Ankylosing spondylitis (AS) is a chronic autoimmune disease that primarily affects the axial joints. Immune cells play a key role in the pathogenesis of AS. This study integrated bioinformatics methods with experimental validation to explore the role of natural killer (NK) cells in AS.

Two microarray datasets, GSE25101 and GSE73754, were selected, and the scRNA-seq data were obtained from GSE194315 and Liu's research. Differentially expressed genes (DEGs) and functional enrichment analysis were performed respectively. Weighted gene co-expression network analysis (WGCNA) was conducted to identify key modules of co-expressed genes and genes involved in NK cell function. The diagnostic value of the identified key genes was evaluated using ROC curves, logistic regression analysis, and a nomogram. Real-time PCR (RT-PCR) was used to quantified the expression of genes. Statistical analysis was conducted using the R software package, and a p-value of less than 0.05 was considered statistically significant.

Pathways enrichment analysis revealed the involvement of NK cell-mediated immune pathways and regulation of the innate immune response, indicating the crucial role of innate immunity, especially NK cells, in AS pathogenesis. The construction of a co-expression network revealed that the MElightyellow module was most relevant to the NK cell-mediated immune pathway. IL2RB, CD247, PLEKHF1, EOMES, S1PR5, FGFBP2 from the MElightyellow module were identified as key genes involved in NK cell-mediated immune response and served as potential diagnostic biomarkers for AS, with moderate to high diagnostic values based on AUC values. Further analysis using scRNA-seq profiling revealed the higher expression level of IL2RB, CD247, PLEKHF1, S1PR5, FGFBP2 in NK cells compared to that in other cell types. CD247, PLEKHF1, EOMES, S1PR5, and FGFBP2 were reduced expressed in AS patients as compare to control group verified by scRNA-seq data, CD247, EOMES, FGFBP2, IL2RB and S1PR5 were reduced expressed verified by RT-PCR, and PLEKHF1, S1PR5, and FGFBP2 was upregulated after TNF-α blocker therapy.

The study revealed the potential role of NK cells and identified IL2RB, CD247, PLEKHF1, EOMES, S1PR5, and FGFBP2 as key genes associated with NK cells in the pathogenesis of AS.

To describe the incidence rates of inflammatory bowel disease (IBD) and tuberculosis (TB) in Korean patients with ankylosing spondylitis receiving biologics.

Data from a Korean claims database between 2010 and 2021 was used to calculate crude incidence rates of TB and IBD using number of events and total patient-years (PYs).

Overall, 43 643 and 43 396 patients were included in TB and IBD cohorts, respectively. Exposure-adjusted incidence rates (EAIRs) of TB for non-exposure, TNF inhibitors (TNFis), and IL-17 inhibitors (IL-17is) were 0.14, 0.25 and 0.12 and of IBD were 0.18, 0.19 and 0.44 per 100 PYs, respectively. Incidence rates during biologic DMARD (bDMARD) non-exposure, adalimumab, etanercept, golimumab, infliximab, secukinumab and ixekizumab exposures for TB were 13.96, 27.79, 14.28, 21.19, 33.62, 12.74 and 0.00 and for IBD were 18.29, 19.98, 22.41, 18.85, 15.73, 44.99 and 0.00 per 10 000 PYs, respectively. Compared with bDMARD non-exposure, adalimumab, golimumab and infliximab exposures were associated with a significantly higher risk of TB. Etanercept and secukinumab exposure showed no significant increase in risk of TB. Compared with bDMARD non-exposure, exposure to biologics did not show a significant difference in risk of IBD.

EAIRs of TB and IBD with use of IL-17is in patients with AS were within anticipated low range. IL-17is had numerically lower incidence of TB, and numerically higher incidence of IBD compared with TNFis. Notably, secukinumab showed no increased risk of TB compared with bDMARD non-exposure. Neither TNFis nor IL-17is showed increased risk of IBD compared with bDMARD non-exposure.

Ankylosing spondylitis (AS) is a systemic inflammatory disorder that predominantly involves the axial skeleton, often leading to irreversible structural damage and disability. Although several therapeutic measurements are available, limitations in efficacy and long-term outcomes remain significant. Therefore, identifying novel biomarkers and therapeutic targets is of critical importance for optimizing clinical management and prognostic evaluation in AS patients.

This study aims to elucidate the immune features and discover potential biomarkers for AS by the integration of deep plasma proteomics and deep learning strategies.

The deep quantitative proteomics was applied to analyze the plasma samples from 104 participants of AS patients with active and stable stages, along with healthy controls. The immune and functional features of AS patients in different stages were assessed. By integrating random forest (RF) with orthogonal partial least squares discriminant analysis (OPLS-DA), a machine learning model-based score matrix was constructed to identify biomarkers. ELISA experiments were performed on an independent cohort of 79 participants to confirm the potential biomarkers for AS.

Patients with AS exhibit significant dysregulation in the distributions and characteristics of immune cells. Several key proteins involved in integrin signaling pathway were significantly differentially expressed in patients with AS, highlighting the pathway's role in the pathogenesis of AS. Four proteins including SAA1, FERMT3, ILK, and TLN1, were identified as potential biomarkers for AS and further verified by ELISA experiments.

By integrating the machine learning-based method with deep proteomics analysis, we explored the pathological mechanism and identified biomarkers for AS. Our study provides insights into the distinct protein expression patterns and pathogenesis of AS and may contribute to diagnosis, long-term monitoring, and therapy for this disease.

Axial spondyloarthritis (axSpA) is a chronic inflammatory arthritis affecting the spine and sacroiliac joints, often accompanied by extra-musculoskeletal manifestations involving the eyes, gut, and skin. Other organ systems, including the heart (aortic insufficiency), lungs (upper-lobe predominant interstitial fibrosis), and kidneys (nephritic syndrome), may also be affected. Immunoglobulin A vasculitis (IgAV), formerly known as Henoch-Schönlein purpura, is the most common systemic vasculitis in children and is typically self-limited. It is characterized by palpable purpura, arthritis or arthralgia, abdominal pain, and renal involvement. Studies suggest a potential link between elevated serum immunoglobulin A levels and active inflammation in axial spondyloarthritis. Here, we present a case of a Caucasian male diagnosed with immunoglobulin A vasculitis, leading to the identification of previously unrecognized axial spondyloarthritis. In addition, we reviewed the current literature on IgAV occurring in patients with axial spondyloarthritis.

