Arthropathy, or joint disease, of the zygapophyseal or “facet” joint (FJA) is a clinical and pathological syndrome that involves the functional failure of facet joints (FJ).1
Improper FJ alignment and load distribution are believed to be the major contributors to the development and progression of FJA, with the earliest changes typically occurring in the regions that experience the greatest mechanical forces.1 In patients with healthy spines, the disc is the primary load bearing structure with only 3-33% of axial load carried through the facets depending on position.2 As discs degenerate with age, they become functionally impaired resulting in up to 70% of the load being transferred through the facets in the older population.3 As a result, with the shifted transmission of force, pathology beginning in a disc progresses to osteoarthritic changes in the FJ at that vertebral level.1,4 Thus, lumbar FJA frequently occurs at the levels most commonly affected by disc degeneration, namely L4-S1.5
Epidemiology, risk factors and primary prevention
FJA noted on imaging is often an asymptomatic, age-related degenerative finding.6-8 Asymptomatic facet degeneration can be found 4% of people in their 20s and upwards of 90% of people over the age of 70 based on data from multiple large scale studies.1,7,8 The rates of FJA in women are nearly twice those in men.7 BMI is also independently associated with increased risk of FJA, up to threefold higher in overweight individuals, and fivefold in obese individuals.7,9 Overall, the increase in prevalence of FJA is largely age dependent, with moderate or severe FJA present in 36% of adults age <45 years, 67% of adults age 45-64 years, and 89% of those age 65 years or older.7 Changes in any component of the three-joint spinal unit lead to predictable changes in other components. Therefore, it is not surprising that concurrent disc-height narrowing is independently associated with doubled odds of FJA at the involved levels.7 Vascular disease is also associated with increased prevalence of FJA, which suggests a modifiable risk factor to degeneration outside the conventional biomechanical paradigm.7,9 Like other synovial joints, FJs are potential pain generators in cases of low back pain (LBP) and have been of clinical interest in that context since the 1910s. Of patients with localized LBP, facet mediated symptoms account for 5-90% of cases depending on the population studied and the means of diagnosis, with more recent studies using placebo-controlled blocks suggesting a rate closer to 15%.1,4,6, 10 Primary prevention is directed at modification of risk factors such as weight management and promotion of a physically active lifestyle.
Patho-anatomy and physiology
Facets consist of the inferior articular process of the superior vertebra and the superior articular process of the inferior vertebra and exhibit features typical of synovial joints including aneural articular cartilage, synovial membrane, capsular pouch, fibroadipose meniscoid, and a fibrous capsule.11 FJs function to stabilize and limit excessive flexion, extension, side-bending, and axial rotation of the spine. The orientation of the joints relative to the sagittal plane is different in the upper levels than the lower levels. Tropism, or differing orientation of paired joints, is common in the general population. Each joint receives dual innervation from the medial branches of the dorsal primary rami of the same level and the level above.1 One in nine patients have been found to have FJ innervation from other nerves, such as the medial branch below the joint or the dorsal root ganglion.1,4 Studies have demonstrated free, encapsulated and un-encapsulated nerve endings in lumbar FJs.1,12. These nerves contain substance P, calcitonin gene-related peptide, and even neuropeptide Y which is typically found in sympathetic efferent fibers.1,12 Many inflammatory mediators and cytokines have been found in facet joint cartilage and synovial tissue in degenerative lumbar spine disorders. Direct pressure on subchondral bone, intramedullary hypertension, trabecular micro-fractures, capsular distension, and synovial inflammation activate nociceptor fibers leading to acute pain.1 Chronic pain is thought to occur due to neuronal sensitization secondary to persistent nociceptive input.
