Spinal Osteoarthritis

Etiology

Despite the lack of evidence to delineate a specific etiology and pathogenesis of spine arthritis, several risk factors are critical in its development. Osteoarthritis traditionally was thought to be a disorder directly linked to "wear and tear." Degenerative changes over time were theorized to lead to osteophyte formation and cartilage loss.[9][10] However, more modern advances in technology have aided in our understanding of this disorder. The etiology of spine osteoarthritis is likely secondary to its multifactorial pathogenesis. Its etiology includes genetic predisposition, epigenetics, dietary changes, sex, and ethnicity differences. Patient age, muscle strength, physical activity, and work-related habits are factors in osteoarthritis development. Together these factors contribute to a low-grade inflammatory state and potentiate degenerative change. Furthermore, the overtraining of muscles with abnormal joint movements can lead to injury, changes to joint alignment, and worsening arthritis. Congenital abnormalities such as the increased sagittal orientation of the facet joints or increased pelvic girth, and unusual lordotic angles also contribute to osteoarthritic degeneration.[10][11][7][12]

Genetically, researchers have linked over 80 gene mutations involved in osteoarthritis. The 143383 nucleotide polymorphism is arguably the most critical, secondary to its role in developing, maintaining, and repairing synovial joints.[10] The heritability of spine osteoarthritis is the highest in the cervical and lumbar regions.[9]

The role of epigenetics in osteoarthritis includes more rapid phenotypic variance for cellular microenvironmental changes. For example, the MMP-13 and IL-1 beta promoter play a significant role in the maintenance of cartilage. The MMP-13 enzyme is associated with cartilage matrix destruction in osteoarthritis. Demethylation of the MMP-13 promoter is associated with an increased expression of the MMP-13 protein, which, in turn, increases cartilage matrix degeneration.[9] 

The most crucial associated risk factor for osteoarthritis among many studies is age.[8][10][12][9] With aging, there is an alteration in the healthy joint cartilage (chondrocytes) and extracellular matrix. These alterations lead to maladaptations in both the chemical and mechanical capacity of the joint. Chondrocytes have a limited number of replications. As cells age, the telomere length lessens, leading to cellular division senescence. Ultimately, this results in the inability to maintain and repair the cartilage extracellular matrix. Disruption predisposes joints to damage after sustained mechanical loads. Additionally, chondrocytes undergo apoptosis as there is a decrease in the expression of extracellular matrix macromolecules as we age — apoptosis is directly correlated with cartilage damage.[9]

Gender and ethnicity also have a role in osteoarthritis. The degree of lumbar lordosis is different between genders. Excessive curvature increases the load on the lumbar facet joints and predisposes the lower spine to degenerative changes. Changes in lumbar lordosis have a significant effect on the development of spine osteoarthritis. This change in lordosis is more pronounced in women and older men.[11] 

The contribution of ethnicity to spine osteoarthritis is mostly variable. Joint mobility is more common in whites than in African Americans. Yet, there is no association between hypermobility and the development of radiographic arthritis between races. Interestingly, there is a correlation between joint hypermobility and low back pain.[13]

Diet and obesity are also directly related to the development of osteoarthritis. Risk factors for metabolic syndrome are independently associated with the development of osteoarthritis, including central obesity, diabetes, high blood pressure, and hyperlipidemia.[14] Atherosclerosis, microvascular disease, and venous stasis may also potentiate the development of osteoarthritis by worsening subchondral bone ischemia within the articular cartilage.  Ischemia leads to osteocyte and chondrocyte apoptosis, stiffening the subchondral bone. The lack of cartilage flexibility causes damage from mechanical loads.[14] Obesity, in itself, is a condition that releases pro-inflammatory cytokines, including IL-6, TNF-alpha, and nitric oxide, and other macromolecules, including leptin, which is released from white adipose tissue and highly correlated with arthritis.[10][14] In fact, leptin influences growth factor synthesis and cartilage anabolism and catabolism via the regulation of STAT molecules.[10] The concentration of leptin is directly proportional to the severity of cartilage destruction within tissues.[10] Reactive oxygen species produced by chondrocytes can also damage the articular cartilage. Dietary intake of antioxidants, including vitamins C and K, can help prevent arthritis.[10]