Background: Ankylosing Spondylitis (AS) is a rare autoinflammatory disorder affecting 0.1-1.4% of the population, with increasing recognition over the past 20 years. Although the specific causes of AS remain unclear, the presence of the HLA-B27 gene is associated with increased risk, though only 1-5% of carriers develop the disease. Despite extensive research, no definitive lab tests exist, and many patients are diagnosed years after symptom onset. Methods: In the present study, in order to investigate the disease's genetic background in correlation with autoimmune diseases, a metanalysis has been performed following PRISMA guidelines using Scopus and PubMed publications towards extracting single-nucleotide polymorphisms (SNPs) of high importance for the disease. Moreover, the polymorphisms have been annotated and analyzed using information from several databases, including PubMed, LitVar2, ClinVar, and Gene Ontology. Results: From 1940 screened titles and abstracts, 57,909 studies were selected, with 539 meeting the inclusion criteria. The genetic background of AS is described through 794 genetic variants, of which 76 SNPs are directly associated with AS (Classes A and B), predominantly located in intronic regions. ERAP1 and IL23R emerged as key genes implicated in AS, while chromosomes 1, 2, and 5 accumulated the most associated SNPs. Functional enrichment revealed strong associations with immune regulation and interleukin signaling pathways, particularly IL6 and IL10 signaling. IL-6 promotes inflammation in AS, while IL-10 tries to suppress it, acting as an anti-inflammatory cytokine. Of the 78 AS-related SNPs, 16 were unique to AS, while 66 were common to autoimmune diseases, especially rheumatoid arthritis (RA) and psoriasis (PsO), suggesting genetic overlap between these diseases. Conclusions: This study creates a comprehensive genetic map of AS-associated SNPs, highlighting key pathways and genetic overlap with autoimmune diseases. These findings contribute to understanding disease mechanisms and could guide therapeutic interventions, advancing precision medicine in AS management.

Axial spondyloarthritis (axSpA) is a chronic inflammatory disorder characterised by inflammation of the axial manifestations. For the military draftees, there are no epidemiological data on axSpA in nationwide and population-based databases. This retrospective, nationwide and population-based study aimed to assess the national and regional trends in axSpA prevalence among draft-eligible military populations in South Korea between 2014 and 2023.

The study included 3 063 805 males examined by the Regional Military Manpower Administration. The annual nationwide prevalence was presented as the prevalence per 10 000 and a 95% CIs. The severity of axSpA was assessed using radiographic scoring of the sacroiliac joint based on the New York criteria. Regional trends of axSpA were evaluated for Seoul, metropolitan areas and provinces, categorised according to transportation accessibility.

The nationwide prevalence of axSpA increased from 10.75 (95% CI 9.68 to 11.81) in 2014 to 21.18 (95% CI 19.37 to 23.00). The prevalence of radiographic axSpA (r-axSpA) followed a similar upward trend, whereas the prevalence of non-radiographic axSpA (nr-axSpA) remained stable. The prevalence of r-axSpA (52.73% in 2015 and 79.52% in 2019) was higher than that of nr-axSpA. Meanwhile, r-axSpA patients with grade 3 sacroiliitis showed the highest prevalence during the recent 3-year follow-up. The mean regional prevalence of nr-axSpA differed significantly among the three regions (p=0.013), whereas there were no differences in the prevalence of r-axSpA (p=0.084).

This epidemiological study revealed an increasing trend in the nationwide prevalence of axSpA over the past decade, primarily driven by an increase in moderate-grade r-axSpA. Therefore, early recognition and awareness of axSpA in young males are essential for initiating appropriate treatment options to slow disease progression.

Sleep disorders are a common symptom in Ankylosing Spondylitis (AS) patients. In this cross-sectional study, we aimed to understand the current status of sleep disorders in AS patients and to analyze potential factors influencing sleep disorders.

A total of 205 AS patients were recruited in the survey. The content included the self-designed demographic data questionnaire, The MOS 36-Item Short Form Health Survey (SF-36), Visual Analogue Scale (VAS), Multidimensional Fatigue Inventory (MF-20), Self-Rating Anxiety and Depression Scale, Pittsburgh Sleep Quality Index questionnaire (PSQI), Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), Bath Ankylosing Spondylitis Functional Index (BASFI) and Bath Ankylosing Spondylitis Metrology Index (BASMI). These data were analyzed using chi-square test, independent sample t-test, Mann-Whitney U test, Pearson correlation analysis, single-factor linear regression analysis, and multiple linear stepwise regression analysis.

The results showed that the average sleep total score was 8.82 ± 4.146, and the prevalence of sleep disorders was approximately 66.8% in AS patients. Age (F = 29.710, P < 0.001), disease duration (F = 13.025, P < 0.001), anxiety (F = 36.060, P < 0.001), depression (F = 11.808, P < 0.001), and quality of life (t = 6.665, P < 0.001) significantly impacted the sleep total score. Pearson correlation analysis revealed a significant negative correlation between SF-36 total score and sleep total score (r = ‒0.449, P < 0.01), while positive correlations were observed for VAS score, fatigue, anxiety, depression, BASDAI, BASFI, BASMI, age, and disease duration (all P < 0.01). Multivariate analysis showed that age, disease duration, nocturnal pain VAS score, total back pain VAS score, peripheral joint pain VAS score, total fatigue score, total anxiety score, and BASMI total score significantly predicted sleep total score (R² = 0.755, F = 45.334, P < 0.001).

These findings suggest that medical professionals should pay increased attention to the observed associations between sleep disorders and clinical factors in AS patients, and consider implementing targeted interventions to address sleep-related issues.

Ankylosing spondylitis is a complex rheumatic disease, characterised by chronic and progressive inflammation of the spine, causing an important health and economic burden for the person with the condition. Evidence shows the unequal impact of the disease in different groups of people, with a higher burden for lower socioeconomic groups. The objective of this study is to evaluate the impact of the use of biologics for the treatment of ankylosing spondylitis on health inequities in Chile.

We conducted an aggregate distributional cost-effectiveness analysis. Data on health outcomes and costs were derived from a cost-effectiveness model of secukinumab, etanercept, certolizumab pegol, infliximab, adalimumab and golimumab versus treatment as usual for the treatment of ankylosing spondylitis from the Chilean healthcare system perspective. Health gains and health opportunity costs were distributed across socioeconomic subgroups. Health and equity impacts, measured using the Atkinson index, were assessed on an equity-efficiency impact plane.

All treatments had a positive impact on equity relative to treatment as usual. At an opportunity cost threshold of 1 Gross Domestic Product per capita/quality-adjusted life-year, secukinumab improved societal welfare irrespective of the Atkinson index value. When varying thresholds (2 and 3 Gross Domestic Product), all assessed technologies contributed to an increase in societal welfare, regardless of the Atkinson index.

