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Inflammatory back pain (IBP) is chronic pain concentrated in the axial spine and sacroiliac joints, distinguishing it from mechanical back pain through specific diagnostic features. While strongly linked to inflammatory conditions, IBP is not diagnostic. IBP is a hallmark symptom of spondyloarthritis, characterized by insidious onset, morning stiffness, and improvement with exercise but not rest. Clinicians must recognize these distinctive features for early diagnosis and appropriate management. This course discusses the association of IBP with ankylosing spondylitis and other seronegative spondyloarthropathies, including psoriatic arthritis, enteropathic arthropathy, juvenile idiopathic arthritis, and reactive arthritis. Patient characteristics, chronicity, and pain progression are also discussed, offering clinicians valuable insights to differentiate IBP from other causes and emphasizing a comprehensive approach to address the complexities of this complex pain syndrome associated with spondyloarthritis. Objectives: Identify diagnostic features of inflammatory back pain to enable accurate differentiation from mechanical back pain. Screen for inflammatory back pain risk factors, including age, chronicity, and specific pain patterns. Implement multimodal treatment approaches. Communicate effectively with patients undergoing treatment for inflammatory back pain. Access free multiple choice questions on this topic.

Inflammatory back pain (IBP) is chronic pain concentrated in the axial spine and sacroiliac joints, distinguishing it from mechanical back pain through specific diagnostic features. While strongly linked to inflammatory conditions, IBP is not diagnostic. Several key characteristics help differentiate IBP from other causes of back pain: Localization of pain: IBP is typically localized on the axial spine, particularly the lumbar spine. Additionally, patients may experience alternating buttock pain from one side to another. Patient characteristics: The patient's characteristics, such as age and chronic pain, are crucial in distinguishing IBP. Associated with the onset of pain before the age of 40, persistent pain lasts for 3 months or more.[1][2] Pain progression: The progression of pain over time is another important factor in diagnosing IBP. The pain often follows an insidious course, gradually worsening over an extended period. Morning Stiffness: Patients with IBP commonly experience morning stiffness, which tends to improve with movement or exercise. This significant feature helps differentiate it from other forms of back pain. Association with inflammatory conditions: While the classic association is with ankylosing spondylitis, IBP may also be present in other seronegative spondyloarthropathies such as psoriatic arthritis (PsA), enteropathic arthropathy, juvenile idiopathic arthritis (RIA), and reactive arthritis. Undifferentiated causes: In some cases, the cause of IBP may be undifferentiated, given the absence or combination of diagnostic features of any of these conditions.[3][4]

The identification of seronegative spondyloarthropathies often follows the presentation of IBP. The etiology of these conditions is complex, typically linked to a systemic inflammatory response triggered by a known or unknown source. This systemic inflammation induces local tissue alterations that may persist in the joint environment. The persistence of inflammation, mediated by pathways like interleukin-17 (IL-17) and tumor necrosis factor (TNF), contributes to an ongoing cycle of imbalanced bone remodeling, leading to axial bone loss.[2] The inflammatory changes and subsequent structural alterations, classically observed in imaging through vertebral bone fusion in conditions like ankylosing spondylitis, provide insight into the insidious onset of chronic pain observed in patients with IBP. These manifestations have been pivotal in directing research toward potential intervention strategies.[1][5]

The assessment of IBP prevalence in the US for adults aged 20 to 69 is approximately 5% to 6%.[6] However, a gap exists between the prevalence of IBP and a relatively lower prevalence of spondyloarthropathies in the US, ranging from only 0.9% to 1.4%. Studies conducted in Asia reveal an even lower incidence of ankylosing spondylitis in that population, near 0.001%. Further, only 36% of Asian populations experiencing IBP meet the criteria for spondyloarthropathy.[7] This gap between the prevalence of IBP and seronegative spondyloarthropathy has prompted some researchers to explore other potential causes or propose that IBP may be distinct from other inflammatory immune-mediated conditions. A UK study observed a minimum prevalence of IBP ranging from 1.7% to 3.4% in primary care.[6] Similarly, a study conducted in Mexico reported a prevalence of 3% for IBP in that population.[6] Notably, the frequency of IBP in different populations varies considerably depending on the diagnostic criteria employed; however, in most studies, the prevalence does not exceed 8%. In at least 1 large study, IBP was found to be more prevalent among non-Hispanic white individuals than non-Hispanic black individuals (5.9% versus 3.3%). Limited evidence currently supports the existence of a significant difference in IBP rates based on gender or age group.[8]

