Axial spondylarthritis is an immune mediated multi system inflammatory condition involving the sacroiliac joints, spine, and peripheral joints.
It affects approximately one percent of US adults.
In the US the prevalence is approximately one percent among adults and the disease prevalence is higher than that of rheumatoid arthritis (0.6).
Axial spondylarthritis is associated with impaired physical function and reduced quality of life.
Diagnosis of axial spondyloarthritis includes ankylosing spondylitis and non-radiographic axial spondylitis arthritis, based on the presence of sacroiliitis on MRI or plain radiography and at least one spondyloarthritis feature or HLA -B 27 positivity, and at least two spondyloarthritis features.
Usually occurs in the second or third decade of life, with less than 5% of patients diagnosed when older than 45 years of age.
It refers to an inflammatory chronic back pain characterized by gradual onset starting before age 45 years, prolonged morning stiffness, improvement with exercise, and lack of improvement with rest.
These are the most common symptoms of axial spondyloarthritis and affects more than 80% of patients.
Typically appears in those younger than 45 years and has a peak age between 20 and 30 years.
Radiographic axial spondyloarthritis is more common among men than women, with a male to female ratio of three to one.
The pain is inflammatory as suggested by: improvement with exercise, pain at night, insidious onset of pain, aged onset younger than 40 years, and no improvement with rest.
Patients with axial spondyloarthritis may also have inflammatory arthritis in large peripheral joints, most commonly knees.
Patients with axial spondyloarthritis may also have an oligoarticular, asymmetric inflammation at tendon insertions, inflammatory eye disease (uveitis); psoriasis; and inflammatory bowel disease.
Approximately 20% of patients with AS have symptoms affecting joints or organs in addition to the axial skeleton such as peripheral arthritis, enthesitis, or uveitis.
Peripheral inflammatory arthritis typically affects large joints, such as the knees and shoulders in asymmetric and oligoarticular, fashion, enthesitis in 30% to 40% of cases and dactylitis or sausage digits in 5 to 7% of cases.
Up to 45% of patients present with ocular pain, erythema, blurry vision, and photophobia and may be associated with floaters and vision loss.
Psoriasis affects 10 to 15% of patients and inflammatory bowel disease affects 8% of patients.
A characteristic feature of AS is inflammation induced bone loss that occurs simultaneously with abnormal new bone formation at specific sites in the skeleton such as the sacroiliac joints, at entheses in the spine, and the peripheral skeleton.
The etiology of axial spondyloarthritis may involve genetic predisposition, gut microbial dysbiosis, and entheseal trauma, with immune cell infiltration of the sacroiliac joints and entheseal insertion areas in the spine.
Immune lymphocytes, neutrophils, and dendritic cells infiltrate the synovium, the entheses, and the bone marrow of the SI joints and spine leading to release of pro-inflammatory cytokines such as TNF, IL 23, IL-17, which activates osteoclasts and causes bony erosions.
IL-23 and IL-17 stimulate mesenchymal stem cells that differentiate into osteoblast, leading to pathologic new bone formation in the SI joints, spine, and peripheral entheses.
Enthesitis, and inflammatory granulation tissue in connective tissue, including the annulus fibrous, and vertebral bone can form bony outgrowths and ultimately bridging of adjacent vertebral bodies, resulting in ankyloses.
Its pathogenesis may involve genetic predisposition, gut microbial dysbiosis and entheseal trauma, with immune cell infiltration of the sacroiliac joints, and entheseal insertion areas in the spine.
No diagnostic criteria for axial spondyloarthritis, and the diagnosis is often delayed 6 to 8 years after symptom onset.
HLA-B27 a major histocompatibility class I molecule expressed on antigen presenting cells such as monocytes and macrophages present a self peptide from the joint to CD 8 positive T cells, initiating a T cell mediated inflammatory response.
Gut microbiome dysbiosis is thought to play a role in pathogenesis of AS: microbial alteration/translocation of gut bacteria and bacterial products through a disrupted intestinal barrier to distant axial as well as peripheral articular and entheseal sites which participates in an inflammatory arthritis response.