Biologic treatment for ankylosing spondylitis, such as secukinumab, may reduce health inequity in the Chilean population. An aggregate distributional cost-effectiveness analysis framework is feasible to implement alongside a cost-effectiveness analysis in the context of the Chilean healthcare system to provide additional information of equity impacts for health technology assessment recommendations and policy making.

The implementation of diverse surgical techniques plays a crucial role in managing ankylosing spinal diseases (ASDs), serving as invaluable tools. Presently, posterior surgery stands out as the predominant approach owing to its familiarity with anatomical structures; however, it comprises various methodologies that require a thorough comprehension for their suitable application. Henceforth, we performed a network meta-analysis to assess and prioritize the efficacy and safety of surgical interventions for ASDs.

The databases PubMed, EMBASE, Cochrane Library, and CNKI (China National Knowledge Infrastructure) were systematically searched for both randomized and non-randomized studies. No restrictions were placed on the initial time periods or languages of the searches. Patients with thoracolumbar fractures accompanied by ankylosing spondylitis and diffuse idiopathic skeletal hyperostosis were included in this study. RevMan 5.4 and Stata 14.2 software programs were utilized for assessing literature quality and conducting data analysis.

A total of 20 trials involving 1116 patients with ASDs were included, encompassing 4 posterior approaches. Network meta-analysis revealed that Percutaneous puncture demonstrated favorable outcomes in terms of surgical duration, intraoperative blood loss, postoperative bed rest time, and hospital stay. Both percutaneous internal fixation and 3D assisted fixation exhibited alternating advantages in postoperative functional recovery.

Based on the available evidence, it is evident that percutaneous instrumentation offers clear advantages over other forms of instrumentation. However, the quality of some studies is suboptimal and further high-quality randomized controlled trials are necessary to provide additional verification.

Rheumatic diseases are chronic immune-mediated disorders affecting multiple organ systems and significantly impairing patients' quality of life. Current treatments primarily provide symptomatic relief without offering a cure. Mesenchymal stem cells (MSCs) have emerged as a promising therapeutic option due to their ability to differentiate into various cell types and their immunomodulatory, anti-inflammatory, and regenerative properties. This review aims to summarize the clinical progress of MSC therapy in rheumatic diseases, highlight key findings from preclinical and clinical studies, and discuss challenges and future directions.

A comprehensive review of preclinical and clinical studies on MSC therapy in rheumatic diseases, including systemic lupus erythematosus, rheumatoid arthritis, ankylosing spondylitis, osteoarthritis, osteoporosis, Sjögren's syndrome, Crohn's disease, fibromyalgia, systemic sclerosis, dermatomyositis, and polymyositis, was conducted. Emerging strategies to enhance MSC efficacy and overcome current limitations were also analyzed.

Evidence from preclinical and clinical studies suggests that MSC therapy can reduce inflammation, modulate immune responses, and promote tissue repair in various rheumatic diseases. Clinical trials have demonstrated potential benefits, including symptom relief and disease progression delay. However, challenges such as variability in treatment response, optimal cell source and dosing, long-term safety concerns, and regulatory hurdles remain significant barriers to clinical translation. Standardized protocols and further research are required to optimize MSC application.

MSC therapy holds promise for managing rheumatic diseases, offering potential disease-modifying effects beyond conventional treatments. However, large-scale, well-controlled clinical trials are essential to establish efficacy, safety, and long-term therapeutic potential. Addressing current limitations through optimized treatment protocols and regulatory frameworks will be key to its successful integration into clinical practice.

Spondyloarthritis (SpA) is a group of chronic inflammatory rheumatic diseases that can present with diverse extra-articular manifestations. However, bladder involvement as the primary clinical presentation has not been previously reported.

We present a case report of a 55-year-old male with a 20-year history of recurrent left lower abdominal pain and lower urinary tract symptoms (LUTS). Despite multiple treatments for presumed chronic prostatitis and cystitis, symptoms persisted. Imaging revealed bladder wall alterations and inflammatory changes in bilateral sacroiliac joints. Laboratory tests showed positive HLA-B27 expression. Histopathological examination of bladder tissue demonstrated chronic inflammation with eosinophilic infiltration and vasculitis. These findings led to a diagnosis of SpA, despite the absence of typical musculoskeletal symptoms. Treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) and tumor necrosis factor (TNF) inhibitors resulted in complete resolution of urological symptoms and normalization of bladder morphology. After one month of continuous management, the patient experienced significant relief from left lower abdominal pain (NRS 2-3) and LUTS. The patient reported complete alleviation of pain (NRS 0) and LUTS at the three-month follow-up. No recurrence was observed during a 1-year follow-up period.

This case highlights the potential for SpA to manifest primarily with urological symptoms, emphasizing the need for clinicians to consider systemic inflammatory conditions in cases of refractory LUTS. The successful diagnosis and management underscore the importance of interdisciplinary collaboration between urology and rheumatology.

Ankylosing spondylitis (AS) is a sustained inflammatory pathology that manifests as increasing rigidity and a continuous decline in spinal flexibility, leading to increasing lumbar pain during rest.

This study primarily aimed to evaluate depression assessments using the Beck Depression Inventory (BDI) and delineate depressive symptomatology in patients diagnosed with AS compared to those without this condition.

A comparative study was conducted in Medical Centers in Málaga, Spain.

A cohort of 102 participants, with a mean age of 46,80 ± 10,54 years, was divided into two sets: 51 individuals diagnosed with AS (cases) and another 51 without AS (controls), each harmonized across variables such as body mass index, age, and sex. Demographic variables were systematically gathered from each participant, and the BDI responses were accurately recorded and subsequently analyzed for comparison.

Of the total sample, the sex distribution was 29.4% male and 70.6% female. BDI scores were higher for the AS group (19.25 ± 15.5) than for the control group (5.33 ± 7). Notably, there were clear statistical differences (P < 0.01) in the BDI categories, with elevated levels observed in participants with AS.

Individuals with AS experienced higher levels of depression than those without AS. Furthermore, there were sex differences within the case group, with a higher percentage of women than men at any level of depression. Notably, there was a moderate inverse correlation between the number of years since diagnosis and depression level.

To investigate the clinical response at week 52 in patients with AS who received secukinumab 300 vs 150 mg after inadequate response to 150 mg at week 16.

ASLeap (NCT03350815) was a randomized, double-blind, parallel-group, multicentre, phase 4 trial. After 16 weeks of open-label secukinumab 150 mg (Treatment Period 1), patients who did not achieve inactive disease [AS Disease Activity Score (ASDAS) <1.3] at both week 12 and 16 were considered to have an inadequate response and were randomized 1:1 to receive secukinumab 300 or 150 mg every 4 weeks until week 52 (Treatment Period 2). The primary efficacy variable was achievement of ASDAS <1.3 at week 52 using week 16 as baseline. Safety was evaluated by the incidence of treatment-emergent adverse events (TEAEs) through week 52.