Epidemiology

Radiographic evidence of spine osteoarthritis is widespread. In patients over the age of sixty, 95% of men and 70% of women have at least one indicator of arthritis. Cervical spine osteoarthritis is present in over 80% of individuals over the age of 55.[8] Specifically, facet joint arthritis is present in 19% of individuals between the ages of 45 and 65 years of age and 57% of patients over the age of 65 in the United States.[7] There have been no reported studies indicating the prevalence of thoracic facet joint arthritis.[8] Lumbar spine osteoarthritis affects approximately 30% of men and 28% of women from the ages of 55 to 64 in the United States. The L4-5 and L5-S1 vertebral levels are most commonly affected due to their higher load and joint mobility.[2] A separate study found lumbar osteoarthritis-related back pain in over 20% of men and 22% of women between the ages of 45 and 64.[8] Sixty-seven percent of patients between the ages of 45 to 64 and 89% of patients over 65 had evidence of facet joint arthropathy on imaging.[7] There may also be ethnic differences in spine osteoarthritis, with a lower prevalence in Asians than whites.[8] Often, osteoarthritic changes of the spine are more advanced in males than in females.[15]

Pathophysiology

As patients age, the functional integrity of their spines deteriorates and predisposes patients to degenerative changes as a result of the alterations in load-bearing forces.[2] This cascade begins with age-related intervertebral disc degeneration.[1] In a healthy spine, the facet joints carry approximately 33% of the load. However, as facet joint and intervertebral disc degeneration develop, this load-bearing increases to 70%.[2] As the posterior spine bears an increased load, the subchondral bone density increases along with osteophyte formation. In turn, it leads to synovial hypertrophy, cartilage necrosis, ulceration, fibrillation, eburnation, instability, and bony overgrowth. All of which can contribute to spinal stenosis.[2]

Arthritis becomes advanced due to the decline in viscoelastic properties of synovial fluid, primarily attributable to hyaluronic acid, which serves as a lubricant and shock absorber for the spine.[2] In addition to the decline of synovial fluid, leukotrienes, and prostaglandins produce inflammation within the facet joints. Inflammation attracts neutrophils and macrophages and produces vasodilation and venous congestion within the joint. The recurring nature of this injury will sensitize pain receptors (nociceptors); over time. Chronic pain then develops.[2] Additionally, inadequate blood supply leads to the pathogenesis of intervertebral disc degeneration. One systematic review demonstrated that stenosis of the middle and fourth lumbar arteries is highly associated with lumbar disc degeneration.[14]

Histopathology

As patients age, their cervical spines begin to go through degenerative changes. Splitting and fissuring of the vertebra and osteophyte formation occur. Aging causes calcified cartilage thickness, and the subchondral bone thickness at the osteocartilaginous junction changes to increase.[15] In contrast, the depth of hyaline cartilage decreases with age. In the lumbar spine, there is an increase in bone formation and an abundance of macrophages present in the subchondral bone of the degenerative tissue.[16] Separately, on histology, limited nerve fibers have been found in the areas of bony pathology.[16]

History and Physical

The typical presentation of patients with symptomatic osteoarthritis of the spine is pain, stiffness, and motion restriction, which is commonly accompanied by referred pain.[8][7] The distribution of a patient's pain depends on the location of the pathology. For example, mid-cervical and lower-cervical facet joints refer pain to the posterior scapular and shoulder regions. The upper cervical complex produces pain in the occipital region and is often associated with headaches. The lumbar spine provides pain located in the buttock and thigh region. Lumbar spine osteoarthritis can be associated with radicular pain above the knee. If radicular symptoms move below the knee, nerve root compression or irritation is likely. Nerve root compression is associated with motor, sensory, and reflex deficits. The clinical exam helps rule out many of the various etiologies of spinal pain, such as neoplasms, disc herniation, and spinal stenosis. However, there are no proven orthopedic examination maneuvers that are diagnostic for spine osteoarthritis. Degenerative osteoarthritis causes localized and unilateral pain. This pain is reproducible upon palpation of the facet joint, relieved with flexion. Radicular symptoms, if present, are limited to above the knee. Pain from hyperextension and rotation from a standing position suggest facet joint arthropathy.[7]

In many cervical spine osteoarthritis cases, patients complain of shoulder, posterior head, and anterior chest pain. If pain persists longer than one to two weeks, or there are neurological symptoms present such as numbness, tingling, loss of grip strength, or there is fever or crepitus on range of motion, patients may require further evaluation. 

