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Evaluate the MRI evidence of active inflammatory and chronic structural damages in radiographic axial spondyloarthritis (r-axSpA) and non-radiographic axial spondyloarthritis (nr-axSpA). A retrospective review of 253 patients who underwent sacroiliac joint (SIJ) MRI between June 2014 and December 2019 was performed. MRI images including short tau inversion recovery scan and T1-weighted spin echo scans were assessed using the Spondyloarthritis Research Consortium of Canada (SPARCC) score and SPARCC MRI SIJ structural score by two independent readers. Higher mean score of inflammatory (SPARCC) was seen in r-axSpA patients when compared with nr-axSpA patients (8.08 4.37, <0.05). Frequencies of MRI structural lesions in r-axSpA patients and nr-axSpA patients were as follows: erosion (65.84 88.23%, =0.002), backfill (33.17 13.73%, <0.001), fat metaplasia (79.21 60.78%, =0.01), and ankylosis (37.13 1.96%, <0.001). Patients with r-axSpA had a higher mean score for fat metaplasia (8.93 4.06, =0.0003) and ankylosis (4.49 0.04, <0.001). More active inflammatory and chronic structural damages except for erosion were seen in r-axSpA patients than nr-axSpA patients, while higher percentage of nr-axSpA patients presented with erosion in MRI.

Background In axial spondyloarthritis (axSpA), 5–10% of patients have comorbid inflammatory bowel disease (IBD). Beyond that, 50–60% display histologic inflammation in ileum/colon biopsies, and fecal calprotectin (F-calprotectin) is elevated in relation to healthy controls. Prior studies have shown such, often subclinical, gut inflammation in axSpA to be associated with more active disease, as measured by clinical indices as well as magnetic resonance imaging – both known risk factors for structural spinal damage development. In light of this, in the current study we aimed to examine whether gut inflammation, assessed by F-calprotectin, is associated with more structural spinal damage in axSpA. Methods Patients with well-characterized non-radiographic or radiographic axSpA (nr-axSpA/r-axSpA; n  = 76/152), according to ASAS or modified New York criteria, enrolled in a population-based cohort study in southern Sweden, were assessed for structural spinal damage (modified Stoke ankylosing spondylitis spinal score [mSASSS]) and gut inflammation (F-calprotectin). mSASSS values were compared between patients with normal (< 50 mg/kg), moderately elevated (50–149 mg/kg) or distinctly elevated (≥ 150 mg/kg) F-calprotectin, reflecting no/some/evident gut inflammation, respectively (one-way ANOVA). Moreover, logistic regression was applied to explore if elevated F-calprotectin (≥ 50 mg/kg) was associated with mSASSS values above the median, adjusted for sex, symptom duration, HLA-B27 status, smoking, CRP, NSAID and anti-TNF therapy. Analyses limited to r-axSpA were also performed. Results In both axSpA patients overall and separately in r-axSpA, mSASSS distributions differed significantly between subjects with normal/moderately/distinctly elevated F-calprotectin, with more damage observed in those with higher F-calprotectin levels. Furthermore, elevated F-calprotectin (≥ 50 mg/kg) was associated with mSASSS values above the median, in both the entire axSpA group (adjusted odds ratio [OR] 2.2 [95%CI 1.1–4.2]); and in r-axSpA alone (adjusted OR 2.9 [1.2–7.1]). Conclusion In the current study, the presence of gut inflammation, assessed by F-calprotectin, was cross-sectionally associated with more structural damage in the spine in patients with axSpA, even after adjustments for known risk factors for spinal damage. Prospective studies are, however, needed to investigate whether gut inflammation may be a predictor of spinal radiographic progression in axSpA.