Disease progression including natural history, disease phases or stages, disease trajectory
The earliest changes of FJA involve the articular cartilage, synovium, and capsule. Cartilage breakdown begins focally and superficially, progresses deeper, encompassing the entire joint, and eventually erodes down to the subchondral bone.14 In early arthropathy the joint capsule might show fibrosis and increased vascularization with inflammatory cells. Extensive fibrocartilage proliferation occurs later.15 Osteophyte formation and remodeling of the subchondral bone with formation of sclerosis and subchondral cysts are characteristic of advanced disease.1
Specific secondary or associated conditions and complications
At any stage of the disease, a degenerative event or mechanical joint injury can initiate an inflammatory response leading to muscle spasms of the spinal erectors and radicular symptoms from leakage of cytokines through the ventral capsule.4,12,13 Prolonged peripheral inflammation can lead to central sensitization due to neuronal plasticity that progresses to a chronic pain syndrome.4,16 Foraminal stenosis, central stenosis, radicular symptoms, and nerve impingement may occur due to joint hypertrophy and synovial cyst formation especially if the cyst projects anteriorly.4 Adult degenerative spondylolisthesis is also related to FJA secondary to failure of motion segments and is more prevalent in those with sagittally oriented FJs.17
Essentials of Assessment
There are no symptoms specific or unique to FJA. Patients present with axial back pain and stiffness. Referred pain is predominantly in the buttock as well as the posterior or anterior thigh, rarely radiating past the knee when at severe intensities.18 Other common causes of acute and chronic LBP can have similar presentations, and no historic or exam features can reliably predict response to diagnostic facet blocks.12 History is most useful in excluding alternative etiologies, in particular radiculopathies, fractures, infections, neoplasms, or rheumatologic conditions.1,4 Some authors suggest that “typical” facetogenic LBP is progressive, although this too is contraversial.4
There are no specific signs or special tests to aid in the facet syndrome diagnosis, which is often guided by the absence of signs that suggest alternate etiologies such as pain worsened with coughing, pain radiating below the knee.20 Patients are typically neurologically intact. Non-midline tenderness, and possibly tenderness over the facet joints, may be weakly associated with a positive response to facet joint interventions.4,19,20 “Facet loading”, or pain upon extension and ipsilateral rotation, was popularized in a small, retrospective study; however, larger, higher quality studies have consistently failed to replicate this finding.19-24
Mobility can be impaired due to pain. Studies have repeatedly failed to identify patient reported activities that are associated with the presence of facetogenic LBP.4
Laboratory studies are not used to diagnose FJA but facilitate exclusion of other etiologies of LBP. Renal and hepatic function studies maybe be needed to guide medication management.
The ability of radiologic imaging to predict response to diagnostic FJ blocks has been conflicting at best. The current recommendation is to avoid imaging for acute LBP within the first 6 weeks of presentation unless red flag symptoms are present.24,25 Plain films of the lumbar spine with stress views (flexion and extension) can be considered to look for possible complications of FJA like spondylolisthesis or dynamic instability of motion segments. The majority of available epidemiologic studies showed no consistent relationship between the presence or severity of FJA on CT, fused PET and CT, and/or MRI and the presence of LBP although some suggest that SPECT findings are weakly associated with response to blocks.1,4,20 There are low to moderate strength recommendations against routine imaging prior to proceeding with a diagnostic FJ procedure.20
Supplemental assessment tools/Early prediction of outcomes
Lumbar medial branch blocks (MBBs) are strongly recommended for patients with suspected facetogenic LBP as the gold standard for diagnosis as well as candidate selection for definitive therapy.4,12,20,26 MBBs, intra-articular injections, and radiofrequency ablation (RFA) must be performed using image guidance for both safety and accuracy, with fluoroscopy typically preferred to CT due to lower costs, faster time, and less radiation exposure.20 MBBs are considered more predictive than intra-articular FJ injections, which are still considered diagnostic but are more technically challenging with higher technical failure rates.20 Some studies suggest reserving intra-articular FJ blocks to younger patient populations where the anatomy allows for easier access and for those with inflammatory etiologies.20 For MBBs, the false positive rate in the lumbar spine is between 17-44% and the false negative rate is about 8%.4,12,26 Interestingly, false-positive responders to medial branch blocks with steroids have been shown to experience benefits that are indistinguishable from those of treatment responders.27 The best outcomes appear to be in studies with dual blocks who achieved at least 80% pain relief following MBB, however, some guidelines suggest using a lower cut off of 50%.20,28-30 The use of dual blocks has consistently shown decreased risks of false positives and higher subsequent success rate with RFA, but some organizations continue to recommend a single block to maximize access to treatment.20 The consequences of false-negative blocks, commonly caused by aberrant joint innervation by non-medial branch nerves or patient failure to distinguish daily pain from procedure-related pain, are serious because it means a safe, effective treatment will be withheld from a patient who otherwise has limited reliable treatment options.4,20
Early predictions of outcomes
Poor postures and repetitive heavy lifting have been reported to increase the risk of future sick leave due to back pain.31 Heavy physical activity has been associated with worsening FJA on imaging, however, specific exercises, actions and tasks have not been studied sufficiently.32
Social role and social support system
