Osteoarthritis and Inflammatory Arthritides of the Aging Spine

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13 Osteoarthritis and Inflammatory Arthritides of the Aging Spine

Because of space limitations, osteoarthritis of the aging spine will be primarily considered in this review. Certain inflammatory arthritides will be considered as a part of the differential diagnosis. Osteoarthritis is an almost ubiquitous disease and a significant source of morbidity. Although it can affect every age demographic, it has an increasing prevalence in the elderly population.1 In the elderly, osteoarthritis is a significant source of disability and has a deleterious effect on a patient’s quality of life. Although a majority of studies have examined the effect of osteoarthritis on hip, knee, and hand joints, osteoarthritis can affect any joint in the body, including those in the spine. Spinal osteoarthritis commonly manifests with back or neck pain. The degeneration caused by spinal osteoarthritis can also result in central canal or neural foraminal stenosis, or both, which may cause neurological deficit, including radiculopathy, neurogenic claudication, or myelopathy.

The treatment of spinal osteoarthritis is a significant burden on health care systems globally. Patients with spinal osteoarthritis are major consumers of pharmaceuticals and allied health resources. Although most patients are treated conservatively, as the population ages, spine surgeons will become increasingly involved in the treatment of spinal osteoarthritis in the elderly. A fuller understanding of the disease, including its risk factors and pathophysiology, is therefore imperative to properly counsel patients on their options for treatment. The following three case examples present patients with severe manifestations of osteoarthritis requiring consultation for possible surgical intervention.

Clinical Case Examples

Clinical Case #1 (Degenerative Lumbar Spondylolisthesis)

Figure 13-1 presents lumbar magnetic resonance imaging (MRI) of a 67-year-old woman with a 30-year history of progressive lower back pain. This pain was exacerbated by activity and relieved by rest. She reported no associated radicular symptoms. Past medical history was significant for morbid obesity, diabetes, and osteoarthritis. Physical exam did not reveal a neurological deficit. The patient had failed to improve despite intensive conservative therapy which included high dosage opiates, physiotherapy, epidural steroid injections, and facet blocks. MRI and plain radiography (see Fig. 13-4) revealed degenerative spondylolisthesis, central canal stenosis, and bilateral synovial cysts. Lateral flexion and extension films demonstrated a 10-mm anterolisthesis of L4 on L5 with 9 mm in extension and 11 mm in flexion. Due to increasing disability and lack of response to conservative measures, the patient was referred for evaluation for surgical intervention.

Clinical Case #2 (Degenerative Cervical Spondylosis)

Figure 13-2 presents axial computed tomography (CT) myelogram images of a 79-year-old woman with moderate neck pain and progressive difficulty with ambulating during the past 4 years. At presentation, the patient was wheelchair bound with limited ability to transfer. Past medical history was significant for osteoarthritis, atrial fibrillation, and multiple peripheral neuropathies. Physical examination revealed gross lower extremity hyperreflexia and weakness and was consistent with myelopathy. Her sensation was diffusely diminished in her hands and arms, but she did have normal sensation in the C4-C5 distribution. She did not have a Hoffman sign, but had extensive hand intrinsic muscle atrophy. She did have crossed adductor reflexes. She was able to flex and extend her neck to 35 degrees and laterally rotate to 40 degrees. The patient’s CT myelogram demonstrated severe spinal cord compression at the C4-C5, C5-C6, and C6-C7 levels. There was anterolisthesis and osteophytic bulging, which resulted in severe spinal canal narrowing.

Clinical Case #3 (Atlantoaxial Instability)

Figure 13-3 presents images from a CT scan of an 85-year-old woman with severe neck pain and occipital neuralgia. The pain had been progressively worsening during the past 12-month period despite analgesia. Past medical history included hypertension, hypothyroidism, and osteoarthritis resulting in bilateral knee arthroplasties. On physical exam no weakness or evidence of myelopathy was detected. Dynamic imaging revealed a C1-C2 atlantodens interval of 4 mm in neutral, increasing to 5 mm in flexion and in extension. CT imaging (see Figure 13-3) demonstrated gross evidence of atlantoaxial instability including pannus. The patient received temporary relief with a greater occipital nerve block. Because of the overwhelming disability attributable to her neck pain and occipital neuralgia, the patient was considered for surgical intervention.

Basic Science

Osteoarthritis is a complex disease and may represent a series of diseases rather than one specific disease entity.1 The consensus definition states that osteoarthritis is a result of both mechanical and biological events that destabilize the normal coupling of degradation and synthesis of articular cartilage, extracellular matrix, and subchondral bone. When clinically evident, osteoarthritis is characterized by joint pain, tenderness, limitation of movement, crepitus, and variable degrees of inflammation without systemic effects.1 Osteoarthritis affects articular joints including the knees and hips. The zygapophyseal or facet joints are the synovial joints in the spine and therefore susceptible to osteoarthritis. Spinal osteoarthritis is therefore a disease of the facet joints due to degeneration, resulting in facet joint incompetence.