Of 322 patients treated with secukinumab in Treatment Period 1, 207 (64.3%) had inadequate response. Similar proportions of patients with inadequate response randomized to secukinumab 300 mg (n = 101) and 150 mg (n = 105) in Treatment Period 2 completed the study (83.8% and 84.3%, respectively). At week 52, 8.8% and 6.7% of patients receiving secukinumab 300 and 150 mg, respectively, achieved ASDAS <1.3. The incidence of TEAEs was similar in both groups through week 52. No new safety signals were observed.

Patients with AS who did not achieve ASDAS <1.3 after receiving secukinumab 150 mg for 16 weeks experienced similar clinical response and safety through week 52 regardless of dose escalation.

ClinicalTrials.gov, http://clinicaltrials.gov, NCT03350815.

This study explored the proteomic landscape of inflammatory protein dysregulation in ankylosing spondylitis (AS), a chronic inflammatory disorder primarily affecting the axial skeleton and strongly associated with the HLA-B27 allele, particularly the HLA-B2705 and HLA-B2704 subtypes prevalent in Chinese populations. Blood samples from HLA-B27-positive AS patients and normal controls (NC) were analyzed using the Olink Target 96 inflammation panel to profile 92 inflammatory proteins. HLA-B27 subtyping was performed via PCR-SSP. To identify key proteins and stratify AS subtypes, we employed machine learning classifiers, including LightGBM models coupled with SHAP value interpretation, alongside traditional statistical analyses. The proteomic analysis revealed significant dysregulation of pro-inflammatory cytokines, such as IL-6 and IL-17A, in AS patients compared to NC, with CXCL9 and NRTN identified as potential biomarkers associated with disease activity. The combination of LightGBM classifiers and traditional statistical methods demonstrated high accuracy in distinguishing AS from NC and effectively stratifying subtypes. These findings provide valuable insights into the inflammatory mechanisms underlying AS pathogenesis and highlight potential biomarkers and therapeutic targets for improving diagnosis and treatment strategies. Future studies with larger and more diverse cohorts, as well as longitudinal designs, are warranted to validate these biomarkers and elucidate their dynamic changes during disease progression.

Aim of this study is to compare the thiol/disulfide variables before treatment, at the 3rd and 6th months of biologic treatment in patients with axSpA.

Consecutive patients with axial spondyloarthritis to whom biologic treatment was initiated in our clinic were enrolled upon consent. Demographics, clinical characteristics, laboratory parameters and treatment agents were collected. Disease activity scores and thiol-disulfide balance parameters were recorded at baseline and 3rd, 6th months of treatment. Statistical analyses were performed in all patients and in subgroups of ankylosing spondylitis and non-radiographic axial spondyloarthritis patients.

In all patients, total thiol levels were significantly increased at 6th month in comparison to baseline values (470.5 ± 74.7 vs 491.9 ± 69.6, p = 0.047). Native thiol levels were increased at 6th month close to significance (438.9 ± 70.4 vs 458.8 ± 63.7, p = 0.060). Moderately strong negative correlations were observed between native thiol levels and disease activity parameters (BASDAI: p = 0,019; ASDAS-CRP: p = 0,035; ASDAS-ESR: p = 0,030), and between total thiol levels and disease activity parameters (BASDAI: p = 0,031; ASDAS-CRP: p = 0,020; ASDAS-ESR: p = 0,026) at 6th month evaluation.

Our results demonstrated oxidative stress reducing effect of biologics in axSpA patients parallel to suppression of disease activity at 6th month of the treatment.

With the intensification of aging issues, inflammatory orthopedic diseases almost occur in the majority of elderly people, which is becoming increasingly severe. Photoacoustic imaging (PAI) is a non-invasive visualization technique for a clear diagnosis of the inflammation areas through detecting acoustic signals generated by the laser irradiation. The combination of "light input" and "acoustic output" provides unprecedented scalability as well as high penetration depth and resolution. This new imaging technology can also present more anatomical information and feedback status of inflammatory activity for the orthopedic diseases. Especially in inflammation imaging, this technology can effectively supplement current clinical imaging methods in diagnosis, staging, and monitoring of pathophysiological processes. With the rapid development of these new technologies, the goals of precise diagnosis, predictive regulation, and ultimately personalized treatment strategies are becoming increasingly realistic. Herein, this article introduces various orthopedic inflammations and related imaging technology applications. It covers the types of PA nanoprobes and their research progress in orthopedic inflammation, as well as the potential applications of PAI in various aspects. The review also discusses the recent researches and emerging translational applications of PAI in orthopedic inflammation, as well as the prospects and future development challenges of clinical transformation.

The objective of this study was to compare health-related quality of life (HRQoL) and work productivity in axial SpA (axSpA) and non-axSpA patients with chronic back pain of <2 years.

Baseline and 2-year data for patients included in the SPondyloArthritis Caught Early cohort were analysed. HRQoL was assessed by the physical (PCS) and mental component summary (MCS) scores of the 36-Item Short-Form Health Survey, and presenteeism, absenteeism, work productivity loss (WPL) and activity impairment (AI) by the Work Productivity and Activity Impairment questionnaire. Linear or zero-inflated negative binomial regression was conducted to compare 2-year outcomes between groups (axSpA and non-axSpA), adjusting for the baseline value, sex, age and use of NSAIDs.

There were 265 axSpA and 108 non-axSpA patients: males 52% vs 26%, mean age 29 vs 31 years, respectively. At baseline, non-axSpA patients showed worse PCS (mean 28.6 axSpA vs 26.6 non-axSpA), presenteeism (31.1% vs 37.3%), absenteeism (8.2% vs 10.3%), WPL (34.7% vs 44.1%) and AI (39.6% vs 48.5%). MCS was not impaired in either group. After 2 years, PCS, presenteeism, WPL and AI significantly improved in both groups; absenteeism only improved in axSpA. In multivariable analysis, axSpA (vs non-axSpA) was associated with 22% less WPL [incidence rate ratio (95% CI): 0.78 (0.62; 0.98)] and 18% less AI [0.82 (0.69; 0.97)].

HRQoL and work productivity are more impaired in non-axSpA (vs axSpA) at baseline and also after 2 years. Although most outcomes improve in both groups, axSpA is associated with larger reductions in WPL and AI.

