Pub Date : 2026-03-01Epub Date: 2025-12-16DOI: 10.1016/j.jbspin.2025.106017
Paul Gervaise , Simon Glatigny , Maxime Breban , Félicie Costantino
{"title":"Dual JAK and IL-23 blockade: A mechanistically supported strategy in refractory psoriatic arthritis. A case report.","authors":"Paul Gervaise , Simon Glatigny , Maxime Breban , Félicie Costantino","doi":"10.1016/j.jbspin.2025.106017","DOIUrl":"10.1016/j.jbspin.2025.106017","url":null,"abstract":"","PeriodicalId":54902,"journal":{"name":"Joint Bone Spine","volume":"93 2","pages":"Article 106017"},"PeriodicalIF":4.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145783520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2025-11-01DOI: 10.1016/j.jbspin.2025.105998
Mustafa Kemal Demir , Onder Ertem , Deniz Konya
{"title":"Hidden nidus on MRI, revealed on CT: Lumbar lamina osteoid osteoma","authors":"Mustafa Kemal Demir , Onder Ertem , Deniz Konya","doi":"10.1016/j.jbspin.2025.105998","DOIUrl":"10.1016/j.jbspin.2025.105998","url":null,"abstract":"","PeriodicalId":54902,"journal":{"name":"Joint Bone Spine","volume":"93 2","pages":"Article 105998"},"PeriodicalIF":4.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145440154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The skeleton is able to secrete hormones and mediate endocrine functions. Particularly, the fibroblast growth factor 23 (FGF23) has received considerable attention for its unique phosphaturic properties, raising the bone to the status of an essential endocrine regulator. Excess in circulating levels of FGF23, not so surprisingly, then associated to mineral imbalance, in hereditary/acquired mineral and skeletal disorders. A key player, FGF23 excess precedes mineral and skeletal disturbances. However, unexpected effects have been described in the recent years. Various demonstrations have been made that FGF23 is directly regulated by non-mineral stress, including: inflammation, iron deficiency, and glycolysis. In turn, an emerging body of research shows association and causality between FGF23 and the cardiovascular system at large, from the iron metabolism to erythropoiesis, and to the cardiac muscle. This review summarizes canonical and novel effects of FGF23. FGF23 cleavage generates C-terminal peptides that also mediate biological functions. In aggregate, FGF23 measurements should be considered for larger application, as its excess can precede hypophosphatemia, explain hypophosphatemia or resistance to phosphate loading, and possibly predict cardiovascular progression in a wide range of uremic and non-uremic conditions.
{"title":"FGF23: A player not only in bone diseases","authors":"Amélie Cifuentes , Zacharie Laskar-Marchesseau , Guillaume Courbon","doi":"10.1016/j.jbspin.2025.105988","DOIUrl":"10.1016/j.jbspin.2025.105988","url":null,"abstract":"<div><div>The skeleton is able to secrete hormones and mediate endocrine functions. Particularly, the fibroblast growth factor 23 (FGF23) has received considerable attention for its unique phosphaturic properties, raising the bone to the status of an essential endocrine regulator. Excess in circulating levels of FGF23, not so surprisingly, then associated to mineral imbalance, in hereditary/acquired mineral and skeletal disorders. A key player, FGF23 excess precedes mineral and skeletal disturbances. However, unexpected effects have been described in the recent years. Various demonstrations have been made that FGF23 is directly regulated by non-mineral stress, including: inflammation, iron deficiency, and glycolysis. In turn, an emerging body of research shows association and causality between FGF23 and the cardiovascular system at large, from the iron metabolism to erythropoiesis, and to the cardiac muscle. This review summarizes canonical and novel effects of FGF23. FGF23 cleavage generates C-terminal peptides that also mediate biological functions. In aggregate, FGF23 measurements should be considered for larger application, as its excess can precede hypophosphatemia, explain hypophosphatemia or resistance to phosphate loading, and possibly predict cardiovascular progression in a wide range of uremic and non-uremic conditions.</div></div>","PeriodicalId":54902,"journal":{"name":"Joint Bone Spine","volume":"93 2","pages":"Article 105988"},"PeriodicalIF":4.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145253818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2025-09-09DOI: 10.1016/j.jbspin.2025.105963
Ana Bento da Silva , Désirée van der Heijde , Floris van Gaalen , Sofia Ramiro
Structural damage of the sacroiliac joints and spine is a feared consequence of axial spondyloarthritis (axSpA), leading to impairments in spinal mobility and physical function, thus contributing to the high disease burden and compromising patients’ quality of life. Inhibiting the progression of structural damage is a major treatment goal. Contrasting with the proven clinical efficacy of available therapies (tumour necrosis factor-alpha inhibitors [TNFi], interleukin-17 inhibitors [IL-17i], and Janus kinase inhibitors [JAKi]), their efficacy in slowing damage progression is not clearly demonstrated. For various reasons, including methodological challenges, such an effect could not be demonstrated in randomised clinical trials (RCT). Instruments for assessing structural damage have several limitations, notably their low sensitivity to change, and RCTs with a placebo control group over a long period are not viable for ethical reasons. Based on observational studies, TNFi seem to exert an inhibitory effect compared to conventional treatment, particularly in patients with risk factors for disease progression, mainly pre-existing syndesmophytes, and with longer treatment duration (> 2 years). Although evidence relating to IL-17i is scarcer, one head-to-head RCT showed no differences between secukinumab (IL-17Ai) and adalimumab (TNFi) in slowing structural damage progression. For JAKi, comparative evidence is lacking. The potential disease-modifying effect appears to be equally promising for TNFi and IL-17Ai, and structural damage inhibition currently does not seem to be a distinguishing feature between drug classes for the treatment of axSpA. The development of more sensitive instruments to capture structural damage appears crucial for conducting comparative studies on the efficacy of current therapies.