Epidemiology and Risk Factors

Spinal osteoarthritis has been demonstrated through radiographic and cadaver studies to affect every adult age group.2,3 The prevalence of clinical spinal osteoarthritis increases with age, with elderly patients having the highest radiographic and symptomatic prevalence.1,3 There is also a significant gender difference in prevalence. Females are more likely than males to suffer from osteoarthritis in general. The gender difference is exacerbated after menopause and therefore greater in the elderly.1

Other risk factors besides age and gender have been reported to be associated with the development of osteoarthritis. Obesity has a strong correlation with developing osteoarthritis. This likely represents added mechanical stress to the facet joints. Previous trauma from sports activities and occupations requiring strenuous physical labor have also been associated with the development of spinal osteoarthritis.1

Pathophysiology

Osteoarthritis is a disease of the articular cartilage and underlying subchondral bone. Although the exact etiology of osteoarthritis is not known, one theory is that cartilage matrix turnover is negatively affected by degenerative forces. This disrupts the balance between cartilage synthesis and degradation. Evidence suggests that collagenase, gelatinase, and stromelysin, which are enzymes involved in cartilage degradation, are increased in osteoarthritic joints.1 The cause for this imbalance is not clear. One proposed theory is that changes to the subchondral bone instigate changes to the cartilage matrix. Radiographic evidence of subchondral bone changes is often present in patients with osteoarthritis. It is theorized that stiffening of the subchondral bone due to microtrauma results in an abnormal environment for the overlying cartilage. This increases cartilage turnover and leads to further degradation of the joint. However, the debate as to whether subchondral bone changes are a result or cause of cartilage degeneration is not settled.1

Also unsettled is the role of the inflammatory response in the pathogenesis of osteoarthritis. Localized inflammation has been demonstrated in certain stages of osteoarthritis, including mononuclear cell infiltrate and synovial hyperplasia. The exact role of this inflammation, be it causative or reactionary, is not clear. Markers of inflammation such as C-reactive protein (CRP) may be elevated as well.1 However, in general, systemic inflammation is not characteristic of osteoarthritis. Its presence would indicate that another pathology such as rheumatoid arthritis or gout should be considered.

Degenerative Mechanics

Osteoarthritic changes at the facet joints can have a cascading effect on a patient’s overall spinal health. The facet joints function as the posterolateral articulation between vertebral segments. As such, they bear weight, restrict anterior and posterior movement of the anterior column, and restrict axial rotation. Arthritic changes in these joints can promote abnormal spine mechanics, increasing degeneration. It is commonly held that facet joint arthrosis is a sequela of disc degeneration.4 However, there is evidence to suggest that facet arthrosis is a long-standing phenomenon present before evidence of disc degeneration.2 Either way, the coupling of facet joint arthritis with disc degeneration can lead to progressive degenerative changes. In the normal spine, facet joints bear between 18% and 25% of the segmental weight load.4,5 Facet joints in degenerative spines can bear upwards of 47% or more in extension.5 This leads to progressive stress on a weakened joint. Sequelae of continued stress on the weakened facet joint include osteophytosis and synovial cyst formation. These can cause radiculopathies if affecting the lumbar or cervical foramina. Specific symptoms vary by levels, with L4-L5 being the most commonly affected.5 Large osteophytes or synovial cysts coupled with anterior osteophytic change can lead to central canal stenosis. This stenosis can result in symptoms of neurogenic claudication when located in the lumbar spine, or symptoms of myelopathy when located in the cervical spine.

Severe osteoarthritis in the facet joints can lead to changes in spinal alignment. Competent facet joints prevent forward sliding of one vertebra upon another. When damaged by osteoarthritis, facet joint incompetence contributes to degenerative spondylolisthesis. This spondylolisthesis is generally mild and asymptomatic but can cause neurological symptoms when the degree is severe. Symptoms may include intractable neck or lower back pain or radiculopathy due to compression of the neural foramen. Osteoarthritic changes of the facet joints can also exacerbate other deformities of the spine, including degenerative scoliosis, as these joints serve as a stabilizing influence on spinal alignment.