Ankylosing spondylitis (AS) is recognized as a long-term inflammatory disorder that leads to inflammation in the spine and joints, alongside abnormal bone growth. In previous studies, we reported that mesenchymal stem cells (MSCs) derived from individuals with AS demonstrated a remarkable inhibition in the formation of osteoclasts compared to those obtained from healthy donors. The mechanism through which MSCs from AS patients achieve this inhibition remains unclear.

To investigate the potential underlying mechanism by which MSCs from individuals with ankylosing spondylitis (AS-MSCs) inhibit osteoclastogenesis.

We analysed fat mass and obesity-associated (FTO) protein levels in AS-MSCs and MSCs from healthy donors and investigated the effects and mechanism by which FTO in MSCs inhibits osteoclastogenesis by coculturing and measuring the levels of tartrate-resistant acid phosphatase, nuclear factor of activated T cells 1 and cathepsin K.

We found that FTO, an enzyme responsible for removing methyl groups from RNA, was more abundantly expressed in MSCs from AS patients than in those from healthy donors. Reducing FTO levels was shown to diminish the capacity of MSCs to inhibit osteoclast development. Further experimental results revealed that FTO affects the stability of the long non-coding RNA activated by DNA damage (NORAD) by altering its N6-methyladenosine methylation status. Deactivating NORAD in MSCs significantly increased osteoclast formation by affecting miR-4284, which could regulate the MSC-mediated inhibition of osteoclastogenesis reported in our previous research.

This study revealed elevated FTO levels in AS-MSCs and found that FTO regulated the ability of AS-MSCs to inhibit osteoclast formation through the long noncoding RNA NORAD/miR-4284 axis.

To evaluate the potential of large language models (LLMs) in health education for patients with ankylosing spondylitis (AS)/spondyloarthritis (SpA), focusing on the accuracy of information transmission, patient acceptance and performance differences between different models.

Cross-sectional, single-blind study.

Multiple centres in China.

182 volunteers, including 4 rheumatologists and 178 patients with AS/SpA.

Scientificity, precision and accessibility of the content of the answers provided by LLMs; patient acceptance of the answers.

LLMs performed well in terms of scientificity, precision and accessibility, with ChatGPT-4o and Kimi models outperforming traditional guidelines. Most patients with AS/SpA showed a higher level of understanding and acceptance of the responses from LLMs.

LLMs have significant potential in medical knowledge transmission and patient education, making them promising tools for future medical practice.

To investigate the expression of Tim-3 on neutrophils in ankylosing spondylitis (AS) patients and its correlation with disease activity, severity, and inflammatory markers.

Sixty-two AS patients from Guangdong Second Provincial General Hospital and 38 healthy controls (HC) were enrolled. Clinical data, physical exams, and laboratory measurements were recorded. Flow cytometry measured Tim-3 and PD-1 expression on neutrophils, real-time PCR quantified mRNA levels and protein expression of Tim-3 was determined by Western blot. We analyzed the correlation between Tim-3 mean fluorescence intensity (MFI) on neutrophils, inflammatory markers, and AS disease activity and severity.

Tim-3 expression on neutrophils was higher in AS patients than in HC, showing a positive correlation with erythrocyte sedimentation rate (ESR), c-reactive protein (CRP), and Ankylosing Spondylitis Disease Activity Score (ASDAS). Active AS patients (ASDAS ≥ 1.3) had increased Tim-3 MFI compared to inactive ones (ASDAS < 1.3). Regular treatment with non-steroidal anti-inflammatory drugs (NSAIDs), biological disease-modifying anti-rheumatic drugs (bDMARDs), and conventional synthetic disease-modifying anti-rheumatic drugs (csDMARDs) over a month significantly reduced Tim-3 MFI in AS patients.

Elevated Tim-3 expression on neutrophils correlates with increased inflammatory markers and AS activity. Treatment lowered Tim-3 MFI, suggesting its potential as an indicator for assessing AS disease activity and severity and as a feedback mechanism to reduce tissue damage from inflammation.

Multiple studies have shown a substantial association between obstructive sleep apnea (OSA) and rheumatic disease. However, traditional studies are susceptible to confounding factors or reverse causal relationships, and the exact causal relationship still needs to be clearly defined. This study aims to use a bidirectional two-sample Mendelian randomization (MR) analysis to investigate the causal association between OSA and rheumatoid immune diseases.

We conducted a two-sample bidirectional MR analysis by using large-scale genome-wide association studies (GWAS) summary statistics to investigate whether there is a causal relationship between OSA and rheumatic disease. Inverse variance weighted (IVW) was used as the primary analysis approach, supplemented by MR-Egger and Weighted median methods. Sensitivity analyses were conducted to ensure the robustness of the results.

The MR predicted ankylosing spondylitis (AS) was associated with risk of OSA (IVW: OR = 1.0239, 95% CI = 1.0086 to 1.0394, P = 0.0021; MR-Egger: OR = 1.0374, 95% CI = 1.0089 to 1.0668, P = 0.0326; weighted median: OR = 1.0287, 95% CI = 1.0109 to 1.0467, P = 0.0014). However, no bidirectional causal association was found between other rheumatic disease and OSA. The sensitivity analysis confirmed the robustness of the results.

Our analysis suggests a potential causal relationship between AS and OSA. There was no direct causal relationship between OSA and other rheumatic disease. We need more experimental research on specific pathological and physiological mechanisms in the future.

To investigate the long-term course of aortic regurgitation (AR) and the width of the proximal ascending aorta (PAA) in patients with ankylosing spondylitis (AS).

This is a follow-up cohort study of patients with AS examined with echocardiography at inclusion (2009 to 2011). Out of the initial 187, a subgroup of 52 patients (54% men, mean age 62 years) was selected for follow-up based on presence/absence of AR at baseline; 26 with AR (18 mild, 7 moderate, 1 severe) and 26 age/sex-matched without AR. These patients were re-examined with echocardiography in 2014 by an independent observer. Severity of AR and PAA diameter were assessed. Related samples Wilcoxon signed rank and Mann-Whitney U tests were used to analyze the change (Δ) in PAA diameter.

Regarding the 26 patients with AR at baseline, two had an aggravated grade, 16 an unchanged grade, and eight a less severe AR versus baseline. Two of the 26 patients with no AR at baseline had a mild grade of AR at follow-up. The mean (SD) ΔPAA diameter was 0 (3) mm, and no statistically significant ΔPAA diameter was found overall or in analyses stratified by sex and baseline presence of AR.

