Lumbar Spondylosis: Degenerative Disease of the Lumbar Spine

Lumbar spondylosis, namely degeneration of the lumbar discs and facet joints, is a common feature of aging. Often, this degeneration may be present without causing symptoms beyond a routine back ache. However, the overgrowth of tissue, hypertrophy of ligamentum flavum, and bony osteophytes that accompanies the degenerative process can also cause narrowing of the lumbar spinal canal (spinal stenosis) and compression of the neural elements with associated leg pain, lower extremity numbness, buttock pain, and weakness.


Degeneration of the disc and facet capsule can also lead to instability and slippage of one vertebral body relative to the one below, a condition known as spondylolisthesis. This too can cause compression of the nerve roots in the canal, by narrowing the space occupied by the nerves.



Structure and Function

The five lumbar vertebrae, designated L1 to L5, lie between the rib cage and the pelvis (see Figure 1). Each vertebra has a body, behind which lies the central canal, bordered as well by the pedicles and the laminae (see Figures 2 and 3). There is an intervertebral disc between the adjacent vertebra. There are also superior and inferior articular processes that make up the facet joint: the inferior articular process of the vertebrae above lying either dorsally (cervical and thoracic spine) or medially (lumbar spine) to the superior articular process of the vertebrae below.


Figure 1: The lumbar spine, highlighted in red: anterior view (left) lateral oblique (center) and posterior view (right). (Courtesy of Wikipedia)


Figure 2: A lumbar vertebral body, superior view to the left, mid-sagittal view to the right. The central canal is denoted with the red star; the superior articular processes that make up the anterior side of the facet joints, are circled in blue. The disc lies between the vertebral bodies, as shown. (Modified from, rID: 82813/Gray’s Anatomy)


Figure 3: Colorized version of the superior view highlighting the pedicles in blue, the laminae in green and the spinous process in orange. The remaining bone, comprising the vertebral body, the articular processes and transverse processes are shown in red.


Along the vertebral column, there are anterior and posterior longitudinal ligaments adjacent to the vertebral bodies (see Figure 4). Posteriorly, the ligamentum flavum runs between adjacent lamina. Hypertrophy of the ligamentum flavum can compress the canal or the neural foramen and put pressure on the nerve roots.


Figure 4: The ligaments of the lumbar spine. To the left is the original from Gray’s Anatomy; to the right, the potential sources of compression are shown in color: the disc in purple, the bony elements (see text) in black; the posterior longitudinal ligament in blue and the ligamentum flavum (Latin for "yellow ligament") is shown of course in yellow.


Osteophytes (bone spurs) can form near the neural foramen as part of the degenerative process. These bone spurs may grow into the spinal canal, resulting in central or lateral recess stenosis, or they can grow into the foramen, causing foraminal stenosis.


When the disc degenerates, it becomes flatter. This will inherently shrink the size of the foramen, but will also alter the geometry of the facet joints as the bone move relative to each other as the disc space narrows. This can stimulate facet joint osteoarthritis with resultant osteophytes, further exacerbating the problem of narrowed space.


Facet instability and disc degeneration can produce a slippage of one vertebral body relative to the one below, a degenerative spondylolisthesis, that further reduces the canal diameter. This type of slippage is distinguished from the isthmic type in which there is a defect of the pars interarticularis. (See In degenerative spondylolisthesis there is no defect in the pars, and because the pars remains intact, the slip is often less than 25% of the width of the vertebral body and rarely greater than 50%. (With isthmic spondylolisthesis, where are bilateral pars interarticularis defects, there are often slips greater than 50%.)


The spinal cord itself terminates at roughly the L1 vertebral level, but the nerve roots that branch off of the lower end of the spinal cord (the conus medullaris) remain within the central canal until they exit at their appropriate neural foramen. The nerves branching off beneath the termination of the spinal cord are said to resemble a horse's tail, hence the name cauda equina.


Lumbar stenosis, thus, can compress the cauda equina or part of it, causing pain, paresthesias, and weakness in the buttocks area and lower extremities. This can result in numbness in the legs and decreased walking distances.



Patient Presentation

Patients with degenerative joint disease alone are usually asymptomatic but can complain of an aching lower back pain. Patients may state that they are unable to bend down to pick up items due to stiffness.


If there is stenosis however, there can be buttock pain or pain radiating down the legs, as well as difficulty walking distances.