The atlantoaxial junction is a common site for arthritic changes, most commonly seen in rheumatoid arthritis. Although classically not associated with osteoarthritis, atlantoaxial osteoarthritis has been reported to have a prevalence ranging between 5% and 18% of patients with spinal osteoarthritis.6 True symptomatic prevalence is probably much smaller. Arthritic changes can affect the lateral mass articulations and the atlantodens articulation. Degeneration at the atlantodens articulation can produce a pannus, similar to that seen in rheumatoid arthritis, causing myelopathic symptoms due to cord compression. More commonly, osteoarthritis at the atlantoaxial junction results in neck pain. This pain generally originates in the suboccipital region. It can radiate both cranially and caudally and can present with severe occipital pain. In general, occipital pain or subaxial neck pain without a suboccipital component most likely does not represent pain from atlantoaxial osteoarthritis, and other sources of pain should be excluded. In cases where the pain generator is difficult to locate based upon symptomatology, C1-C2 facet blocks can be a diagnostic aid if they relieve the neck pain.

Natural History

The natural history of spinal osteoarthritis is difficult to define. Most patients will present with back or neck pain, the etiology of which can be hard to determine. Some investigators feel that facet joints are a significant pain generator. Facet joints are innervated by branches of the dorsal rami of the same level and, the level above. After the capsule of the facet joint is innervated with nociceptive fibers. However, studies using facet blocks to examine facet joint contribution to spinal pain report varying prevalence from 7% to 75%.5 In addition, a large study of the prevalence of spinal osteoarthritis in women demonstrated a peak in incidence of osteoarthritis in the mid thoracic spine region. However, this radiographic peak did not correlate with any clinical symptoms. The same study did demonstrate a peak at the L4-L5 segment, which correlated with increased symptom scores.3 This study underlines the variability of clinical symptoms with significant radiographic findings.

In general, osteoarthritis is a progressive disease. Whereas disease modifying agents are currently employed in the treatment of gout, rheumatoid arthritis, and psoriatic arthritis, the treatment of osteoarthritis is primarily symptomatic. This treatment may be beneficial to most, but some patients still develop enough spinal degeneration to result in significant morbidity and disability. Decreased mobility coupled with deconditioning portends significant physical decline. Thus, while most patients will stabilize with current therapy, some patients will progress to developing significant pain, neurological deficit, and disability. These patients are the most likely to present to a spine surgeon for evaluation and treatment.

Clinical Practice Guidelines

Evaluation

Elderly patients presenting with significant neck or back pain should be evaluated with plain radiographs to look for evidence of facet joint arthrosis. Those presenting with neurological deficit should be evaluated with MRI or CT myelogram to determine the extent and location of neural compromise. MRI offers a noninvasive assessment of soft tissue disease, whereas CT myelograms can provide additional information on bony compression and provide for surgical planning for instrumentation.

Rheumatological consultation may be necessary to exclude other inflammatory disorders. Diffuse idiopathic skeletal hyperostosis (DISH) has a high prevalence in the elderly. It commonly manifests with calcification and ossification of soft tissues including ligaments and affects the spine. Symptoms usually involve pain and stiffness. Although it may be present concomitantly with osteoarthritis, DISH is usually radiographically distinct and recognizable by osteophytic change, often affecting the anterior longitudinal ligament, with preservation of the disc space. Rheumatoid arthritis can also cause signs and symptoms similar to osteoarthritis. Cervical degeneration with pannus formation is seen with advanced rheumatoid arthritis.

Exclusion of other pain generators is imperative. Radiographic evidence of arthrosis does not necessarily correlate with symptoms. Patients with significant back and hip pain should be evaluated for such conditions as trochanteric bursitis. Treatment via steroid injection may alleviate both hip and back pain. Evaluation of hip osteoarthritis should also be undertaken. A hip–spine syndrome has been postulated for several years as a cause of spine pain in patients with severe hip osteoarthritis. Recent evidence has suggested significant improvement in back pain scores and improvement in Oswestry disability scores in patients undergoing hip replacements for hip osteoarthritis.7 Because osteoarthritis commonly affects multiple joints, evaluation of the hip should be performed in patients with lower back and hip pain.

Conservative Therapy

Conservative therapy for spinal osteoarthritis consists of reduction of risk factors and amelioration of symptoms. Obesity worsens symptoms of osteoarthritis, likely by increasing the load on the stressed facet joints. Weight loss should therefore be included in any treatment regimen. Lack of activity can lead to deconditioning and weight gain. Encouragement of physical activity is important in treating symptomatic cases of spinal osteoarthritis. Patients with severe obesity or deconditioning may find it difficult to begin an exercise regimen. Our group has had success with aquatic exercise therapy, which promotes increased activity while lessening the axial load on the spine. A trial of physiotherapy should be considered in patients before becoming operative candidates.

Analgesia for spinal osteoarthritis commonly includes nonsteroidal antiinflammatory drugs. Elderly patients may have multiple comorbidities and the risks of these medications should be evaluated before they are prescribed. Local application of heat may have some benefit in controlling symptomatic neck or back pain. Opiates may also play a role in management of the disease. These should be carefully prescribed in the elderly because they may have significant side effects. Pain treatment procedures also may benefit patients, especially those who are not candidates for surgery. Facet joint blocks can provide symptomatic relief of facet-mediated pain. They also may serve to elucidate those facets contributing to spinal pain. Epidural steroid injections can also be beneficial in treating spinal pain and radicular symptoms.