{"title":"Transforming myth into reality: a narrative review on the effect of therapies in slowing structural damage progression in axial spondyloarthritis","authors":"Ana Bento da Silva , Désirée van der Heijde , Floris van Gaalen , Sofia Ramiro","doi":"10.1016/j.jbspin.2025.105963","DOIUrl":"10.1016/j.jbspin.2025.105963","url":null,"abstract":"<div><div>Structural damage of the sacroiliac joints and spine is a feared consequence of axial spondyloarthritis (axSpA), leading to impairments in spinal mobility and physical function, thus contributing to the high disease burden and compromising patients’ quality of life. Inhibiting the progression of structural damage is a major treatment goal. Contrasting with the proven clinical efficacy of available therapies (tumour necrosis factor-alpha inhibitors [TNFi], interleukin-17 inhibitors [IL-17i], and Janus kinase inhibitors [JAKi]), their efficacy in slowing damage progression is not clearly demonstrated. For various reasons, including methodological challenges, such an effect could not be demonstrated in randomised clinical trials (RCT). Instruments for assessing structural damage have several limitations, notably their low sensitivity to change, and RCTs with a placebo control group over a long period are not viable for ethical reasons. Based on observational studies, TNFi seem to exert an inhibitory effect compared to conventional treatment, particularly in patients with risk factors for disease progression, mainly pre-existing syndesmophytes, and with longer treatment duration (><!--> <!-->2 years). Although evidence relating to IL-17i is scarcer, one head-to-head RCT showed no differences between secukinumab (IL-17Ai) and adalimumab (TNFi) in slowing structural damage progression. For JAKi, comparative evidence is lacking. The potential disease-modifying effect appears to be equally promising for TNFi and IL-17Ai, and structural damage inhibition currently does not seem to be a distinguishing feature between drug classes for the treatment of axSpA. The development of more sensitive instruments to capture structural damage appears crucial for conducting comparative studies on the efficacy of current therapies.</div></div>","PeriodicalId":54902,"journal":{"name":"Joint Bone Spine","volume":"93 2","pages":"Article 105963"},"PeriodicalIF":4.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145042466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
To evaluate the diagnostic performance of synovial fluid (SF) biochemical markers and assess the value of combining their measurements into a composite score for identifying septic arthritis (SA).
Methods
Patients who underwent arthrocentesis with SF biochemical analysis (proteins, glucose, lactate dehydrogenase (LDH), lactate) were included in the initial cohort (IC) (May 2018-May 2021) or the validation cohort (June 2021–March 2023). Using IC data, we compared marker levels in SA vs. non-SA and vs. crystal-related arthritis (C-rA) subgroup. Based on receiver operating characteristic (ROC) curves, we identified two thresholds (one optimizing sensitivity, the other specificity) to assign a score of 0–2 for each biomarker. We developed a composite score by combining the individual scores for discriminative biomarkers and assessed its diagnostic performance.
Results
We included 190 SF (170 patients) in the IC; 36 SF (18.9%) were septic. Glucose level was lower in SA than non-SA and C-rA, but lactate and LDH levels were higher (P < 0.001). The composite score was developed with a 0–6 scale, with the following thresholds: glucose (≤ 7 and ≤ 1.5 mmol/L), lactate (≥ 4.5 and ≥ 7.5 mmol/L), and LDH (≥ 600 and ≥ 1200 UI/L). A composite score ≥ 3 had 100% sensitivity and 73.9% specificity for SA diagnosis in the IC cohort, and a score≥ 5 had 55.5% sensitivity and 97.8% specificity. These findings were consistent in the validation cohort.