Chronic LBP can lead to multifactorial disability and work absenteeism. Biopsychosocial factors such as depression, poor coping skills, lack of home/community support, somatization, secondary gain issues (e.g., ongoing litigation), and greater disease burden (e.g., high dose opioid use, previous spinal surgery) can lead to harder to treat pain and worse interventional outcomes. Poor patient selection, including the aforementioned reasons, for invasive treatments is perhaps the most common reason for treatment failure.1,20
Lumbar facet interventions are the second most common procedure performed in interventional pain practices in the US.20 From 2000 to 2013, in the Medicare population alone, MBBs and RFAs increased at a rate of 213% and 522% respectively.33 Review of the FJ injections allowed by Medicare Part B in 2006 found that 63% did not meet the program requirements for reimbursement, 38% had a documentation error, 31% had a coding error, 8% did not establish medical need, and 14% had overlapping errors.34 A more recent review of the Marketscan commercial claims and encounters database from 2007 to 2016 demonstrated a 130.6% overall increase in utilization with an annual 12.2% associated increase in cost.20 Increasing utilization alters the risk to benefit ratio of treatments and has raised increased scrutiny on the parts of government regulatory agencies and payers, in US and internationally.20
Sedation for spinal procedures has also received scrutiny in recent years and remains a debated topic. Sedation for facet procedures has been justified using both patient centric (e.g.: reduce procedure related discomfort or anxiety) and physician centric perspectives (e.g.: increase patient satisfaction, decrease body movements during procedure, reduce no-show rates, and expedite workflow).20 There is also the potential for higher reimbursement for procedures done under sedation. Despite these potential benefits, sedation can increase false-positive rates of the procedures and carries intrinsic risks to the patients. Most guidelines recommend against routine use of sedation, and avoidance of opioids for sedation if possible.20,30
Rehabilitation Management and Treatments
Available or current treatment guidelines
Multiple organizations have published guidelines on management of LBP stemming from FJA with many undergoing multiple revisions and updates through the years. The North American Spine Society (NASS) as a combined effort with American Academy of Physical Medicine & Rehabilitation (AAPMR) and American Association of Neurological Surgeons and Congress of Neurological Surgeons (AANS/CNS) released guidelines in 2020 and last updated them in January of 2021.29 The American Society of Regional Anesthesia and Pain Management (ASRA)20, and American Society of Interventional Pain Physicians (ASIPP)30 released updated guidelines in 2020. A non-exhaustive list of additional guidelines includes the American College of Occupational and Environmental Medicine (ACOEM) updated in 2021, the Centers of Medicare and Medicaid Services (CMS) updated in 2021, and Spine Intervention Society (second edition updated in 2014). Some of the published guidelines have received major scrutiny and criticism by experts for poor methodology and discordance with clinical practice.36
At different disease stages
No studies have evaluated non-interventional therapy for injection-confirmed FJ pain, so treatment is extrapolated from patients with non-specific LBP.4,37 Most experts and guidelines recommend a 3 month trial of conservative management, which may include a combination of NSAIDs and other non-opioid oral analgesics, muscle relaxers, exercise-based rehabilitation, weight reduction, topical agents, thermal remedies, integrative treatments, and addressing psychological comorbidities.4,20,30 Exercise therapy, especially physical therapy (PT), has the strongest evidence for efficacy compared to all other non-interventional treatments.4 PT, which has overall better outcomes than a home program, should address posture, range of motion, muscular strengthening, activity/risk factor modification, and provide pain neuroscience education for those with chronic pain.4 Acupuncture and chiropractic or osteopathic manipulation have low quality evidence for short term pain relief; but when compared to sham, other non-interventional treatments, or physical exercise, the results are inconclusive.4 Early interventional modalities are sometimes performed for very painful presentations and may aid in therapy participation.37 Opioids should be used with caution, as new guidelines published by CDC in 2016 noted early opioid exposure increased the risk of long-term use.38 If using opioids, clinicians should prescribe the lowest effective dose of immediate-release formulations for three to seven days maximum.38
If symptoms have been present for more than three months and have not responded to conservative treatment, interventional methods are often pursued. These interventions include intra-articular corticosteroid injections, MBBs, and RFAs. Therapeutic intra-articular injections are considered inconclusive with weak to moderate evidence for adequate treatment for lumbar facet joint pain although may be an appropriate choice in younger patients in whom RFA is relatively contraindicated.20,29,30 Therapeutic nerve blocks with added steroid remain controversial, but have some moderate evidence to support their use.20,30 Approximately 90% of responsive patients received an average of 5 to 6 procedures over a 2 year period.12 At the end of one year, 69% of therapeutic MBB patients showed significant improvement in pain compared to 90% in the RFA group.33 There is good evidence for RFA efficacy up to 6 months and moderate evidence for long term pain relief in appropriately selected patients.20,29,30,33 The efficacy of RFA for functional improvement is limited, with only low quality evidence available to suggest that RFA has greater effect than placebo.39 Serious complications from RFA are rare (<1%).4,20
If RFA has yielded positive results, it can be repeated every six months with expected relief lasting up to 13-24 months for repeat treatments.12,20,28 Opioid therapy for chronic LBP is a controversial topic and not generally recommended. There is no good evidence that opioids improve pain or function with long-term use, and complete relief of pain is unlikely.38 Clinicians should use extreme caution when considering increasing opioid dosages for chronic LBP and should follow current guidelines.38 There is a lack of evidence for arthrodesis and surgery for spondylosis or facet-mediated pain. Surgery can be indicated in patients with symptomatic spondylolisthesis and/or dynamic instability of the spine.