Warning signs or red flags should also merit consideration as part of the initial evaluation of osteoarthritis of the spine. Review of systems should include numbness, loss of bowel or bladder continence, fever, chills, or the presence of saddle anesthesia.

Physical exam should include inspection and palpation of the area of reported history. Furthermore, active and passive range of motion testing of the spine should also be completed. Pronounced or reduced lordosis or kyphosis should also be documented, and the patient's gait and posture should also undergo assessment. Point tenderness over the spinous process requires differentiation from paraspinal muscle hypertonicity. Muscle strength, sensation, and deep tendon reflex testing are indicated depending on the location of the patient's pain. If there is a concern for myelopathy, the patient will experience upper motor neuron symptoms such as spasticity, an ataxic gait, hyperreflexia, or a positive Babinsky sign on the exam. Special tests are also necessary if radiculopathy is suspected, such as the Spurling test and straight leg raise.

Evaluation

History and physical exam are essential in the diagnosis of spine osteoarthritis. However, a broad differential diagnosis is critical to rule out other, more threatening causes of back pain. Labs or imaging are often part of the evaluation of osteoarthritis of the spine. Less common but potentially severe etiology of back pain include infection, neoplasm, inflammatory disease, myelopathy, and aortic aneurysm or dissection.[8] Any of these suspected etiologies of back pain require advanced imaging or testing to make the diagnosis. Plain films are a standard first test in the evaluation of osteoarthritis. Plain radiographic imaging is inexpensive and often easy to obtain. Current guidelines suggest plain films are an appropriate imaging modality in the absence of radicular symptoms when back pain has persisted longer than six weeks.[1] 

Plain films in an acute setting should be limited to patients with spinal pain suggestive of systemic disease or trauma — other more advanced imaging modalities, including MRI and CT. When there is high suspicion for a possible infection, neoplasm, or persistent and or severe neurological deficits such as severe lumbar radiculopathy, the patient requires advanced imaging. More severe etiologies of a patient's pain are more common in an older population. A herniated nucleus pulposus can occur at all levels of the spine but most often occurs in the lower cervical (C5 to C6 and C6 to C7) and lumbar segments (L4 to L5 and L5 to S1). Early evaluation in an elderly population with advanced imaging is recommended for persistent pain.[8] Fluoroscopically guided injections and blocks are the standard of care for diagnosing facet joint-mediated low back pain.[2] Furthermore, medial branch blocks and dual comparative anesthetic blocks have been validated to diagnose facet joint pain as well.[2]

Treatment / Management

Treatment of spine osteoarthritis includes conservative management, pharmacological interventions, and invasive procedures. The various treatment modalities get determined by the etiology of the osteoarthritis, duration of the patient's pain, neurological symptoms, and physical exam findings. The American College of Physicians Clinical Guidelines Committee (ACPCGC) guideline helps direct clinicians in managing low back pain. The committee's goal is to avert unnecessary costs associated with non-evidence-based management of low back pain.[17] The ACP recommends superficial heat, massage, acupuncture, or spinal manipulation as first-line therapy for acute or subacute non-radicular low back pain. Conservative management should be the initial treatment for chronic, mechanical low back pain. The classification of low back pain falls into three categories: acute, subacute, and chronic. Acute back pain lasts under four weeks, subacute four to 12 weeks, and chronic back pain longer than 12 weeks in duration. Non-interventional therapies that show a small to moderate improvement of pain and function in low back pain include exercise, cognitive behavioral therapy, physical therapy, acupuncture, massage, spinal manipulation, and low-level laser therapy.[17]

One of the most beneficial traditional therapy techniques is exercise therapy.[2][1] Specifically, land-based exercises are of the most significant benefit in increasing lumbar spine bone mineral density.[18] Unfortunately, many patients with obesity have limited mobility, leading to additional weight gain and worsening of osteoarthritis symptoms. To overcome this, clinicians should create patient-specific treatment regimens. Providing supervised exercise sessions can ensure adequate exercise intensity and alleviate the fear associated with mobility.[19] Clinicians should also consider aquatic exercise when appropriate.[20] In one meta-analysis, water-based exercise was more effective than no exercise at all in preventing age-related bone deterioration. Studies assessing swimming as part of aquatic exercise regimens often do not delineate the intensity or duration of the therapy. The best treatment for improving lumbar spine bone mineral density incorporates an intense water-based exercise regimen and moderate to vigorous intense therapy for 60 minutes, three times per week, for seven months.[18]

