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Section 8, Chapter 1: Rheumatoid Arthritis

Tamir Ailon, MD, MPH


Rheumatoid arthritis (RA) is an inflammatory arthropathy that affects multiple joints in the extremities and axial skeleton. It is characterized by joint destruction which is thought to arise from autoimmune-mediated inflammation. Attenuation of ligamentous support structures around affected joints may lead to instability. RA is commonly associated with osteopenia and osteoporosis. Relative immunodeficiency is another hallmark and may arise from the disease itself or from the suppressive medications utilized in its treatment.

In the spine, the cervical region is the most typically involved by RA—its manifestations here have been extensively studied. For example, spinal fusion for atlantoaxial instability is a well-established treatment.1 Though less characteristic and by no means pathognomonic, lumbar spine pathology in patients with RA is not infrequent. It may manifest in a variety of forms, including disc space narrowing, endplate erosion, facet erosion, facet cysts, spinal stenosis, spondylolisthesis, scoliosis, osteoporosis and compression fractures.2-8 Up to 50% of patients with RA have back pain; those that experience back pain report higher levels of disability and depression.2,9 Low back pain is associated with disease activity; however, the relationship between this symptom and radiological findings is unclear.10 Spinal fusion appears to achieve comparable clinical outcomes in patients with and without RA, albeit with a higher risk of complications in the former group. This chapter will discuss the clinical and radiographic features that characterize RA involvement of the lumbar spine and highlight key aspects of the management and outcomes of treating such patients.


Back Pain

Back pain has a higher prevalence among patients suffering from RA than in the general population. Helliwell at al.2 reported the point prevalence of chronic back pain in a population of patients with RA of 33%; the majority of these patients had pain for between 6-12 months. The majority of RA patients report their primary area of pain in the peripheral joints or cervical spine, however 13.5% report the low back as their primary pain site.11 Yamada et al.10 demonstrated a prevalence of 4-week severe low back pain (visual analogue score > 50) of 23.9%. On multivariate analysis, risk factors for severe pain included female sex, smoking and RA disease activity. Of these factors, high disease activity was the most strongly associated with incidence of severe low back pain (OR 6.97). Conversely, radiological findings – including scoliosis, spondylolisthesis, vertebral fracture, disc degeneration and spinopelvic parameters – were not significantly associated with incidence of severe low back pain. The strong correlation between disease activity and low back pain may be explained by higher pain sensitivity which causes patients to self-report greater low back pain and peripheral joint tenderness. Alternatively, or additionally, the inflammatory response in the lumbar spine associated with high RA disease activity may inherently induce severe pain in the low back and peripheral joints.

The specific causes of back pain in RA are not clear and are not necessarily distinguishable from those in patients without RA. Despite the prevalence of joint erosions in the lumbar zygapophyseal joints of RA patients, the typical syndrome of facet-mediated pain (hip and buttock pain, early morning stiffness, aggravation by extension) is present in the minority of patients.2 Spondylolisthesis and associated instability may contribute to back pain in RA patients, however it is more frequently identified in mechanical low back pain associated with spondylosis than in those with RA. The etiology of back pain is likely multifactorial and may include facet joint disease, compression fractures associated with osteoporosis, spondylolisthesis with associated instability, and gait anomalies associated with lower limb joint RA involvement.

Neurologic Symptoms

In RA, neurologic symptoms, when present, are typically associated with cervical lesions. Upper cervical lesions including atlantoaxial and vertical subluxation cause myelopathy due to dynamic and static compression of the spinal cord. Lower cervical lesions produce similar patterns of spinal cord dysfunction due to destructive changes in the cervical spine and associated vertebral subluxation. Neurologic symptoms associated with lumbar spine involvement receive less attention, likely attributable to their lower incidence and reduced propensity to cause significant impairment. Kawaguchi et al.6 reported on 106 patients with RA, of which 57% had abnormal radiologic findings in their spine. In this group, 42% had concurrent lumbar and cervical lesions. Symptoms potentially attributable to lumbar involvement occurred in 10-20% of RA patients and included leg pain, leg numbness, and neurogenic claudication.


Lawrence et al.12 first described the distinct radiographic features of lumbar disease associated with RA. These features include disc space narrowing without osteophytosis, facet joint erosion, spondylolisthesis and osteoporosis. The reported prevalence in this study was only 3-5%, however, subsequent studies have shown the lumbar pathology characterizes approximately half of patients with RA.6,13 Using quantitative MRI, Yamada et al.14 demonstrated a very high prevalence of endplate (71%) and facet erosion (77%) suggesting that this modality has greater sensitivity for RA-associated lumbar pathology.