Coordination of care
The physiatrist’s role is to coordinate a multidisciplinary approach to treatment, including ensuring consistent pain education and messaging is provided to the patient by the care team.
Patient & family education
Intensive physical rehabilitation and pain neuroscience education, typically referred to as “Back School” or “Back Boot Camp” can improve the quality of life in patients who suffer from chronic LBP and prevent recurrent injuries.40 Patient education appears to reduce the negative consequences of fear-avoidance behavior that occurs when attempting active exercise-based rehabilitation and thus promotes treatment compliance. Patient and family education should be focused on risk factor modification, the importance and safety of physical activity in recovery, and institution of a feasible home exercise program after discharge.
Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills
Facet arthropathy is often asymptomatic; medicalization of normal degenerative changes should be avoided. Symptomatic facet arthropathy is best confirmed via MBBs after an initial trial of conservative treatment fails to yield desired improvements. If the patient has failed conservative treatment and injection is the next step, the site of pain can be palpated and confirmed under the fluoroscope before performing a diagnostic MBB. By attempting to confirm the level of pain prior to the injection, the accuracy and potential efficacy of the procedure may improve. Routine imaging is not required, although it may help exclude alternative dangerous etiologies or findings. Radiofrequency ablation remains the current standard for management of chronic facetogenic pain but cut offs for candidate selection and aspects of the procedural techniques remain controversial.
Cutting Edge/Emerging and Unique Concepts and Practice
The use of ultrasound guidance for intra-articular injections and MBBs has garnered interest, with multiple studies demonstrating its feasibility and benefits including lack of radiation exposure and possibly faster performance time.20,42-45 Ultrasound is not a feasible tool for image guidance in patients with elevated BMIs, which unfortunately is up to 40% of the US population.20 In addition, reports of endoscopic guidance for lumbar medial branch neurotomy have been described with overall comparable outcomes and low complications.46 Techniques for percutaneous facet fusion are available, but long-term published results are not.47. There has been a recent interest in regenerative techniques such as platelet rich plasma (PRP) or stem cell therapies for FJA and other spinal degenerative conditions.48
Gaps in the Evidence-Based Knowledge
There is an ongoing need for more and better designed studies examining the efficacy of interventional and conservative management options.
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- Adams MA, Hutton WC. The mechanical function of the lumbar apophyseal joints. Spine (Phila Pa 1976). 1983;8(3):327-330. http://www.ncbi.nlm.nih.gov/pubmed/6623200.
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- Suri P, Miyakoshi A, Hunter DJ, et al. Does lumbar spinal degeneration begin with the anterior structures? A study of the observed epidemiology in a community-based population. BMC Musculoskelet Disord. 2011;12:202. doi:10.1186/1471-2474-12-202.
- Brinjikji W, Luetmer P, Comstock B, Bresnahan B, et al. Systematic literature review of imaging features of spinal degeneration in asymptomatic populations. AJNR Am J Neuroradiol. 2015;36(4):811-6. https://pubmed.ncbi.nlm.nih.gov/25430861/.
- Suri P, Katz JN, Rainville J, Kalichman L, Guermazi A, Hunter DJ. Vascular disease is associated with facet joint osteoarthritis. Osteoarthritis Cartilage. 2010;18(9):1127-1132. doi:10.1016/j.joca.2010.06.012.
- MacVicar J, MacVicar AM, Bogduk N. The Prevalence of “Pure” Lumbar Zygapophysial Joint Pain in Patients with Chronic Low Back Pain. Pain Med. 2021;22(1)41-48. https://pubmed.ncbi.nlm.nih.gov/33543264/
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- Manchikanti L, Abdi S, Atluri S, et al. An update of comprehensive evidence-based guidelines for interventional techniques in chronic spinal pain. Part II: guidance and recommendations. Pain Physician. 2013;16(2 Suppl):S49-283. http://www.ncbi.nlm.nih.gov/pubmed/23615883.
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- Boszczyk BM, Boszczyk AA, Korge A, et al. Immunohistochemical analysis of the extracellular matrix in the posterior capsule of the zygapophysial joints in patients with degenerative L4-5 motion segment instability. J Neurosurg. 2003;99(1 Suppl):27-33. http://www.ncbi.nlm.nih.gov/pubmed/12859055.
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Original Version of the Topic
Amit Bhargava, MD. Lumbar zygapophyseal joint arthropathy. 5/19/2013.
Previous Revision(s) of the Topic
Clifford Richard Everett, MD, Mark Bauernfeind, MD, Maria Vanushkina, MD. Lumbar zygapophyseal joint arthropathy. 3/27/2017.
Maria A Vanushkina, MD
Nothing to Disclose
Patrick O’Connor, MD
Nothing to Disclose
Clifford Everett, MD
Nothing to Disclose