Background Radiographic axial spondyloarthritis (r-axSpA) is a chronic inflammatory disease that primarily affects the axial skeleton and entheses, leading to pathological spinal bone formation and systemic bone loss. Treatments with tumor necrosis factor inhibitors (TNFi) and interleukin-17 inhibitors (IL-17i) have shown efficacy in reducing inflammation and potentially impacting bone remodeling in r-axSpA. Osteoclasts, crucial for bone resorption, are derived from the monocytic cell lineage and regulated by proinflammatory cytokines. This study aimed to evaluate the osteoclast development capacity from peripheral blood monocytes in patients with r-axSpA with different treatment strategies and compare it to controls. Methods This study included 28 patients with long-standing r-axSpA receiving various treatments, including disease-modifying anti-rheumatic drugs (DMARDs) and NSAIDs, as well as 16 blood-donor controls. Disease activity was assessed using the Ankylosing Spondylitis Disease Activity Score (ASDAS). CD14 + monocytes were isolated from blood samples and differentiated into osteoclasts in vitro by stimulation with three different conditions: (I) macrophage colony-stimulating factor (M-CSF), (II) M-CSF and receptor activator of nuclear factor-κβ (RANKL), and (III) M-CSF, RANKL, and tumor necrosis factor-alpha (TNF). Osteoclast and osteoclast precursor formation were assessed using tartrate-resistant acid phosphatase (TRAP) staining, and TRAP5b concentration in supernatants was measured by ELISA. Results The frequency of CD14 + monocytes was similar in patients with r-axSpA and controls, but the capacity to develop osteoclasts and osteoclast precursors was significantly decreased in the r-axSpA patients. Stratification of the patients based on treatment with or without biological DMARDs (bDMARDs) revealed no significant differences in ASDAS or frequency of CD14 + monocytes. Notably, only r-axSpA patients receiving bDMARDs exhibited a reduced ability to develop osteoclasts and osteoclast precursors compared to those not on bDMARDs and controls. Lower Trap5b concentrations in supernatants corroborated these findings. Conclusions Our study demonstrates that patients with r-axSpA exhibit a reduced capacity for osteoclast formation from CD14 + monocytes isolated from peripheral blood. The process was modulated by treatment with bDMARDs, which might explain the previously shown sparing effect of bDMARDs on bone mineral density in r-axSpA.

ObjectivesTo identify clusters of highly correlated genes enriched in biological functions and specific molecular pathways involved in the pathogenesis of radiographic damage in axial spondyloarthritis (axSpA) and to discover molecular biomarkers of radiographic progression and disease severity.MethodsA total of 144 patients with axSpA were included. First, RNA from peripheral blood mononuclear cells was sequenced in a cohort of 24 patients with axSpA. Hub genes were measured in a n=60 validation cohort through microfluidic PCR. A 5-year follow-up enabled the classification of the patients into fast/moderate or slow progressors. Machine learning approaches were applied to identify a predictive biomarker of progression by integrating gene expression data with clinical variables. An independent cohort of 60 patients with axSpA, with spine radiographs taken 5 years prior, underwent serum proteomic analysis using a Proximity Extension Assay.ResultsUnsupervised clustering analysis using transcriptomics revealed two distinct groups of patients with axSpA, differentiated by their clinical profiles. Weight gene correlation network analysis identified six gene modules differentially expressed between the two clusters. Patients in cluster 2 exhibited higher disease activity, greater functional impairment and more structural damage. Molecular alterations linked to structural damage revealed a specific circulating inflammatory proteome profile associated with disease severity. A predictive model composed of two genes and basal total modified Stoke Ankylosing Spondylitis Spinal Score emerged as a key biomarker for identifying moderate-to-fast radiographic progression.ConclusionsThis study identified molecular pathways involved in radiographic damage and discovered potential proteomic biomarkers of disease severity and transcriptomic predictors of radiographic progression in axSpA.

Spondyloarthritis (SpA) encompasses a group of chronic inflammatory diseases with overlapping genetic, clinical, and radiographic features. Axial spondyloarthritis (axSpA), a subset of SpA, predominantly involves the sacroiliac joints and spine, often progressing to ankylosis, severe disability, and functional impairment. Psoriatic arthritis (PsA), another SpA subtype, is characterized by a heterogeneous phenotype that includes peripheral arthritis, enthesitis, and axial involvement, frequently associated with psoriasis. Bone remodeling in axSpA and PsA is driven by a dynamic interplay between inflammatory cytokines and the uncoupling of anabolic and catabolic processes, resulting in bone erosion, systemic and local bone loss, and pathological new bone formation. In axSpA, tumor necrosis factor-alpha (TNFα) and interleukin-17A (IL-17A) drive osteoclastogenesis via the RANKL pathway while suppressing osteoblast-mediated bone formation through WNT/β-catenin signaling. Mechanical stress, combined with inflammatory mediators, promotes mesenchymal stem cell differentiation and new bone formation, which manifests as syndesmophytes and contributes to progressive ankylosis. Conversely, PsA is distinguished by concurrent bone erosion and neoformation, driven by IL-17A, IL-22, and IL- 23, with axial disease exhibiting asymmetrical, bulky para-syndesmophytes rather than the fine, hair-like syndesmophytes typical of axSpA. Advanced imaging modalities, particularly MRI, have elucidated key mechanisms of disease progression, revealing processes such as fat metaplasia and reparative changes. This review explores the intricate molecular and cellular mechanisms underlying bone remodeling in SpA, emphasizing both shared pathways and disease-specific features. It aims to enhance the understanding of these processes to support the development of more precise and effective therapeutic approaches tailored to axSpA and PsA.

