Structural Damage In Ankylosing Spondylitis Research Articles

Proposal of simplified CT syndesmophyte score (sCTSS) and comparison with CTSS in patients with ankylosing spondylitis

The CT syndesmophyte score (CTSS) can evaluate spinal progression more precisely than mSASSS in ankylosing spondylitis (AS); however, it is complex and time consuming. Here, we propose a simplified CTSS (sCTSS) for measuring spinal structural changes in AS. Patients with AS were recruited from a single tertiary hospital. Baseline and 2-year follow-up whole spine CT images were used to calculate CTSS and sCTSS. The sCTSS used the anterior and posterior vertebral corners, and ranged 0–184. Intraclass correlation coefficients (ICC) were calculated, as well as the smallest detectable changes. Fifty AS patients were included. For reader 1, the mean sCTSS at baseline and 2-year follow-up were 11.7 ± 14.6 and 15.8 ± 16.1, whereas those for reader 2 were 12.0 ± 12.5 and 15.8 ± 15.7, respectively. The ICCs for CTSS at baseline and at 2-year follow-up were 0.97 (95% confidence interval [CI] 0.96–0.99) and 0.98 (0.97–0.99), respectively, and that for changes over the 2 years was 0.48 (95% CI 0.23–0.67). For sCTSS, the ICCs were 0.96 (95% CI 0.92–0.97), 0.97 (95% CI 0.94–0.98), and 0.58 (95% CI 0.36–0.74), respectively. Detection rates for syndesmophyte progression were comparable between CTSS and sCTSS. The detection rate for syndesmophytes on only lateral side was 13.2 and 11.4%, and 11.4 and 15.2% at baseline and 2-year follow-up (reader 1 and 2). sCTSS and CTSS showed similar detection rates for syndesmophyte progression. sCTSS may be a reliable method for evaluating spinal structural damage in AS.

The impact of smoking status on radiographic progression in patients with ankylosing spondylitis on anti-tumor necrosis factor treatment.

Ankylosing spondylitis (AS) is characterized by back pain which can lead to spinal ankylosis. Anti-tumor necrosis factor (TNF) dramatically alleviates symptoms, but spinal damage can still be progressive even during anti-TNF treatment. Smoking is a one of well-known risk factors for structural damage in AS. However, it has not been confirmed that smoking can affect radiographic progression even during anti-TNF treatment. To investigate factors associated with radiographic progression during anti-TNF treatment with a focus on smoking status which is known as one of poor prognostic factors for AS. We conducted a retrospective cohort study of AS patients who began the first-line anti-TNF treatment between 2001 and 2018 according to availability of smoking data. All enrolled patients were observed until the last visit, the first-line anti-TNF discontinuation, or December 2019. Radiographic damage was assessed using the modified Stoke Ankylosing Spondylitis Spinal Score (mSASSS). The mSASSS progression rate (units/year) was calculated using the baseline mSASSS, the final mSASSS during observation period, and the duration between them. Univariable and multivariable logistic regression analyses were performed to identify associated factors of mSASSS progression rate > 1 unit/year. Among 459 AS patients, 185 (40.3%) patients were never smokers, 62 (13.5%) were ex-smokers and 212 (46.2%) were current smokers at baseline. Ex- and current smokers had higher mSASSS progression rates than never smokers [never smoker 0.1 (0.0-0.7), ex-smoker 0.6 (0.0-1.5), and current smoker 0.6 (0.0-1.5) units/year, P < 0.001]. In the multivariable logistic analysis, current smoking [adjusted odds ratio (OR) 1.69, 95% CI 1.01-2.82, P = 0.047] and higher baseline mSASSS [adjusted OR 1.03, 95% CI 1.01-1.04, P < 0.001] were associated with a mSASSS progression rate > 1 unit/year. Current smoking is a modifiable risk factor for radiographic progression in patients with AS on anti-TNF treatment. Quitting smoking should be strongly recommended.

AB0675 Infliximab in Ankylosing Spondylitis: Effect on Structural Damage Progression

BackgroundTumor necrosis factor-α (TNF-α) inhibition has been evolutionary in the treatment of ankylosing spondylitis (AS). Conventional radiography reflects chronic structural damage in AS rather than the underlying inflammatory processes that...