Additionally, physical therapy improves patient pain and function.[2] Specifically, physical therapy focused on flexion-based maneuvers to address lumbar stabilization and spinal stenosis, in addition to a home-based exercise program, is a highly effective option in patients with both acute and chronic spinal pain. However, studies with a higher power are needed to validate the effectiveness of exercise in lumbar spine osteoarthritis.[21] One research study suggests improvement of function as early as two weeks after physical therapy.[22] Nonetheless, aerobics, weight-bearing, and resistance exercise all show increases in lumbar spine bone mineral density in postmenopausal women.[21] Abdominal muscle strengthening enhances the quality of life in older adults with lumbar osteoarthritis.[23] Yoga has also proven to be an effective treatment modality for chronic low back pain.[1] The combination of exercise and psychological treatment may be of greater efficacy for chronic low back pain than any single intervention.[24]

Diet and nutritional supplements also play a role in managing osteoarthritis and should be combined with exercise therapy.[19] Studies suggest a higher intake of saturated fat quickens the progression of osteoarthritis. An increased intake of monounsaturated and polyunsaturated fat decreases the radiographic progression of osteoarthritis. Patients should reduce their consumption of omega-six fatty acids while increasing their intake of omega-three fatty acids. Omega six is associated with the development of bone marrow lesions. Patients can increase their intake of omega-three fatty acids by consuming eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Consumption of EPA and DHA reduces the pro-inflammatory burden. Evidence suggests that the use of EPA and DHA, found in oily fish, can improve pain scores in individuals with osteoarthritis. A significant benefit was found with a low dose of fish oil supplement when compared to a high dose of anti-inflammatory. There may be efficacy in prescribing a low-dose treatment of one to two capsules per day of fish oil supplements.[19]

Obesity is a risk factor for osteoarthritis; thus, weight management is paramount.[19] For every five kilograms of weight gain, there is a 36 percent increased risk of developing osteoarthritis. Studies have demonstrated that a five percent loss in body weight can attenuate some joint pain, while a loss of at least 10 percent can produce a moderate to considerable reduction in joint pain. Joint pain in obese individuals is primarily in the load-bearing joints, including the lumbar spine.[20] For many obese patients, it is difficult to lose or maintain weight loss. In these patients, it is reasonable to refer to a bariatric surgeon for surgical intervention. Patients who undergo bariatric surgery via vertical banded gastroplasty reduced their body mass index (BMI) by 14.3 kg/m². The reduction in BMI corresponds to improvements in multiple pain and disability indexes. Other studies have demonstrated similar results. The frequency of back pain decreased in 83 percent of patients, and the severity of back pain subsided in 82 to 90 percent of patients after six to 22 months following surgery. In those with severe chronic axial back pain, the severity of pain was lessened by 44 percent after bariatric surgery.[20]

Acetaminophen is a first-line treatment for low back pain.[8] NSAIDs had small to moderate effects on pain and minimal impact on function NSAIDs are first-line pharmacological therapy for chronic low back pain. If ineffective, tramadol or duloxetine are second-line therapy. Skeletal muscle relaxants are adjunct treatments for acute and subacute low back pain. Risks and benefits should be weighed before prescribing these medications.[17] However, the use of antispasmodic drugs chronically for low back pain has no supporting evidence.[2] Systemic steroids do not affect acute or subacute low back pain.[17] Opioids are for short-term management of chronic low back pain only, but the ACP guideline cautions against their use.[17] Opioids do have a more significant effect on pain relief and patient mood when compared to NSAIDs in patients with chronic pain. Caution is necessary with opioid prescriptions due to their addictive potential and side-effect profile.[8]