IBP is a chronic pain condition characterized by an insidious onset of pain localized to the lower back and buttocks. The pathophysiology stems from a systemic inflammatory response to an insult, leading to the localization of inflammatory mediators in the axial skeletal joints and triggering proinflammatory intracellular changes. This persistent inflammatory condition results in a cycle of unbalanced bone remodeling associated with bone loss and potential for bone fusion. Ankylosing spondylitis: Ankylosing spondylitis and other forms of spondyloarthritis affect the axial skeleton, involving the interplay between bone, ligaments, tendons, and cartilage. SpA-specific gut microbiota activates innate lymphoid cells that produce proinflammatory cytokines. Inflammatory processes occurring in the entheses and joints contribute to bone erosion, while mechanical stress triggers the generation of IL-17. The human leukocyte antigen (HLA) B27 gene plays a significant role in several key pathogenic processes, although non-HLA genes have also been identified.[9] Inflammation initiates changes in bone, leading to new bone formation, such as syndesmophytes. PsA: The cause of PsA is unknown, although some factors have been suggested. Genetic factors play a role in PsA pathogenesis, as evidenced by a higher prevalence within certain families and among twins and an association with specific histocompatibility antigens. Additionally, several environmental factors, including infections and trauma, have been linked to PsA. Immunologic mechanisms are indicated by the shared inflammatory response observed in psoriatic skin and synovial lesions and inflammation in soft tissues and the spine, features shared with axial spondyloarthritis.

PsA: The cause of PsA is unknown, although some factors have been suggested. Genetic factors play a role in PsA pathogenesis, as evidenced by a higher prevalence within certain families and among twins and an association with specific histocompatibility antigens. Additionally, several environmental factors, including infections and trauma, have been linked to PsA. Immunologic mechanisms are indicated by the shared inflammatory response observed in psoriatic skin and synovial lesions and inflammation in soft tissues and the spine, features shared with axial spondyloarthritis. Enteropathic arthropathy: The development of arthritis and inflammatory bowel disease (IBD) may involve the influence of gastrointestinal bacteria. For example, in a study involving rats raised in a germ-free environment and transgenic for the HLA-B27, there were no reported instances of joint or intestinal inflammation.[10] Moreover, individuals with Crohn disease and ankylosing spondylitis exhibited increased levels of immunoglobulin M (IgM) and IgG antibodies to collagen types I, III, IV, V, and Klebsiella pneumoniae compared to healthy controls.[11] Additionally, these patients display a positive antibody response to K pneumoniae serotypes, a phenomenon not observed in patients with celiac disease or healthy controls. JIA: Joint damage in JIA arises from the formation of inflamed synovial tissue, known as pannus. This process involves synoviocyte proliferation and infiltration by inflammatory cells. Vascular factors, cytokines, adhesion molecules, and chemokines facilitate infiltration into the synovium, and inflammatory cells are also present in the synovial fluid. Consequently, the pannus extends and adheres to intraarticular cartilage, resulting in cartilage degradation at the pannus-cartilage junctions.[12] Reactive arthritis: Major causative organisms for reactive arthritis include Campylobacter, Salmonella, and Shigella.[13]

Though not a diagnostic criterion, IBP has been established as a sentinel condition for seronegative spondyloarthropathies. Histopathologic studies in patients with spondyloarthropathies, compared to those with rheumatoid arthritis, reveal heightened vascularity, the proliferation of CD163+ macrophages, and increased levels of polymorphonuclear leukocytes.[14] The synovial membrane undergoes inflammation and thickening due to the infiltration of immune cells such as T cells, B cells, and macrophages. These cells release cytokines such as TNF-α and interleukins (IL-1, IL-6, and IL-17), exacerbating inflammation and contributing to tissue damage. In addition to synovial inflammation, IBP is associated with erosion of the adjacent bone tissue. This erosion results from the activation of osteoclasts, triggered by the release of cytokines such as TNF-α and receptor activator of nuclear factor kappa-B ligand (RANKL) by immune cells.

IBP is differentiated from mechanical back pain by its insidious onset, alleviation with exercise, absence of improvement with rest, and nocturnal pain that improves upon rising and movement. Its connection to seronegative spondyloarthropathies suggests that an inciting illness or systemic inflammatory process might precede IBP.[3]