Another hypothesis for the pathogenesis of axial spondylosis is that repeated trauma to entetheal sites in genetically predisposed people leads through recruitment of neutrophils and production of neutrophilic inflammation and activation of pro-inflammatory cytokines such as IL–23, IL-17, and TNF.
Diagnosis is based on history of inflammatory back pain, or symptoms of peripheral arthritis or enthesitis, human leukocyte antigen B27–positive [sensitivity, 50%; specificity, 90%] and elevated C-reactive protein level [sensitivity, 35%; specificity, 91%), and imaging findings consisting of sacroiliitis on plain radiography (sensitivity, 66%; specificity, 68%) or magnetic resonance imaging (sensitivity, 78%; specificity, 88%).
Physical exam includes assessment of spinal tenderness and range of motions and evaluation for flexibility in of the spine.
Evaluating the flexibility and range of motion of the spine has a sensitivity of 68 to 79% and a specificity of 36 to 45% for diagnosing axial spondyloarthritis.
Other findings include peripheral joint arthritis, skin rash, ocular erythema, pain and photophobia.
HLA-B 27 has a sensitivity of 50% and a specificity of 90% and C reactive protein is elevated in 40% of patients: these are not diagnostic because 6% of US population is positive for HLAB 27 and CRP level may be elevated in multiple conditions.
Management:
First-line treatments are physical therapy and nonsteroidal anti-inflammatory drugs (NSAIDs).
Fewer than 25% of patients achieve complete symptom control with NSAIDs.
Approximately 75% of patients require biologic drugs such as tumor necrosis factor inhibitors [anti-TNF agents], interleukin 17 inhibitors [anti–IL-17 agents]) or targeted synthetic disease-modifying antirheumatic agents (Janus kinase [JAK] inhibitors) to reduce symptoms, prevent structural damage, and improve quality of life.
Anti-TNF agents significantly improved ASAS20 score measuring pain, function, and inflammation in 58% to 64% of patients compared with 19% to 38% for placebo.
Similar outcomes were attained with anti–IL-17 agents (48%-61%, vs 18%-29% with placebo) and JAK inhibitors (52%-56%, vs 26%-29% with placebo).
Anti-TNF agents, anti–IL-17 agents, and JAK inhibitors have been associated with reduced radiographic progression of axial spondyloarthritis.
Axial spondyloarthritis predominantly affects the sacroiliac joints and spine but is also associated with extraskeletal manifestations such as uveitis, psoriasis, and inflammatory bowel disease.
Chronic back pain and stiffness can occur over time leading to new bone formation, structural damage, and ultimately fusion of the sacroiliac joints in the spine in some patients, known as bamboo spine.
If at least four of the five criteria are identified, it has a sensitivity of 79.6% and a specificity of 72.4% in diagnosing inflammatory back pain.
In a patient with at least three months of inflammatory back pain, plain x-rays may show sacroiliitis with a sensitivity of 48%.
Anti—TNF agents, anti—IL-17 agents, and JAK inhibitors have been associated with reduced radiographic progression of axialspondyloarthritis.
An under recognized cause of chronic low back pain is axial spondyloarthritis, an inflammatory rheumatic disease that predominately involves spine and sacroiliac joints.
T-weighted MRI of the pelvis or symptomatic spinal area can show sacroiliitis or spondylitis with the sensitivity of 85%.
MRI of the sacroiliac joints is the preferred imaging test for evaluating axial spondyloarthritis in patients whose radiographic images are not diagnostic.
In axial spondyloarthritis the disease is predominantly of the axial skeleton, but peripheral joints, and entheses, and extra articular organs such as the skin, eyes, and intestines are also frequently affected.
Nonsteroidal anti-inflammatory drugs are the mainstay of treatment.
Other biologic agents such as antitumor necrosis factor alpha may be employed.
Sulfasalazine is commonly utilized, especially for patients with peripheral arthritis, although its role in management has not been clinically demonstrated.
Physical therapy is recommended for all patients with AS except for those with advanced spinal fusion.
Physical therapy is important for muscle strengthening, maintaining range of motion, and appropriate posture.
Oral glucocorticoids and conventional synthetic disease modifying antirheumatic drugs, such as sulfasalzine and methotrexate are not recommend to treat AS.