Osteophytes from vertebral body or facet arthritis may impinge on isolated nerve roots, causing neurogenic pain or paresthesias suggestive of a disc herniation, but for an anatomically distinct reason. In disc herniations, the disc itself puts pressure on the nerve roots. In degenerative spondylosis the combination of ligamentum flavum hypertrophy, facet hypertrophy, and mild disc bulging (versus large disc herniation) combine to significantly narrow the spinal canal.


The back pain of lumbar spondylosis is often described as “mechanical”, meaning that motion provokes the pain. Nonetheless, spondylosis can lead to subtle instability of the vertebral bodies which can initiate compensatory muscle spasm (to limit the motion). This muscular pain can endure throughout the day and evening, and thus cause a component of rest pain as well. This can make diagnosis a bit more difficult as rest pain normally suggests a cause outside of arthritis.


Lumbar stenosis can cause neurogenic claudication. (The word claudication comes from a Latin verb claudicare, meaning ‘to limp’, but these days refers to lower extremity pain and not a limp, per se.) The adjective “neurogenic” is used to distinguish this pattern of symptoms from vascular (or “classic”) claudication, which is caused by peripheral arterial insufficiency. Both types of claudication, thus, are produced by ischemia, but in neurogenic claudication the ischemic tissue are the spinal nerve roots, whereas in vascular claudication it is the leg muscles themselves that are ischemic as a result of decreased blood flow.


One way to differentiate the two types of claudication is that the neurogenic variety is often relieved by bending over, for example, riding a bicycle or pushing a shopping cart. Spinal flexion tends to maximally open the spinal canal, whereas extension of the spine as seen with upright standing tends to compress the central canal. (This is analogous to Phalen’s maneuver compressing the carpal tunnel, with pressure relieved by holding the wrist in a neutral position.)


The location of the symptoms may be informative too: neurogenic claudication usually causes symptoms proximally, in the buttock and posterior thigh primarily, whereas vascular claudication, mediated by decreased blood flow to the muscles, appears first distally in the calf.


On examination, patients with vascular claudication may show signs of arterial insufficiency such as cool, brittle, shiny skin on the legs, and weak or absent pulses. Whereas patients with neurogenic claudication more likely have normal skin color, texture, and temperature in their lower extremities and normal palpable pulses.


Historically, students have been taught that vascular claudication can be identified by its “dose-dependent” symptoms, meaning that the pain of vascular claudication is initiated and worsened with movement and ameliorated by rest, in a crescendo/decrescendo pattern. By contrast, symptoms of neurogenic claudication were taught to be less related to the duration of activity and more to spinal position (flexion and extension). A recent study found that the “classic symptom attributes used to differentiate neurogenic from vascular claudication are at best weakly valid independently.” Nonetheless, the study did find that the collected presence of classical symptoms, namely, pain located above the knees, triggered with standing and relieved with spinal flexion strongly supports the diagnosis of neurogenic claudication.



Objective Evidence

Lab studies are usually not indicated unless there is concern for an infectious or neoplastic process. An electromyelogram (EMG) with nerve conduction studies can often help differentiate lower lumbar radiculopathy due to stenosis from peripheral neuropathy due to diabetes.


Radiographs in the setting of spondylosis (see Figures 5 and 6) may show disk-space narrowing, facet-joint hypertrophy, spondylolisthesis, end-plate sclerosis, and osteophytosis.


Figure 5: Lateral radiograph of the lumbar spine, showing degenerative narrowing of the L5/S1 disc space (red arrow), contrasted to the normal space (shown in green) at the levels above. (Courtesy of Diagnostic Testing for Degenerative Disc Disease by Michael W. Hasz)


Figure 6: Lateral radiograph of the lumbar spine, showing degenerative spondylolisthesis of L4-5 level (red arrow). (Courtesy of Minimally invasive versus traditional open transforaminal lumbar interbody fusion for the treatment of low-grade degenerative spondylolisthesis: a retrospective study. Sci Rep 10, 21851 (2020).


Advanced imaging such as CT and MRI can confirm the diagnosis of spinal stenosis and can show both narrowing of the central canal and neural foramina. The MRI, however, is the gold standard for confirming lumbar stenosis because cerebrospinal fluid and the nerve roots are seen on this modality. The central canal is considered stenotic when measured to have less than a 100mm^2 cross-sectional area or less than a 10mm A-P diameter on CT scan.