Most patients with AS had an unchanged grade of AR and PAA diameter at follow-up 3 to 5 years after the initial echocardiography. These findings suggest that the average progress of AR in patients with AS is slow and that progression of PAA dilatation seems rare. Key points • Aortic regurgitation (AR) is not uncommon in patients with ankylosing spondylitis (AS) and caused by aortic root dilatation and/or cusp fibrosis/retraction, but little is known about its course. • According to this repeated echocardiography study in median 4.3 years after the baseline evaluation, the majority of patients had no progress of AR or increase in the proximal ascending aorta diameter. • AR in AS is rarely rapidly progressive.

The Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and Ankylosing Spondylitis Disease Activity Score with C-reactive protein (ASDAS-CRP) are commonly used to measure disease activity in patients with AS.

This study was conducted to determine the power of hematological indices to serve as disease activity markers in AS patients treated with tumor necrosis factor (TNF) inhibitors.

A total of 222 patients with AS were recruited and classified into active disease (BASDAI ≥ 4, n = 158) and remission (BASDAI < 4, n = 64) groups. The active group was treated with TNF inhibitors for 3 months. Composite indices such as BASDAI and ASDAS-CRP were measured to assess disease activity. Hematological indices as alternative disease activity markers including neutrophil-to-lymphocyte ratio (NLR), neutrophil-to-hemoglobin and lymphocyte (NHL) score, systemic immune-inflammation index (SII), and platelet-to-lymphocyte ratio (PLR) were assessed.

Patients with active AS showed higher NLR, NHL score, SII, and PLR than those in remission. ASDAS-CRP and BASDAI values at baseline were significantly associated with all hematological indices, including NLR, NHL score, SII, and PLR. Similar to the improvement of BASDAI and ASDAS-CRP scores following TNF inhibitors treatment, NLR, NHL score, SII, and PLR markedly decreased after treatment with TNF inhibitors for 3 months (p < 0.001 for all, respectively). All hematological indices closely predicted major improvement (∆ ≥ 2.0 of ASDAS-CRP) following treatment with TNF inhibitors.

This study indicated that four hematological indices may be useful markers of disease activity and predictors of treatment response to TNF inhibitors in patients with AS. Further studies in larger populations are needed to validate the usefulness of hematological indices as measures of disease activity in patients with AS.

 Existing evidence is insufficient to support that acupuncture is effective in treating ankylosing spondylitis (AS) due to the constraints of acupuncture site and manipulation, and relatively straightforward study treatments and indicators.

 By incorporating high-quality original literature, this study aims to evaluate the effectiveness of acupuncture for AS and to demonstrate acupuncture as a non-drug supplementary and alternative means for treating AS.

 We searched seven databases from their inception to March 31, 2023. Only randomized controlled trials (RCTs) with PEDro score ≥ 6 that compared traditional acupuncture alone or in combination with non-acupuncture therapy on diagnostic AS were considered. The PEDro, ROB2, and STATA tools were used for quality evaluation and statistical analysis.

 A total of 21 RCTs covering 1884 patients were included. Meta-analysis showed that acupuncture had positive effects on Western medicine effective rate (RR = 1.223, 95%CI: 1.150, 1.301, P < 0.001), traditional Chinese medicine effective rate (RR = 1.175, 95%CI: 1.111, 1.243, P < 0.001), pain score (visual analogue scale, SMD = -0.666, 95%CI: -0.801, -0.531, P < 0.001), spinal function including bath ankylosing spondylitis function index score (SMD = -0.827, 95%CI: -0.945, -0.708, P < 0.001), bath ankylosing spondylitis disease activity index score (SMD = -1.069, 95%CI: -1.190, -0.949, P < 0.001), and bath ankylosing spondylitis metrology index score (SMD = -0.699, 95%CI: -0.887, -0.511, P < 0.001), ankylosing spondylitis quality of life score(SMD = -0.619, 95%CI: -0.917, -0.322, P < 0.001), C-reactive protein levels (SMD = -0.980, 95%CI: -1.092, -0.868, P < 0.001) and erythrocyte sedimentation rate value (SMD = -0.701, 95%CI: -0.810, -0.591, P < 0.001).

 Though with a high risk of bias, the high-quality studies indicate that acupuncture is a beneficial complementary and alternative therapy for AS patients, as it can reduce pain intensity and improve effective rate, spinal function, and anti-inflammatory response.

Baduanjin qigong exercises have previously been reported to improve Ankylosing Spondylitis (AS) symptoms. The aim of this study was to examine the effectiveness of 12-week Baduanjin qigong exercises in patients with AS.

Fifty-nine patients with AS aged 18-64 were included in the study. The participants were divided into two groups. The intervention group performed Baduanjin qigong online exercise program, control group received home exercises for 45 min twice a week for 12 weeks. Before and after the 12-week exercise program, patients were evaluated using the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI)-Functional Index (BASFI)-Metrology Index (BASMI), chest expansion measurement, Pittsburgh Sleep Quality Index (PSQI), Fatigue Severity Scale (FSS), Hospital Anxiety and Depression Scale (HADS), and Ankylosing Spondylitis Quality of Life Questionnaire (ASQoL).

When the groups were compared after the intervention, there was a significant difference in favor of the intervention group in the BASMI (p: 0.00-0.04), FSS (p:0.01), and chest expansion (p:0.04). Also, the delta values of the groups were compared; the intervention group was found to be superior in terms of PSQI (p:0.01), BASFI (p:0.00), and BASMI (p:0.04).

Baduanjin qigong should be added to rehabilitation programs as a complementary method to improve fatigue levels, chest expansion, flexibility, functionality, and quality of life in patients with AS.

Surgery to correct the cervicothoracic kyphotic deformity in ankylosing spondylitis (AS) can be associated with serious neurovascular risks. According to the literature, there are no clinical reports documenting the use of vertebral column decancellation (VCD) in the treatment of cervicothoracic kyphotic deformity in patients with AS. The purpose of the present study was to retrospectively analyze and evaluate the effect of VCD on cervicothoracic kyphotic deformity in patients with AS.

Records of eight patients with cervicothoracic kyphotic deformity who underwent VCD at C7 in our institution were retrospectively reviewed. The mean duration of clinical follow-up after surgery was 19 months. The cervical lordosis (CL) and C2-C7 sagittal vertical axis (SVA) were meticulously measured on full-length spine radiographs. The chin-brow vertical angle (CBVA) was measured on clinical photographs. Outcome measures utilized included the Neck Disability Index (NDI), the Japanese Orthopaedic Association (JOA) Score, and a Visual Analog Scale (VAS) for neck pain. The data analysis was performed using SPSS version 26.0 for Windows. For paired data adhering to a normal distribution, we utilized paired sample t-tests to analyze preoperative and postoperative imaging parameters. Statistical significance was established at a p value threshold of < 0.01.