ObjectiveTo evaluate the prevalence and anatomical distribution of inflammatory and structural MRI lesions in axial spondyloarthritis (axSpA) and compare these between patients with isolated axial involvement and those with peripheral manifestations.MethodsData from the Assessment of SpondyloArthritis International Society (ASAS) Classification Cohort were analysed. Peripheral involvement was defined as past or current arthritis/dactylitis/enthesitis. Sacroiliac joint (SIJ) and spinal MRI lesions typical of axSpA were classified per ASAS lesion definitions and centrally read with multi-reader majority agreement (lesion present if called by the majority; SIJ ≥4/7, spine ≥5/9 readers). Comparisons between patients with and without peripheral manifestations were made.ResultsAmong 199 axSpA patients with SIJ MRI, 67 also had spinal MRI. Subchondral SIJ bone marrow oedema (BMO) was observed in 49%, without quadrant preference or subgroup differences. Other SIJ inflammatory lesions ranged from 4%–18%. Erosions (35%) and fat lesions (22%) were the most frequent structural lesions. In the spine, BMO, fat lesions and syndesmophytes/ankylosis were detected in 38%, 25% and 5%, respectively, with similar subgroup frequencies. Among 40 patients with both SIJ and whole spine MRI, inflammatory lesions were observed in both sites in 18%, SIJ only in 38%, and spine only in 20%. Structural lesions occurred in both sites in 19%, SIJ only in 30%, and spine only in 5%, with no subgroup differences.ConclusionThe prevalence and anatomical distribution of ASAS-defined MRI lesions was similar across axSpA subgroups. Notably, 20% exhibited spine-only inflammation, suggesting potential added diagnostic and monitoring value of spinal MRI, warranting further study.

Background Axial spondyloarthritis (SpA) leads to structural bone lesions in every part of the vertebral column. These lesions are only partially visualized on conventional radiographs, omitting posterior parts of the vertebral column and the thoracic spine, that may nevertheless contribute to impaired spinal mobility and function in patients with axial SpA. Methods In this prospective and blinded investigation, we assessed the distribution of structural spinal lesions using magnetic resonance imaging (MRI) of the whole spine in 55 patients with axial SpA classified according to the Assessment in Spondyloarthritis International Society (ASAS) criteria. After assessment of spinal mobility and function two blinded radiologists independently evaluated MRIs of 23 vertebral units in every patient. Non-parametric statistical methods, Spearman‘s correlation and linear regression models were used to analyze structural lesion distribution and the relationship with clinical spinal mobility and function parameters. Results In 55 patients with axial SpA (13 females, average disease duration 14.9 years) 657 ventral and 139 dorsal vertebral body structural bone lesions and, notably, 534 facet joint lesions could be visualized. The median number of lesions per patient was higher in the thoracic (8.5, range 1.0–41.0) than in the lumbar (7.5, range 0.0-27.5) and the cervical spine (3.5, range 0.0-24.5). A negative correlation was noted between the number of osteoproliferative structural bone lesions and impairment of spinal mobility and function in univariate, but not in multivariate analyses. Conclusion MRI of the whole spine revealed a high prevalence of lesions in dorsal parts of the vertebral column and in the thoracic spine in patients with axial SpA that may not be adequately visualized on conventional radiographs. These findings could further contribute to a better understanding of reduced mobility of the spine typically associated with axial SpA and assist diagnostics.

ObjectivesTo determine which anatomical sites and which ultrasonographic entheseal lesions are best able to discriminate between spondyloarthritis (SpA) patients and healthy controls (HC).MethodsWe included patients with psoriatic arthritis (PsA) and axial SpA (axSpA), from six Swiss hospital outpatient clinics, as well as HC. Participants completed quality of life and physical activity questionnaires and underwent a clinical examination of both joints and entheses, followed by a detailed musculoskeletal ultrasound examination including nine entheseal sites bilaterally. Entheses were scored according to the Outcome Measures in Rheumatology criteria, with an additional evaluation of bursae and power Doppler (PD) in the 2–5 mm zone.ResultsOverall, 121 participants were included, including 41 with PsA (mean age in years (SD), percentage male: 54.5±11.0, 63.4%), 39 with axSpA (45.1±10.0, 51.3%) and 41 HC (43.9±10.9, 56.1%), with a total of 2178 entheses evaluated. The PsA and axSpA groups showed no significant differences regarding inflammatory markers or disease activity scores.In the univariable analysis, all ultrasonographic lesions at the enthesis showed a significant association with SpA vs HC. Only B-mode inflammatory lesions (OR=1.38, p=0.034) and active enthesitis (OR=4.45, p=0.030) retained this association in multivariable analyses. While 4/9 entheses were associated with SpA in univariable analyses, only the distal patellar ligament insertion remained significantly associated with SpA (OR=1.74, p=0.039) in multivariable analyses.ConclusionTo distinguish SpA patients from controls, the sonographic scoring system used should account not only for the presence of specific entheseal lesions (structural and inflammatory) but also for the individual site affected.