CT is more sensitive for detecting bony abnormalities such as facet joint hypertrophy and osteophytes, whereas MRI (see Figure 7) is sensitive for detecting spinal stenosis from ligamentous hypertrophy and disc degeneration.


Figure 7: A sagittal T2-weighted MRI image demonstrating the darker discs at the L4-L5 and L5-S1 levels (blue stars), indicating dissection and degeneration, contrasted with the brighter signal within the L3-L4 disc, denoted by the yellow star. The normal posterior disc border at L3-L4 is contrasted with the protrusion of the L4-L5 disc (shown by red line). (Courtesy of Diagnostic Testing for Degenerative Disc Disease by Michael W. Hasz)


Figure 8: A matched pair of sagittal and axial views. The pair above, in the blue box, shows age-normal degenerative changes. The axial view shown at right is taken at the level of the blue line coursing through the disc in the figure at left. The space of the canal and recesses is shown by the yellow circle. Below, in the pain in the red box, stenosis is seen. In the sagittal view at left, the decreased anterior-to-posterior space is outlined by the orange bracket. At right, the smaller space of the stenotic canal and recesses is shown by the orange circle. (Images courtesy of Nader M. Hebela.)

It is important to note that many people over the age of 60 may show signs of spinal stenosis on imaging even if they have no symptoms. Thus, although these imaging modalities are sensitive, they are not clinically specific.


Lastly, CT myelogram is an option for patients who cannot undergo an MRI. In a CT myelogram, dye is injected intrathecally, and radiographs and a CT scan are obtained to reveal neural structure impingement as well as bony abnormalities.



About 10% of the adult population suffers from lumbar spondylosis, with women and men affected equally. The peak incidence of seeking care for lumbar spondylosis is ~age 65. Degenerative changes of course increase with age, but decreasing activity at older ages may make the degenerative condition less symptomatic. Lumbar spondylosis with stenosis most commonly occurs at the L4-5 level.



Differential Diagnosis

The differential diagnosis of lumbar spondylosis is based on the presenting symptoms. If the chief complaint is back pain, following musculoskeletal entities must be considered: muscular strains; disc disease; degenerative arthritis; inflammatory arthropathies; and, less likely, infection and malignancy. (In patients at risk, osteoporotic compression fracture is also on the differential diagnosis.) If the chief complaint is claudication, the main diagnostic entities to consider are vascular insufficiency, diabetic neuropathy, and large central disc herniations.

Note also that back pain can have a non-musculoskeletal cause. Abdominal aortic aneurysms, gynecologic disorders such as endometriosis and tubal pregnancy, gastrointestinal disorders such as ulcers and pancreatitis, and kidney stones may present with back pain.



Red Flags

The compression of multiple nerves in the cauda equina often leads to unilateral or bilateral lower extremity pain and sensorimotor changes, rarely bowel/bladder dysfunction, which can manifest as incontinence or urinary retention (with overflow incontinence and increased post-void residuals).


Night pain can be present with lumbar degenerative disc disease/degenerative joint disease, as noted, but severe night pain - enough to wake the patient - especially if there are systemic complaints such as fever or weight loss, should raise suspicion of spinal infection or metastasis.


Treatment Options and Outcomes

Needless to say, not all back pains require medical treatment and diagnostic investigations may discover incidental findings that are not the true cause of symptoms.


If pain requires intervention, a non-operative approach is the best first option. Such treatment includes a period of relative (but not complete) rest, use of NSAIDs, hot or cold compresses, and physical therapy. Physical therapy is aimed at core strengthening and muscular rehabilitation. Stationary biking (and other exercises that incorporate lumbar flexion) are usually better tolerating for patients than exercises like walking or jogging that require some lumbar extension.


Steroid injections and hyaluronic acid injections can be trialed prior to considering a more aggressive approach.


In cases of progressive neurologic deficits or unremitting and extremely debilitating pain, a patient may elect to proceed with a surgical procedure.


Laminectomy, which involves the partial or total excision of a lamina, may be used to remove osteophytes and fibrotic ligaments. Fusion can be performed in cases of spinal instability or degenerative spondylolisthesis (see Figure 9), although more recent studies are beginning to question the benefits of fusion versus laminectomy and decompression alone.


see below, this needs to be updated


Figure 9: Lateral radiograph of the lumbar spine: Fusion of the degenerative anterior spondylolisthesis of L4 in patient shown in the figure should place figure number here, 5 and 6?. (Courtesy of Minimally invasive versus traditional open transforaminal lumbar interbody fusion for the treatment of low-grade degenerative spondylolisthesis: a retrospective study. Sci Rep 10, 21851 (2020).