Conclusion
A combined score based on SF markers including glucose, LDH, and lactate may be an effective method for rapidly ruling out SA. A multicentric study is warranted to confirm these results.
{"title":"A new biochemical score from synovial fluid for diagnosing septic arthritis","authors":"Isabelle Sacco , Chayma Saadan , Laura Pina Vegas , Xavier Chevalier , Bérénice Souhail , Raphael Lepeule , Nadia Oubaya , Jean-Philippe Bastard , Soraya Fellahi , Florent Eymard","doi":"10.1016/j.jbspin.2025.105980","DOIUrl":"10.1016/j.jbspin.2025.105980","url":null,"abstract":"<div><h3>Objectives</h3><div>To evaluate the diagnostic performance of synovial fluid (SF) biochemical markers and assess the value of combining their measurements into a composite score for identifying septic arthritis (SA).</div></div><div><h3>Methods</h3><div>Patients who underwent arthrocentesis with SF biochemical analysis (proteins, glucose, lactate dehydrogenase (LDH), lactate) were included in the initial cohort (IC) (May 2018-May 2021) or the validation cohort (June 2021–March 2023). Using IC data, we compared marker levels in SA vs. non-SA and vs. crystal-related arthritis (C-rA) subgroup. Based on receiver operating characteristic (ROC) curves, we identified two thresholds (one optimizing sensitivity, the other specificity) to assign a score of 0–2 for each biomarker. We developed a composite score by combining the individual scores for discriminative biomarkers and assessed its diagnostic performance.</div></div><div><h3>Results</h3><div>We included 190 SF (170 patients) in the IC; 36 SF (18.9%) were septic. Glucose level was lower in SA than non-SA and C-rA, but lactate and LDH levels were higher (<em>P</em> <!--><<!--> <!-->0.001). The composite score was developed with a 0–6 scale, with the following thresholds: glucose (≤<!--> <!-->7 and ≤<!--> <!-->1.5<!--> <!-->mmol/L), lactate (≥<!--> <!-->4.5 and ≥<!--> <!-->7.5<!--> <!-->mmol/L), and LDH (≥<!--> <!-->600 and ≥<!--> <!-->1200 UI/L). A composite score ≥<!--> <!-->3 had 100% sensitivity and 73.9% specificity for SA diagnosis in the IC cohort, and a score≥<!--> <!-->5 had 55.5% sensitivity and 97.8% specificity. These findings were consistent in the validation cohort.</div></div><div><h3>Conclusion</h3><div>A combined score based on SF markers including glucose, LDH, and lactate may be an effective method for rapidly ruling out SA. A multicentric study is warranted to confirm these results.</div></div>","PeriodicalId":54902,"journal":{"name":"Joint Bone Spine","volume":"93 2","pages":"Article 105980"},"PeriodicalIF":4.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145187497","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2025-09-26DOI: 10.1016/j.jbspin.2025.105977
Margarida Lucas Rocha , Sofia Ramiro , Alexandre Sepriano
{"title":"Axial spondyloarthritis and polymyalgia rheumatica: When differential diagnosis is not that obvious","authors":"Margarida Lucas Rocha , Sofia Ramiro , Alexandre Sepriano","doi":"10.1016/j.jbspin.2025.105977","DOIUrl":"10.1016/j.jbspin.2025.105977","url":null,"abstract":"","PeriodicalId":54902,"journal":{"name":"Joint Bone Spine","volume":"93 2","pages":"Article 105977"},"PeriodicalIF":4.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145187443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2025-12-16DOI: 10.1016/j.jbspin.2025.106018
Tiantaixi Tu , Nuoyan Zhou , Ye Yang , Tongtong Zheng , Qingfeng Xie , Xinwang Ying
{"title":"Potential targets of air pollutants inducing ankylosing spondylitis: Evidence from eQTL Mendelian randomization and colocalization","authors":"Tiantaixi Tu , Nuoyan Zhou , Ye Yang , Tongtong Zheng , Qingfeng Xie , Xinwang Ying","doi":"10.1016/j.jbspin.2025.106018","DOIUrl":"10.1016/j.jbspin.2025.106018","url":null,"abstract":"","PeriodicalId":54902,"journal":{"name":"Joint Bone Spine","volume":"93 2","pages":"Article 106018"},"PeriodicalIF":4.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145783598","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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