Review: The Interleukin‐23/Interleukin‐17 Axis in Spondyloarthritis Pathogenesis: Th17 and Beyond

Spondyloarthritis (SpA) represents a group of immune-mediated inflammatory diseases that exhibit overlapping clinical features, genetic predisposition, and pathogenic mechanisms (1), and affect 0.5–1.5% of the population (2). Disease can be undifferentiated, or manifest as reactive arthritis, psoriatic arthritis (PsA), arthritis associated with inflammatory bowel disease (IBD), or ankylosing spondylitis (AS). Enthesitis is an important pathologic feature of SpA, and contributes to both axial and peripheral arthritis, although synovitis also occurs. Structural damage in AS is dominated by new bone formation that can result in spinal fusion and marked functional limitation. Trabecular bone loss is also prominent, and paradoxically, occurs in close proximity to vertebral osteoproliferation. It can take years from the onset of symptoms to fulfill modified New York criteria for AS. Consequently, newer classification systems have been developed to identify individuals with early axial SpA (3,4) who may benefit from aggressive treatment. Tumor necrosis factor inhibitors (TNFi) have had a major impact on the treatment of SpA (5). Their ability to reduce new bone formation in AS continues to be debated (6), although recent results are encouraging (7). TNFi are not beneficial in all patients, and thus there is a need for greater understanding of pathogenic mechanisms and translation of this knowledge into more effective therapies. Over the last decade our knowledge of the role of IL-23 and IL-17 cytokine pathways in immunity and immune-mediated inflammatory diseases, from multiple sclerosis (MS) to IBD, arthritis, and psoriasis has grown exponentially (8–11). For SpA, there has been a striking convergence of evidence from genetic studies (12–15), animal models (16–19), translational studies (20–23), and now a therapeutic trial (24) firmly implicating the IL-23/IL-17 axis in pathogenesis (25). In this review we outline key evidence accumulated over the last several years that forms the basis for this conclusion, and provides a background on which to build and refine models of pathogenesis, from inflammation to dysregulated bone formation. These developments, together with the availability of biologics and small molecules that target the IL-23/IL-17 axis, provide an unprecedented opportunity for advances in the treatment of SpA.

Imaging of ankylosing spondylitis

Conventional radiography can visualize bone erosion, sclerosis, joint space narrowing and new bone formation in sacroiliac joints and the spine, but is unfortunately not very sensitive in early disease. Diagnosis of ankylosing spondylitis (AS) is dependent on presence of bilateral moderate or unilateral severe radiographic sacroiliitis, as part of the modified New York criteria for AS. This has, until recently (see MRI below), delayed the diagnosis by 7-10 years. Furthermore, the modified Stokes ankylosing spondylitis spine score (mSASSS), which is the most sensitive radiographic method for monitoring structural damage in AS, is not very reproducible or sensitive to change, so improved methods for structural damage assessment are highly needed. MRI has resulted in a major improvement in the evaluation and management of patients with SpA. Firstly, it permits earlier diagnosis, as MRI findings of active sacroiliitis form part of the recent ASAS criteria for axial spondyloarthritis. Secondly, MRI can provide objective evidence of currently active inflammation in patients with SpA. MRI is by far the best available method for detecting and monitoring inflammation in the spine and sacroiliac joints, and several validated assessment systems exist. Until the introduction of MRI, disease activity assessment was restricted to patient-reported outcomes, such as the Bath ankylosing spondylitis disease activity index (BASDAI) and functional index (BASFI), because disease activity could not be assessed in a sensitive manner by biochemical (mainly C- reactive protein (CRP)) or physical evaluation. Furthermore, MRI can visualize structural damage (erosion, fat infiltration, syndesmophytes and ankylosis) in the sacroiliac joint and spine, but the clinical role of MRI for monitoring structural damage remains to be established. Finally, certain MRI findings (inflammation at the vertebral corners) have predictive value with respect to subsequent development of radiographic syndesmophytes. However, clarification of the prognostic value of MRI in clinical practice requires further research. Despite contrast-enhanced Doppler US has been reported to have a high negative predictive value for the detection of sacroiliitis, the role of US in assessment of sacroiliac and spine involvement in AS and other types of axial SpA is minimal.

Advances in musculoskeletal imaging and their clinical utility in the early diagnosis of spondyloarthritis

Interest in imaging ankylosing spondylitis (AS) and related spondyloarthropathies has increased in recent years. MRI is regarded as the most sensitive imaging modality to detect early inflammatory lesions in the sacroiliac joints and in the spine. Standard radiography plays a major role in evaluating potential disease-modifying properties of the recently introduced, symptomatically effective anti-tumor necrosis factor-alpha agents. Various radiographic scoring methods have been developed to assess and monitor spinal structural damage in AS. The modified stoke ankylosing spondylitis spine score is the method of choice based on its sensitivity to change. MRI is emerging as a useful tool to detect AS early, but this remains a challenge. Recent progress in MR technology with the advent of whole body MRI has expanded the potential role of imaging in AS. Further data are needed before MRI can replace radiographs for earlier diagnosis of AS.