Conservative therapy of spinal osteoarthritis is generally symptomatic. Recent evidence has suggested that alendronate and other bisphosphonates may have a role in disease modification. Alendronate can reduce osteophyte progression and disc space narrowing in patients with spinal osteoarthritis. In a randomly selected subgroup of the Fracture Intervention Trial, which examined the effectiveness of alendronate, patients receiving alendronate demonstrated a significantly reduced increase in osteophyte progression and disc space narrowing from T4 to L5.8 However, this was a secondary analysis and not a primary endpoint of the main study. After the results suggest that alendronate as a modifier of spinal osteoarthritis progression should be given further consideration.

Operative Therapy

The surgical treatment of painful spinal osteoarthritis remains controversial. No large-scale randomized trials exist to support intervention for neck or back pain or even mild neurological deficit.9,10 Evaluation for surgery should be tailored for each individual patient. Those patients with progressive neurological deficits or those who have failed extensive conservative therapies would seem to be better candidates for intervention. The type of intervention offered should be customized, because the goals of surgery will be different for each patient.

Instrumented Spinal Fusion

In recent years, the number of instrumented spinal fusion procedures has increased, despite a lack of evidence of their effectiveness at treating axial spinal pain and radicular pain.9,10 Conceptually, fusion procedures are attractive, because spinal osteoarthritis leads to facet joint instability. Those patients with axial spine pain demonstrably caused by facet arthrosis (i.e., improved with facet anesthetic blocks) may benefit from stabilization. However, there is no conclusive evidence to support this indication for fusion.9,10 Patients with extensive neurological compression may be candidates for instrumented fusion procedures. More extensive decompression can be performed without concern for posterior element instability. Patients with significant deformity due to osteoarthritic changes may also benefit from corrective procedures.

Most degenerative spondylolisthesis may be successfully treated conservatively. However, those with significant axial pain or neural compression may benefit from surgical intervention if they have failed conservative therapy. Our group has had success in reduction of degenerative grade I or grade II spondylolisthesis using transforaminal interbody allograft and posterior segmental instrumented fusion. This technique allows for aggressive neural foraminal decompression and reduction of listhesis, and forgoes the associated morbidity of an anterior approach procedure.

Atlantoaxial instability may be another indication for surgical intervention. Patients with intractable neck. occipital pain, or both that is attributable to C1-C2 instability may be good candidates for surgical intervention. Recent case series data suggest that C1-C2 fusion can effectively reduce pain by 65%.6 Atlantoaxial fusion would also be indicated in patients with significant pannus and myelopathy secondary to cord compression.

Clinical Case Examples

Discuss Treatment, Clinical Challenges, and Future Treatments

References

1. Creamer P., Hochberg M.C. Osteoarthritis. Lancet. 1997;350(9076):503-508.

2. Eubanks J.D., Lee M.J., Cassinelli E., et al. Does lumbar facet arthrosis precede disc degeneration? A postmortem study. Clin. Orthop. Relat. Res.. 2007;464:184-189.

3. Kramer P.A. Prevalence and distribution of spinal osteoarthritis in women. Spine. 2006;31(24):2843-2848.

4. Niosi C.A., Oxland T.R: Degenerative mechanics of the lumbar spine, Spine J., Suppl. 6:2004, 202S-208S.

5. Kalichman L., Hunter D.J. Lumbar facet joint osteoarthritis: a review. Semin. Arthritis Rheum.. 2007;37(2):69-80.

6. Schaeren S., Jeanneret B. Atlantoaxial osteoarthritis: case series and review of the literature. Eur. Spine J. 2005;14(5):501-506.

7. Ben-Galim P., Ben-Galim T., Nahshon R., et al. Hip Spine Syndrome: The effect of total hip replacement surgery on low back pain in severe osteoarthritis of the hip. Spine. 2007;32(19):2099-2102.

8. Neogi T., Nevitt M.C., Ensrud K.E. The effect of alendronate on progression of spinal osteophytes and disc space narrowing. Ann. Rheum. Dis.. 2008;67:1427-1430.

9. Fouyas I.P., Statham P.F., Sandercock P.A. Cochrane review on the role of surgery in cervical spondylotic radiculomyelopathy. Spine. 2002;27(7):736-747.

10. Gibson J.N., Waddell G. Surgery for degenerative lumbar spondylosis: updated Cochrane Review. Spine. 2005;30(20):2312-2320.

11. Rosen D.S., et al. Minimally invasive lumbar spinal decompression in the elderly: outcomes of 50 patients aged 75 years and older. Neurosurgery. 2007;60(3):503-509. discussion 509-510