofrequency ablation, patients should be encouraged to engage in daily therapeutic spine exercises to maximize functional recovery and minimize recurrence of symptoms.

Cutting Edge/Emerging and Unique Concepts and Practice

Emerging concepts emphasize low back pain to be multifactorial and influenced by biological, psychological, and social factors rather than solely structural degeneration. It is increasingly viewed as a condition with variable pain trajectories rather than isolated episodes, with some patients recovering quickly while others develop persistent or fluctuating symptoms.26,27 Risk stratification tools such as the STarT Back screening tool and Örebro Musculoskeletal Pain Questionnaire may help identify patients at risk for chronic pain and disability to guide more targeted treatment approaches.28 This shift toward a biopsychosocial and stratified care model represents an evolving concept in the management of lumbar spondylosis-related low back pain.

Gaps in the Evidence-Based Knowledge

Current literature shows the limitations in the diagnostic value of patient history, physical examination and imaging findings for diagnosing low back pain secondary to lumbar spondylosis. There are no well-established diagnostic criteria for spinal osteoarthritis or lumbar spondylosis-related pain, making it difficult to determine the primary pain generator in many patients. Further research is needed to better identify diagnostic criteria, improve patient selection for interventional treatments, and evaluate long-term outcomes of emerging therapies for lumbar spondylosis-related low back pain.

References

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  2. Madden V, Ayoub A, Thomas J, Thomas I. Spondylolysis: A Narrative Review of Etiology, Diagnosis, and Management. International Journal of Environmental Research and Public Health. 2026 Jan 26;23(2):153. doi: 10.3390/ijerph23020153
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  4. Theodore N. Degenerative Cervical Spondylosis.The New England Journal of Medicine. 2020;383:159-168. DOI: 10.1056/NEJMra2003558
  5. Näther P, Felix Kersten J, Kaden I, et al. Distribution Patterns of Degeneration of the Lumbar Spine in a Cohort of 200 Patients with an indication for Lumbar MRI. International Journal of Environmental Research and Public Health. 2022 Mar 21;19(6):3721. doi: 10.3390/ijerph19063721
  6. Tsujimoto R, Abe Y, Arima K, et al. Prevalence of Lumbar Spondylosis and its Association with Low Back Pain Among Community-Dwelling Japanese Women. BMC Musculoskeletal Disorders. 2016 Dec 1;17:493. doi: 10.1186/s12891-016-1343-x
  7. Dragsbæk L , Jensen T, Kjær P, et al. Associations Between Sum Scores or Combinations of MRI Findings in the Lumbar Spine and Low Back Pain-Related Outcomes: A Systematic Review.European Journal of Pain. 2025 Jul 18;29(7):e70076. doi: 10.1002/ejp.70076
  8. Hamoor B, Lai S, Xiong G, et al. Intervertebral Disc Degeneration. Nature Reviews Disease Primers. 2026 Feb 5;12(1):5. doi: 10.1038/s41572-025-00681-8.
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  10. Suri, Pradeep, et al. “Does Lumbar Spinal Degeneration Begin with the Anterior Structures? A Study of the Observed Epidemiology in a Community-Based Population.” BMC Musculoskeletal Disorders, vol. 12, Sept. 2011, p. 202. PubMed Central,https://doi.org/10.1186/1471-2474-12-202.
  11. Chiarotto A, Boers M, Deyo RA, et al. Core outcome measurement instruments for clinical trials in nonspecific low back pain. Pain. 2018;159(3):481-495. doi:10.1097/j.pain.0000000000001117
  12. Perolat R, Kastler A, Nicot B, et al. Facet joint syndrome: from diagnosis to interventional management. Insights Imaging. 2018;9(5):773-789. doi:10.1007/s13244-018-0638-x
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  21. Evans L, O’Donohoe T, Morokoff A, Drummond K. The role of spinal surgery in the treatment of low back pain. Med J Aust. 2023;218(1):40-45. doi:10.5694/mja2.51788
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Original Version of the Topic

D.J. Kennedy, MD, Renata Jarosz, MD, Ryan Demirjian, MD. Lumbar spondylosis without myelopathy. 9/20/2013.

Previous Revision(s) of the Topic

Ameet Nagpal, MD and Alan Swearingen, MD. Lumbar spondylosis without myelopathy. 2/14/2018.

Ameet Nagpal, MD, MS, MEd, Adedeji Olusanya, DO, MPH, Austin Bevil, DO. Lumbar Spondylosis Without Myelopathy/Radiculopathy. 5/31/2023

Author Disclosure

Thomas Chai, MD,
Nothing to Disclose

Royce A Copeland, DO
Nothing to Disclose

Bernardo E Gonzalez, MD
Nothing to Disclose

Sara G Nalli
Nothing to Disclose

Ishita Mahajan
Nothing to Disclose