All eight patients successfully completed the surgery. With an average VCD osteotomy angle of 47.6° ± 8.1° (±SD), the mean preoperative CBVA was 81.1° ± 17.6° (±SD), while the immediate postoperative value was 19.9° ± 5.7° (±SD). The overall average correction was 61.2° ± 18.9°. The mean preoperative cervical sagittal imbalance was 93.4 ± 27.3 mm (±SD), while the immediate postoperative value was 40.2 ± 18.9 mm (±SD). The overall average correction was 53.2 ± 28.1 mm. None of the eight patients experienced intraoperative complications, including nerve or vascular injury, cerebrospinal fluid leakage, or any other related complications. In the cohort of eight patients, the mean values for estimated blood loss, surgical time, and hospital stay were 1313 mL, 248 min, and 18 days, respectively. In comparison to preoperative scores, statistically significant improvement was noted in all patients in the postoperative period with regard to NDI, JOA, and VAS (p < 0.01, using a paired t-test).

The VCD procedure proves to be a dependable and efficient approach for addressing cervicothoracic kyphotic deformities. It achieves remarkable corrections in cervical kyphosis and CBVA.

Chinese Clinical Trial Registry: 2400090375.

To evaluate erosive pathological lesions on a skeleton from medieval Transylvania.

A skeleton from a Székely archaeological site in Transylvania was examined and radiocarbon dated to Cal 1300 CE - 1415 CE.

The skeletal remains were examined macroscopically and with radiographic imaging. A differential diagnosis was conducted following established protocols.

The individual was estimated to be a probable adult female. Periarticular erosive lesions involving multiple synovial joints, particularly on the small joints of the hands and feet, were observed.

A differential diagnosis identifies lesions characteristic of rheumatoid arthritis dating prior to the mid-15th century.

The significance of this diagnosis is great since researchers debate the antiquity and spread of rheumatoid arthritis. Some researchers hypothesize that RA originated in the Americas and spread to Europe after the mid-15th century. However, this study asserts that RA existed in Europe prior to European colonization of the Americas.

Only 30-40 % of the skeletal material was excavated, potentially impacting the differential diagnosis.

This case encourages researchers to explore the presence of RA in other medieval groups within and beyond Transylvania as a means to reconstruct the antiquity and geographical distribution of the condition.

Inflammatory arthritis is recognized to increase cardiovascular disease risk, but its association with degenerative aortic stenosis is not well understood.

This prospective cohort study used participants from the UK Biobank, focusing on 4 major types of inflammatory arthritis, including rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, and gout. The primary outcome was the incidence of degenerative aortic stenosis. The primary analysis used Cox proportional hazards models to evaluate the association between inflammatory arthritis and the long-term risk of degenerative aortic stenosis, as well as to explore potential effect modifiers. Genetic risk was evaluated using polygenic risk scores and self-reported family history of cardiovascular diseases.

The study included 497 567 participants, with 271 129 women (54.5%) and 468 015 White individuals (94.1%). The median age was 58 years. Over a median follow-up of 12.58 years, 4571 cases (0.9%) of degenerative aortic stenosis were identified. Compared with the control group, rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, and gout were associated with increased risks of degenerative aortic stenosis by 54% (hazard ratio [HR], 1.54 [95% CI, 1.28-1.85]), 72% (HR, 1.72 [95% CI, 1.19-2.50]), 176% (HR, 2.76 [95% CI, 1.43-5.32]), and 36% (HR, 1.36 [95% CI, 1.20-1.54]), respectively. These associations were independent of genetic risk (P for interaction>0.05). Additionally, we identified significant interactions between sex (P for interaction=0.036), age (P for interaction<0.001), and socioeconomic status (P for interaction=0.014) with rheumatoid arthritis, ankylosing spondylitis, and gout on the incidence of degenerative aortic stenosis, respectively.

Inflammatory arthritis is significantly associated with an increased long-term risk of degenerative aortic stenosis, underscoring the need for enhanced risk assessment for degenerative aortic stenosis in these populations.

Cervical fractures in patients with ankylosing spondylitis (AS) are complex and carry significant morbidity and mortality due to the progressive rigidity and brittle bone characteristic of the disease. This meta-analysis highlights the management techniques and outcomes of cervical fractures in patients with ankylosing spondylitis over the past 10 years. A systematic review was conducted using databases such as PubMed, Cochrane Library, Scopus, and Web of Science, covering studies published between 2014 and 2024. Outcomes assessed included neurological outcomes, complications, mortality, reoperations, and length of hospital stay. The Joanna Briggs Institute (JBI) checklist was used to evaluate bias. Sixty-six (66) articles with 1972 patients were analyzed. The mean age of patients was 57.02 years, with a male-to-female ratio of 9.8:1, p < 0.001. Most fractures occurred at C6- C7 (36.66%) and C5- C6 (27.74%). Posterior fusion was the most commonly performed surgery (40.0%), followed by combined anterior-posterior fusion (28.3%), and anterior fusion (22.9%). Nonsurgical management was reported in 8.8% with a failure rate of 1.2%. The reoperation rate was highest in the anterior fusion group (11.1%), and lowest in the combined fusion group (1.7%). Good neurological outcomes were observed in 63.4% of cases, while poor outcomes were noted in 33.7%. The overall mortality rate was 2.9%. Cervical fractures in ankylosing spondylitis present significant challenges due to spinal rigidity, altered biomechanics, and high complication risks. Posterior fusion remains the most utilized approach, while combined anterior-posterior fusion demonstrates lower reoperation rates. Conservative management, including external immobilization, is viable for carefully selected stable fractures. Prospective studies with standardized outcomes are essential to optimize treatment strategies and enhance patient outcomes.

Associations between ulcerative colitis (UC) and ankylosing spondylitis (AS) have been reported in multiple studies, but the common etiologies of UC and AS remain unknown. Thus, in the current study, we aimed to investigate the shared genes and relevant mechanisms in UC and AS.

Using datasets for UC (GSE113079) and AS (GSE1797879), we initially identified differentially expressed genes (DEGs) through differential expression analysis. The DEGs from both datasets were intersected to identify common DEGs, relevant to both UC and AS, which were used in receiver operating characteristic (ROC) curve analysis to confirm key genes in the shared pathway. Gene set enrichment analysis (GSEA) was used to obtain information on key gene pathways and interactions with UC or AS-related diseases, followed by immune infiltration analysis. Finally, peripheral blood samples of AS and UC were used to verify the mRNA expression of the eight key genes using reverse transcription-polymerase chain reaction (RT-PCR).