Laminectomy or foraminotomy (widening of the foraminal space) may be employed as sole treatment for spinal stenosis depending on the cause of the narrowing (Figure 10). The degree of decompression is chosen by the surgeon. So-called pedicle-to-pedicle decompression incorporates partial resection of the spinous process, lamina, and ligamentum flavum, a facetectomy, and decompression of the foramina. Fusion is added to this procedure when there is spinal instability present, either from the degenerative process itself or surgical-induced instability from the necessary removal of bone. In general, if there is removal of 50% of the articular processes, fusion is necessary.


Figure 10: A schematic superior view of a normal lumbar vertebral body (top left) with a patent canal, showing in yellow; a similar view with lumbar spondylosis in which soft tissue and bony overgrowth along with disc protrusion produce a highly stenotic canal (top right). Shown at bottom left is a bilateral laminectomy as indicated by the green arrows, along with removal of the overgrown tissue in the canal itself. Shown at bottom right is a pedicle-to-pedicle decompression, with sacrifice of the articular processes (pink star). This provides even greater decompression, but the absence of the facets necessitates the addition of surgical fusion to stabilize the spine.


Laminotomy, which removes only a small part of the lamina, can be used as an alternative to laminectomy.


An alternative to laminectomy is interspinous distraction, in which an instrument distracts adjacent spinous processes forcing the spine into flexion, although there is increasing evidence that the benefits of this treatment do not persist over time.


Alternative therapies for lumbar spondylosis include yoga, transcutaneous electrical nerve stimulation (TENS), chiropractic, aromatherapy, acupuncture, and deep tissue massage.


Surgery has been associated with greater symptomatic improvement as compared to non-operative treatment at one to eight years, but this difference narrows through the years. Improvements in function and patient satisfaction are also noted with surgery, although recurrence of spinal stenosis adjacent to the level of decompression can occur. Reoperation rates are between 10% to 23% after ten years. Common surgical complications seen in greater than 10% of patients include wound infections, UTIs, and blood loss requiring transfusion. Deeper infections, neurologic injury, and dural tears are rare complications.



Risk Factors and Prevention

Age is the greatest risk factor in the development of lumbar degenerative spondylosis. Obesity (which increases the load on the spine), family history, and trauma or injury to the back are also known associations with these degenerative conditions as well as spinal stenosis. Specific occupations and sports that involve bending or heavy lifting can increase the risk of DJD and DDD. Women are at a greater risk of developing DJD and spinal stenosis than are men. DJD, DDD, spondylolisthesis, spondylolysis, and congenitally shortened pedicles predispose an individual to spinal stenosis. The last scenario, known as congenital stenosis, usually becomes apparent in the 2nd through 4th decades. Shorted pedicles are a common feature of achondroplasia. Prior surgical interventions such as laminectomy and fusion are additional risk factors. Lastly, certain endocrinopathies and iatrogenic causes, such as Cushing’s syndrome, Paget’s disease, acromegaly, and exogenous steroid use, are associated with spinal stenosis.


Weight loss, proper technique when bending and lifting, and exercising good posture can help prevent the development of DJD and DDD. Physical activity that promotes core strengthening and back flexibility may also be beneficial.




Short-legged dog breeds, including dachshunds, basset hounds, corgis, and shih tzus, are very commonly affected by lumbar degenerative disc stenosis. Up to a quarter of dachshunds acquire the disease.



Key Terms

Spondylosis, degenerative disc disease (DDD), nucleus pulposus, annulus fibrosus, degenerative joint disease (DJD), facet joint arthritis, osteophytes, spinal stenosis, central stenosis, foraminal stenosis, neurogenic claudication, Romberg test, laminectomy, facetectomy, foraminotomy, discectomy




Describe the process of disc and joint degeneration and understand how both conditions can lead to spinal stenosis. Differentiate neurogenic and vascular claudication. Identify the imaging findings associated with degenerative spondylosis.




Meg’s notes

Risk factors starts to throw in DJD and DDD, but not listed elsewhere in text.

Review highlights and red text areas for clarification.

Confirm Fig 9 caption