Cadaveric studies have demonstrated endplate and facet joint erosion in the lumbar spine of RA patients.3 Facet joint erosions occur in the cartilage and subchondral bone ostensibly as a result of inflammatory synovitis. Although vertebral endplates (discovertebral junctions) are not synovial joints, they share the characteristic of being lined by predominantly hyaline articular cartilage. Endplate erosion is thought to originate at the discovertebral junction as an enthesopathy, progressing to disc space loss as a function of inflammatory degeneration of collagen.14 Despite the fact that the radiographic findings of endplate and facet erosion are not unique to RA, the erosive pathophysiological process may play an important role in the development of lumbar disease in this condition.

Patients with RA involvement of their lumbar spine and those with degenerative lumbar disease both exhibit radiographic disc space narrowing; however, the absence of osteophyte formation typifies the former.2,6,12 This is also true when comparing peripheral joint manifestations of RA and those of osteoarthritis. Osteophyte formation may be limited in the lumbar spine and peripheral joints by high concentrations of osteoclasts and osteoclast differentiation factor, both prevalent in areas of rheumatoid pannus invasion into bone.15,16


As with management of cervical and peripheral manifestations of RA, the main treatment of associated lumbar pathology is with medicine. Patients are typically treated with disease modifying antirheumatic drugs (DMARDs). This has led to a dramatic reduction in the prevalence and severity of clinical manifestations of RA. There are many publications on management of disease in the cervical spine. Surgical treatment of symptomatic patients with pain or neurologic deficits arising from atlantoaxial subluxation, atlantoaxial impaction and subaxial subluxation comprises decompression and fusion. In this setting, surgery is associated with improvement in neurologic function, reduction in pain and improved quality of life.17

There exist a paucity of studies characterizing the surgical treatment of lumbar spine disease in rheumatoid patients. There are limited reports – comprising case reports and series – of successful treatment of a variety of lumbar spine pathologies with decompression and either posterolateral or interbody fusion. 3,4,7,18 Where comparisons have been made with non-RA lumbar surgery, comparable clinical outcomes but a higher rate of complications has generally been reported in patients with RA.18 Furthermore, Kang et al.19 demonstrated that significant improvement of roughly equal magnitude in RA and non-RA patients was attenuated in the former group after the first year. The authors attributed the RA group’s decline in outcome to a higher rate of delayed postoperative complications such as adjacent segment disease, non-union and implant-related complications. The rate of pseudarthrosis is higher in patients with RA;19 this is attributable to the disease process which entails an imbalance between bone resorption and formation due to excessive proinflammatory cytokines.20 DMARDs, immunosuppressive drugs and glucocorticoids also adversely affect new bone formation and, accordingly, likely contribute to higher rates of non-union.

Osteoporosis occurs in the majority of patients with RA due to a variety of causes outside the scope of the present discussion. Thus, it is perhaps not surprising that implant-related problems occur more commonly with instrumented fusions in patients with RA.5,18 They are also prone to adjacent segment disease including proximal junctional failure, particularly due to fracture of the upper instrumented vertebra. Increased biomechanical stress of the adjacent segment after lumbar fusion contributes to the development of symptomatic adjacent segment disease.21 Such stress acts on the facet joint and discovertebral junction which, as mentioned previously, are implicated in the pathology of RA thus providing a potential explanation for the relatively high incidence of adjacent segment disease in this population.18

Endplate erosion may complicate placement of interbody grafts leading to subsidence and loss of anterior column support.18 Additional care must therefore be taken in the selection and placement of interbody grafts to minimize this risk. Whereas some authors have argued for long constructs to maximize points of fixation,5 others believe that short segment fixation with cement augmentation is preferred. Wound complications, especially infections, are more common in RA patients, likely owing to their relative immunodeficiency. Strategies to mitigate this increased risk should include consultation with the treating rheumatologist and perioperative modification of immunosuppressive therapies, disease modifying agents and the antibiotic regimen.4


Although cervical spine pathology predominates in rheumatoid patients, lumbar disease is not infrequent. There are characteristic but not necessarily distinct clinical and radiographic manifestations of rheumatoid arthritis that affect the lumbar spine. Patients with rheumatoid arthritis report higher rates of low back pain; those that report back pain have greater disability and depression. Surgical treatment generally involves decompression and fusion and is associated with improved clinical outcomes albeit with an increased risk of complications relative to patients without rheumatoid disease.


  • Although the cervical manifestations of rheumatoid arthritis (RA) are more prevalent and associated with greater neurologic impairment, lumbar disease remains prevalent and may significantly contribute to pain and disability in RA patients.
  • Radiographic manifestations of rheumatoid involvement of the lumbar spine may include facet and endplate erosions, disc space narrowing without osteophytosis, spondylolisthesis, scoliosis, osteoporosis and compression fractures.
  • Many radiographic features of RA are shared by degenerative lumbar disease; however, the latter tends to be associated with more robust osteophyte formation.
  • Surgical treatment, typically comprising lumbar decompression and fusion, produces comparable clinical outcomes to patients without RA but is associated with a higher risk of complications including, in particular, adjacent segment disease, implant-related problems and wound-related complications.


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