Patients with chronic low back pain associated with osteoarthritis should be screened for depression and treated appropriately with cognitive behavioral therapy or antidepressants. Statin therapy also lowers the risk of developing osteoarthritis of the spine and prevents disease progression in patients with hyperlipidemia. Statin therapy exerts a chondroprotective effect and decreases inflammatory cytokines.[25][19] Homeopathic medicine may also be beneficial as an adjunctive treatment for chronic low back pain. Studies have also shown that homeopathy can reduce NSAID use in these patients and reduce the number of associated adverse events.[22] Several studies suggest prostaglandins, gabapentin, and vitamin B1 improved pain and patient walking distance compared to other medications and placebo.[26] There is no evidence that supplementation of antioxidant vitamins A, C, and E shows benefit in osteoarthritis. Vitamin D supplementation has shown improved structural and functional outcomes when plasma levels are above 50 nmol/L. Vitamin K has a role in bone and cartilage mineralization. Adequate levels should be maintained.[19](A1)

Spinal manipulation is a viable treatment option for those with acute and chronic back pain. The clinical significance of the benefits of spinal manipulative therapy has been variable across studies and will require more research.[8][4][27] Traction therapy, transcutaneous electrical nerve stimulation (TENS unit), and massage techniques are adjunctive treatment options. Evidence is lacking to support their efficacy.[2][8] However, one meta-analysis demonstrated that TENS was useful in pain reduction for patients with chronic low back pain if treated for less than five weeks. This treatment modality may reduce the number and amount of pain medications needed for pain control.[28](A1)

Invasive techniques in treating spine osteoarthritis include facet joint injections, epidural injections, acupuncture, medial branch nerve ablation, and surgical intervention.[8][26] Some studies suggest that epidural injections show short-term improvements in pain and quality of life for up to two weeks. Calcitonin injections showed no benefit when compared with placebo or paracetamol. Facet joint injections have increased in popularity in recent years; however, there is little supporting evidence for their use.[1][2][8] Surgical intervention is reserved for clearly identifiable structural pathologies that are amenable to surgical intervention, neurological symptoms secondary to the spinal cord or nerve root compression, or when non-operative intervention has failed.[24] Surgical intervention is recommended for cauda equina syndrome and spinal stenosis with progressive or severe neurological deficits.(A1)

Furthermore, a herniated disc with radicular pain and mild to moderate neurological deficits for greater than four to six weeks may require surgery. Spondylolisthesis with progressive or severe neurological deficits is also an indication for surgery. Back pain resulting in significant functional impairment and has lasted for more than a one-year duration warrants surgical intervention consideration.[1][8]

Of the five studies that compared surgical treatment versus non-surgical treatment, one study found no difference in pain at the two-year follow-up appointment. The other four studies suggested surgical treatment consistently improved pain but not walking ability over different periods, and five to 18 percent of these patients suffered from unwanted side effects post-surgery. However, the studies were of low-quality evidence, and further research is needed to make clinical recommendations.[26] Patients with lumbar spinal stenosis and accompanying neurogenic claudication have greater success with surgery. Surgical treatment is superior in relieving low back pain but not functional status when compared to non-surgical treatment options. Before any surgical intervention, clinicians must evaluate patients' psychosocial factors. Hysteria, hypochondriasis, depression, disability, workers' compensation, extended pre-operative sick leave, litigation, and reinforcement of pain by other family members are all predictive of poor pain tolerance and outcomes after spine surgery. Patients should stop smoking, NSAID use, and steroids before spine surgery, particularly spinal fusion surgery, as all of these factors have a significant adverse effect on fusion success rates. A detailed list of surgical options is beyond the scope of this review. However, fusion can be considered in patients with severe pain secondary to one or two levels of degenerative disease without stenosis or spondylolisthesis. It should not be an intervention when multiple levels of degenerative changes are present; intensive physical and cognitive therapy is preferred.[24](A1)

Cauda equina syndrome (CES) is a severe condition most commonly caused by a lumbar spine disc herniation in patients 31 to 50 years old. Most often, the disc herniation occurs between L4 and L5. Any space-occupying lesion, including spinal stenosis, cysts, infections, and tumors, can compress the cauda equina and should be on the differential diagnosis. CES is defined as having five characteristic features, including bilateral neurogenic sciatica, saddle anesthesia, bladder dysfunction, decreased anal tone, and sexual dysfunction. It is important to note that symptoms of CES can initially be subtle. Thus, a thorough history is paramount in guiding the diagnosis and treatment of this condition, which can be difficult in the setting of severe pain. However, clinical diagnosis is challenging. Even experienced clinicians have a 43 percent false-positive rate in the diagnosis of CES.