When distinguished from other causes of back pain using accepted diagnostic criteria, IBP can serve as a referral criterion for rheumatologic evaluation. This is especially pertinent when supported by a positive HLA-B27 laboratory test and sacroiliitis evident in imaging studies that align with the established pain criteria. Up to 50% of patients with axial spondyloarthropathy may exhibit an increased acute phase response, marked by elevated erythrocyte sedimentation rate and C-reactive protein levels. However, similar elevations in these values are also typically associated with rheumatoid arthritis.[15][16] Ankylosing spondylitis: A positive Schober test is observed during the physical examination. This test evaluates the mobility and flexibility of the lumbar spine by marking 2 points on the lower back—1 point 10 cm above the sacrum and the other 5 cm above the first mark. The distance between these 2 points is measured while the patient stands upright and again while bending forward as much as possible. A Schober test is considered positive if there is less than a 5 cm increase in distance between the 2 marks on the lower back when the patient bends forward.[17] Radiographic findings of the sacroiliac (SI) joints can range from subtle joint space narrowing and sclerosis to erosive changes. Eventually, this progression may lead to bony ankylosis (fusion). For diagnostic purposes, ankylosing spondylitis is confirmed with the combination of at least 1 associated clinical criterion and at least 1 imaging criterion, meeting the severity and duration criteria for findings. PsA: Magnetic resonance imaging (MRI) of axial SI joints shows bone marrow edema in the iliac and sacral bones, sclerosis, chronic changes in periarticular fat accumulation, erosions, and new bone formation. Enteropathic arthropathy: X-rays can reveal joint abnormalities like swelling and bone loss, although these manifestations can also be present in patients without IBD symptoms. MRI effectively detects joint changes but may not consistently correlate with back pain. Therefore, its recommendation is reserved for patients exhibiting back pain and IBD symptoms. JIA: Patients with JIA often exhibit a positive antinuclear antibody (ANA), an elevated erythrocyte sedimentation rate (≥40 mm/hour), hypergammaglobulinemia, and anemia (hemoglobin concentration ≤11 g/dL) may be observed.[12]

A referral to a rheumatologic specialist may be warranted after establishing a diagnosis of IBP using accepted criteria, particularly when accompanied by positive HLA-B27 testing and confirmation of sacroiliitis through imaging. Timely and collaborative efforts between healthcare professionals contribute to a more effective and patient-centered approach to addressing the complexities of IBP and its underlying causes. The initial treatment for IBP begins with patient education regarding the nature of their condition and the expected course. Patients should be informed regarding the possibility of associated conditions, prompting further investigation into underlying causes through laboratory evaluation and imaging. Emphasizing the importance of smoking cessation is crucial. Additionally, discussing sources of psychosocial support is essential. Physical therapy consultation is often recommended, given the favorable response of IBP and its associated inflammatory conditions to exercise and movement therapies. The initial pharmacologic approach for IBP, whether symptomatic of axial spondyloarthropathy or not, typically involves a trial of nonsteroidal anti-inflammatory drug (NSAID) therapy, often necessitating a maximum dose. This initial treatment should span 2 to 4 weeks, during which effectiveness is evaluated. Identifying an effective medication can be utilized as needed for symptom control. In cases where NSAID therapy proves ineffective for symptom control in patients with known axial spondyloarthropathy, the next medications include TNF inhibitors or an alternative, such as secukinumab.[18] If a patient initially responds to a TNF inhibitor but experiences a loss of efficacy, a switch to a second TNF inhibitor is recommended. However, for patients intolerant to 1 or 2 TNF inhibitors or with an inadequate response (typically after 3 months of therapy for each TNF inhibitor used), it is advisable to switch to an anti-IL-17 antibody like ixekizumab or secukinumab or a JAK inhibitor such as tofacitinib or upadacitinib. These medication classes compromise the immune response, necessitating careful consideration of immune function, malignancy diagnosis, heart health, or coexisting demyelinating diseases.

In cases where NSAID therapy proves ineffective for symptom control in patients with known axial spondyloarthropathy, the next medications include TNF inhibitors or an alternative, such as secukinumab.[18] If a patient initially responds to a TNF inhibitor but experiences a loss of efficacy, a switch to a second TNF inhibitor is recommended. However, for patients intolerant to 1 or 2 TNF inhibitors or with an inadequate response (typically after 3 months of therapy for each TNF inhibitor used), it is advisable to switch to an anti-IL-17 antibody like ixekizumab or secukinumab or a JAK inhibitor such as tofacitinib or upadacitinib. These medication classes compromise the immune response, necessitating careful consideration of immune function, malignancy diagnosis, heart health, or coexisting demyelinating diseases. Surgical intervention may be indicated in cases of IBP with axial spondyloarthritis under various circumstances, such as severe hip involvement causing persistent pain or severe limitation in mobility and quality of life, atlantoaxial subluxation with neurologic impairment, and severe flexion deformities resulting in impaired ability to gaze in a forward direction.[19][20] It is crucial to consider the unique aspects of each condition, including its progression and response to treatment, to ensure comprehensive and effective management. Please refer to separate resources for more specific information on managing individual conditions.[9][12][21]