Our results revealed that GMFG, GNG11, CLEC4D, CMTM2, VAMP5, S100A8, S100A12 and DGKQ are potential diagnostic biomarkers of AS and UC. Rimegepant, eptinezumab, methotrexate, atogepant, and ubrogepant were identified as potential drugs for S100A12 and S100A8 in patients with UC and AS. GSEA showed that these key genes were associated with antigen processing and presentation, natural killer cell mediated cytotoxicity and the T cell receptor signaling pathway in AS and UC, and were significantly associated with immune cells in various immune-related pathways. Subsequent functional experiments revealed significant increases in the mRNA expressions of S100A12 and VAMP5 in patients with AS and UC. Additionally, CLEC4D mRNA expression was notably higher in patients with UC than in healthy controls.

Key genes and shared pathways were identified in UC and AS, which may improve understanding of their relationship and guide diagnosis and treatment strategies.

Background: Ankylosing spondylitis (AS) is a chronic inflammatory disorder with a significant genetic predisposition. Genome-wide association studies (GWAS) have identified immune-related loci, including the G Protein-Coupled Receptor 35 (GPR35) gene, as potential contributors to AS pathogenesis. This study aimed to evaluate the association between the rs4676410 polymorphism in the GPR35 gene and both AS susceptibility and disease activity in a Turkish population. Methods: This case-control study included 200 participants (100 AS patients and 100 healthy controls). DNA was isolated from blood samples, and the rs4676410 polymorphism was analyzed using real-time polymerase chain reaction (PCR). Disease activity in AS patients was assessed using the Bath AS Functional Index (BASFI), Bath AS Disease Activity Index (BASDAI), and disease activity scores including C-reactive protein (ASDAS-CRP) scores. Statistical analyses were conducted using IBM SPSS 26. Results: The rs4676410 polymorphism was significantly associated with AS susceptibility. The AA genotype and A allele were more prevalent in AS patients, indicating an increased risk of developing AS. Among disease activity measures, ASDAS-CRP scores were significantly higher in patients with the AA genotype (p = 0.043), while no significant differences were observed for BASFI and BASDAI scores across genotypes. Conclusion: The findings suggest that the rs4676410 polymorphism in the GPR35 gene is associated with AS susceptibility and may influence disease activity through elevated inflammatory responses. These results highlight the potential of the AA genotype and A allele as genetic markers for AS and underscore the importance of integrating genetic insights into personalized treatment approaches.

Many studies on osteoblasts have suggested that Wnt5a plays a crucial role in excessive osteoblast activity, which is responsible for ectopic new bone formation, but research on osteoclasts in ankylosing spondylitis (AS) remains relatively limited. This study aimed to explore whether Wnt5a influences osteoclastmediated bone resorption in curdlan-injected SKG mice, a model that mimics AS. Compared to the Vehicle group, the Wnt5a treatment group exhibited statistically higher clinical arthritis scores and increased hindpaw thickness values. Micro- computed tomography (microCT) analysis of hindpaws revealed a significant increase in inflamed and ectopic bone density in the Wnt5a-treated group compared to the Vehicle group. Histological examination also showed pronounced inflammation and structural bone damage in the bone marrow of ankles in the Wnt5a-treated group. Intriguingly, microCT analysis of the femur revealed that trabecular bone loss was markedly observed in the Wnt5a-treated group. Both the number of TRAP-positive osteoclasts and their activity were statistically greater in the Wnt5a-treated group compared to the Vehicle group. Serum markers of bone resorption, but not bone formation, were also significantly elevated in the Wnt5a-treated group. Notably, promotion of osteoclast differentiation by Wnt5a was inhibited following treatment with anti-Wnt5a. These findings suggest that targeting Wnt5a could be a promising strategy for mitigating pathological bone features in AS by modulating osteoclast activity. [BMB Reports 2025; 58(2): 75-81].

Many studies on osteoblasts have suggested that Wnt5a plays a crucial role in excessive osteoblast activity, which is responsible for ectopic new bone formation, but research on osteoclasts in ankylosing spondylitis (AS) remains relatively limited. This study aimed to explore whether Wnt5a influences osteoclastmediated bone resorption in curdlan-injected SKG mice, a model that mimics AS. Compared to the Vehicle group, the Wnt5a treatment group exhibited statistically higher clinical arthritis scores and increased hindpaw thickness values. Micro- computed tomography (microCT) analysis of hindpaws revealed a significant increase in inflamed and ectopic bone density in the Wnt5a-treated group compared to the Vehicle group. Histological examination also showed pronounced inflammation and structural bone damage in the bone marrow of ankles in the Wnt5a-treated group. Intriguingly, microCT analysis of the femur revealed that trabecular bone loss was markedly observed in the Wnt5a-treated group. Both the number of TRAP-positive osteoclasts and their activity were statistically greater in the Wnt5a-treated group compared to the Vehicle group. Serum markers of bone resorption, but not bone formation, were also significantly elevated in the Wnt5a-treated group. Notably, promotion of osteoclast differentiation by Wnt5a was inhibited following treatment with anti-Wnt5a. These findings suggest that targeting Wnt5a could be a promising strategy for mitigating pathological bone features in AS by modulating osteoclast activity. [BMB Reports 2025; 58(2): 75-81].

Transosseous lacerations represent a particular type of discoligamentous injury of the cervical spine and occur in ankylosing diseases of the spine, with ankylosing spondylitis and diffuse idiopathic skeletal hyperostosis (DISH) being the primary entities. The altered biomechanics of the spine due to the underlying disease pose special challenges in the diagnostics and treatment. Even low-energy trauma can cause severe injuries of the cervical spine, which are often difficult to accurately diagnose due to the difficult assessability of the conventional projection radiography used in the primary diagnostics. In addition to a correct diagnosis a differentiated treatment concept is crucial as treatment courses can be complicated by pre-existing comorbidities, which are present in the majority of cases. Due to a high rate of secondary neurological deficits without adequate stabilization, surgical stabilization is generally recommended. Unlike the treatment of "classical" discoligamentous injuries in the mobile cervical spine, long segment dorsal instrumented spondylodesis is the standard of care for these cases, whereby ventral stabilization is also of value, either as a stand-alone or possibly additive procedure. The intraoperative site, which deviates from that of a normal patient, can present an additional challenge.

The potential impact of ankylosing spondylitis (AS) on cancer risk remains unclear. This study seeks to investigate the relationship between AS and different types of cancers.

A literature search on PubMed, EMBASE and Cochrane Library up to 10 July 2023 was conducted. Two investigators selected eligible studies and extracted relevant data. The study used the random-effects model to explore the causality between AS and cancer, utilizing relative risk (RR) as a measure for the study.