Nonetheless, it is essential to diagnose this condition early in its course to improve prognosis and prevent residual neurological deficits and potential litigation. The gold standard imaging for diagnosis is MRI. Urgent surgical management is required if CES is present.[29][30]

Differential Diagnosis

The differential diagnosis of conditions that cause back pain is extensive and varies by region. In the cervical area, possible etiologies include [1][8]:

• Rheumatic diseases: fibromyalgia, polymyalgia rheumatica, rheumatoid arthritis, ankylosing spondylitis, degenerative joint disorders, diffuse idiopathic skeletal hyperostosis
• Trauma: fractures, dislocations, soft tissue injury
• Regional conditions: myofascial pain, osteomyelitis, septic discitis, septic arthritis, synovial cyst, torticollis syndrome
• Bone conditions: Paget disease, osteomalacia, osteoporosis, metastatic tumor
• Neurological: meningitis, cerebral palsy, paralysis of cervical muscles.

Many of the etiologies of low back pain have similar presentations. The mechanical origin of low back pain is the most common cause, representing 97% of cases of acute back pain. Lumbar strain or sprain is the number one cause of mechanical low back pain accounting for 70% of cases. 

While the list is not comprehensive, the etiologies of thoracolumbar back pain include:

• Mechanical: lumbar strain/sprain, degenerative conditions, herniated disc, spinal stenosis, compression fracture, spondylolisthesis, fracture, congenital disease
• Non-mechanical: neoplasia, infection, inflammatory conditions, Scheuermann disease, Paget disease
• Visceral disease: pelvic organ disease, renal disease, aortic aneurysm, gastrointestinal disease

Prognosis

Approximately 80% of the United States experiences low back pain at least one time during their life.[1] Twenty-three percent of patients develop chronic low back pain after an acute event.[4] Many individuals exhibiting osteoarthritic changes on radiography do not have pain.[2][1] As a result of the complex nature of the spine, it is challenging to identify the source of back pain. Less than 15% of cases have an identifiable etiology, which makes treatment difficult.[4] 

Neck pain is also widespread and affects greater than one-third of the general population at some point in their lives. As patients age, osteoarthritic change to the cervical spine becomes more common. Most cases of neck pain are self-limited, lasting less than one week, and not necessarily perceived as neck pain.

Osteoarthritis is a chronic, degenerative disease. In most cases, patients are asymptomatic. Arthritis is a product of aging. Prognosis often is a function of the severity of osteoarthritis. For example, severe lumbar radiculopathy caused by arthritic changes and spinal stenosis can require surgical intervention. Patients whose osteoarthritic back pain is so critical they require surgical intervention have a worse prognosis than patients with milder symptoms.

Complications

The osteoarthritis cascade causes many complications as the disease progresses. Osteoarthritis of the spine can cause pain, functional impairment, and disability. Pathologically osteoarthritis can cause spinal stenosis, herniated nucleus pulposus, myelopathy, radiculopathy, spondyloarthritis, and spondylolisthesis.[2][1] Most back pain cases are not disabling and acute, but many cases get referred to the hospital after initially presenting to an outpatient clinic. Of the 2.2 million annual visits for low back pain in the United Kingdom seen by their primary physician, 10 to 20 percent received a referral to the hospital.[8]

Spondylosis is a complication that can cause radiculopathy, myelopathy, and vascular impingement. 

Spinal stenosis can lead to two clinical syndromes, including cervical myeloradiculopathy and lumbar neurogenic claudication. Stenosis of the lumbar spine can manifest as persistent or intermittent pain, weakness, and dermatomal sensory symptoms exacerbated by standing or walking and relieved by sitting or lying down. 

Herniated discs cause persistent low back pain in one to two percent of the population from 35 to 45 years old.

Degeneration in the lumbar spine can eventually lead to degenerative spondylolisthesis, which most commonly occurs at L4 on L5, in which the superior vertebral segment slides forward on the inferior segment as a result of the weakened facet joint.[8] If this is severe, it can become a surgical emergency.