ObjectiveTo investigate the extent and performance of structural lesions in sacroiliac joints on MRI (MRI-SI) in patients with axial spondyloarthritis (axSpA), chronic back pain, postpartum back pain, runners and healthy subjects.MethodsMRI-SIs in 172 subjects, including 47 patients with diagnosed axSpA fulfilling the Assessment of SpondyloArthritis international Society (ASAS) criteria, 47 patients with chronic back pain, 7 women with postpartum back pain, 24 runners and 47 healthy individuals, were scored by two well-trained readers for erosions, fatty lesions, sclerosis and ankylosis, using an adjusted Spondyloarthritis Research Consortium of Canada scoring method. In addition, cut-off values proposed by the Imaging workgroups of Leiden and the ASAS were tested.ResultsOf the axSpA patients, 37 (79%) had structural lesions. Most frequently reported structural lesions were erosions in 35 (75%) patients and fatty lesions in 19 (40%) patients. Erosions and fatty lesions were uncommon in chronic back pain, runners and healthy individuals. There was a statistically significant difference in the prevalence of erosions, fatty lesions and ankylosis between axSpA and chronic back pain. Ankylosis was rare in both groups. Comparing axSpA to non-axSpA, Leiden cut-off definitions were more specific than ASAS cut-offs.ConclusionsStructural changes resembling axSpA may occur in individuals who do not have axSpA, but at a lower rate than inflammatory changes. Erosions and fatty lesions are most specific. Using cut-off definitions for these structural lesions results in good discrimination between axSpA and non-axSpA. In axSpA, structural lesions primarily occur in concordance with ongoing inflammation.

The aim of the study was to compare clinical characteristics of patients with axial spondyloarthritis (axSpA)/ankylosing spondylitis (AS) and with axial psoriatic arthritis (axPsA).Materials and methods. A total of 100 patients were examined: 45 with axSpA/AS (group 1) and 55 with axPsA (group 2). Patients of group 1 were included according to axSpA/AS criteria; patients of group 2, according to CASPAR (ClASsification criteria for Psoriatic ARthritis) criteria, and having axial involvement (axPsA). Axial involvement was detected in case of radiologically significant sacroiliitis (SI, bilateral grade ≥2 or unilateral grade ≥3), or active MRI significant sacroiliitis, or ≥1 syndesmophyte(s) of the cervical and/or lumbar spine. Patients were evaluated for the presence of inflammatory back pain (IBP) by ASAS (Assessment of Spondyloarthritis International Society) criteria.Results and discussion. Patients of group 1 were younger (p < 0.001), more often were HLA-B27 positive (p < 0.001), and more often had IBP (p = 0.001). Patients of group 2 had older age (> 40 years) at back pain onset (p < 0.001) and more often had peripheral arthritis (p < 0.001), dactylitis (p = 0.004), and skin psoriasis (p < 0.001). Nail psoriasis was found only in group 2 patients (p < 0.001). Group 1 patients more often had heel enthesitis (p = 0.005). Group 2 patients had worse axial disease activity scores: BASDAI (Bath Ankylosing Spondylitis Disease Activity Index; p = 0.006) and ASDAS-СRP (Ankylosing Spondylitis Disease Activity Score with C-reactive protein level determination; р < 0.001); and worse patient-reported outcomes: BASFI (Bath Ankylosing Spondylitis Functional Index; p = 0.004), patients’ pain (p = 0.005) and patients’ global assessments (p = 0.036). Patients of group 2 had more syndesmophytes of the lumbar (р = 0.009) and cervical (р = 0.007) spine. Only in group 2 patients, chunky “non-marginal” syndesmophytes (in 32.1%), as well as spinal lesions without sacroiliitis (in 20.0%) were found. Patients of group 2 had more joint erosions (р = 0.001), osteolysis (р = 0.015), juxta-articular bone formation (р < 0.001) and joint ankyloses (р = 0.02). All patients of group 1 and only 80% of group 2 (р = 0.003) met ASAS criteria for axSpA. AxSpA/AS and axPsA seem to be two different diseases. In our cohort of patients, axPsA patients had worse disease status compared to axSp and AS.