The differential diagnosis of IBP encompasses mechanical, nonmechanical, and visceral sources. It is crucial to exclude pain sources stemming from cancer or vertebral body compression fractures. Recall that the characteristic features of IBP include age of onset less than 40, back pain duration exceeding 3 months, insidious onset, morning stiffness, and improvement with exercise. In contrast, causes of mechanical back pain typically exacerbate with movement and exercise and often correlate with injury, presenting a more acute onset.[22] Patients should undergo an assessment for neurologic deficits that may indicate compression of the spinal cord or cauda equina syndrome. Additionally, patients with a high clinical suspicion of vertebral osteomyelitis or epidural abscess warrant an immediate MRI. In a study assessing the efficacy of traditionally considered indicators of cancer as the cause of back pain, it was discovered that a history of malignancy and strong clinical suspicion of cancer were the most valuable factors directing the evaluation toward a potential cancer-related origin of back pain.[23]

NSAIDs constitute the first-line treatment for seronegative spondyloarthropathies, showcasing substantial efficacy in alleviating IBP. Additionally, NSAIDs have proven effective in enhancing the duration of morning stiffness and chest expansion in related arthropathies. When integrated with other demonstrated effective interventions, such as exercise and physical therapy, these medications can significantly improve the overall quality of life for patients experiencing IBP.[24][25] While direct evidence linking IBP to increased mortality is limited, ankylosing spondylitis and other spondyloarthropathies involving the axial spine are associated with a 36% to 76% increased risk of acute coronary syndrome (ACS) and a 50% increased risk of venous thromboembolism. Notably, female patients with PsA demonstrate nearly double the risk of ACS compared to the general population. However, given the relatively young age at which these diseases and associated IBP manifest, the absolute risks of ACS, venous thromboembolism, or stroke in these populations remain modest.[26]

The immunologically mediated process associated with IBP also correlates with a cycle of unbalanced bone remodeling, leading to osteoporosis, which becomes notable within the first 10 years of diagnosis. Individuals with ankylosing spondylitis face twice the likelihood of experiencing vertebral fractures as the general population, with extensions most commonly occurring in the cervical region.[27] Spinal cord injury is 11 times more common in ankylosing spondylitis, and patients with long-standing disease are at an increased risk of cauda equine syndrome. Additionally, individuals with axial spondyloarthropathy may be at higher risk of renal disease, with an 8% increase in abnormal urinalysis than the general population.[28][29][30] The chronic use of NSAIDs for patients with IBP carries associations with various possible complications. NSAIDs have links to the exacerbation of peptic ulcer disease, an increased risk of cardiovascular events in at-risk populations, incitement of renal injury or failure, and exacerbation of existing reactive airway disease. Initiating NSAID administration should involve careful consideration of the patient’s underlying disease process associated with IBP, other comorbid illnesses, and concurrent medications, particularly glucocorticoids, anticoagulants, diuretics, and selective serotonin reuptake inhibitors (SSRIs).[31][32]

After confirming the diagnosis of IBP using accepted criteria, a referral to a rheumatologic specialist may be indicated, particularly in those with positive HLA-B27 testing and confirmation of sacroiliitis by imaging. In addition, a physical therapy referral is likely warranted as IBP and its associated inflammatory illnesses have shown favorable responses to exercise and movement therapies. This multidisciplinary approach aims to optimize patient outcomes and enhance overall well-being.

The initial intervention for patients with IBP should begin with education, providing insights into the anticipated course of the condition and emphasizing the need for further evaluation to identify potential sources of the inflammatory process. Patients should be advised to cease smoking, as it may exacerbate symptoms, and they should receive referrals to sources of psychosocial support. Notably, physical therapy, focusing on exercise and postural training, is an essential component of the treatment plan, as these interventions can offer significant benefits in managing the course of the disease.[19]

A few key facts to remember about IBP are as follows: Timely recognition of IBP is crucial for initiating appropriate interventions and preventing complications associated with spondyloarthropathies. Regular monitoring of patients with IBP, including imaging and laboratory assessments, helps track disease progression and modify treatment strategies accordingly. Encouraging patients to adopt a healthy lifestyle, including regular exercise and smoking cessation, can contribute to symptom control and overall well-being. Screening individuals in high-risk groups, such as those with a family history or specific genetic markers, may aid in the early detection of IBP. A multidisciplinary approach involving rheumatologists, primary care providers, physical therapists, and other specialists enhances the overall management of IBP. Genetic factors, including the presence of HLA-B27, play a significant role in developing IBP. Understanding genetic predispositions can guide diagnostic and management strategies.

Managing IBP requires clinical skills, strategic planning, ethical considerations, shared responsibilities, effective communication, and coordinated care. An interprofessional team approach is paramount for optimizing patient outcomes and enhancing the overall quality of care. Collaborative responsibilities among healthcare professionals, including rheumatologists, primary care providers, nurses, therapists, and pharmacists, are integral to effectively managing IBP. Healthcare professionals are responsible for educating patients about the nature of IBP, treatment options, potential complications, and the importance of lifestyle modifications. Interprofessional communication should support shared decision-making, involving patients in discussions about their care and treatment options.