Journal of Bone and Mineral Research最新文献

{"title":"Potential clinical pitfalls in FGF23 measurement.","authors":"Iris Hartley, Kelly Roszko","doi":"10.1093/jbmr/zjag147","DOIUrl":"https://doi.org/10.1093/jbmr/zjag147","url":null,"abstract":"","PeriodicalId":185,"journal":{"name":"Journal of Bone and Mineral Research","volume":" ","pages":""},"PeriodicalIF":6.5,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149190120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: Hypophosphatasia: low penetrance of pathogenic and likely-pathogenic ALPL variants identified through an unselected biorepository.","authors":"","doi":"10.1093/jbmr/zjag146","DOIUrl":"https://doi.org/10.1093/jbmr/zjag146","url":null,"abstract":"","PeriodicalId":185,"journal":{"name":"Journal of Bone and Mineral Research","volume":" ","pages":""},"PeriodicalIF":6.5,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149163918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: Atypical fractures at non-classical sites associated with anti-resorptive therapy: a systematic review.","authors":"","doi":"10.1093/jbmr/zjag132","DOIUrl":"https://doi.org/10.1093/jbmr/zjag132","url":null,"abstract":"","PeriodicalId":185,"journal":{"name":"Journal of Bone and Mineral Research","volume":" ","pages":""},"PeriodicalIF":6.5,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149147461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Treatment of male osteoporosis: a narrative review and position statement by the ECTS Clinical Action Group.","authors":"Anne Sophie Sølling, Julien Paccou, Athanasios D Anastasilakis, Ian R Reid, Maria P Yavropoulou, Barbara Hauser, Anda Mihaela Naciu, Suzanne N Morin, Jane Cauley, Bo Abrahamsen, Willem F Lems","doi":"10.1093/jbmr/zjag145","DOIUrl":"https://doi.org/10.1093/jbmr/zjag145","url":null,"abstract":"<p><p>Osteoporosis in men is under-recognized and under-treated despite a substantial disease burden and poorer fracture-related outcomes than in women. Secondary osteoporosis is highly prevalent in men, making the identification and management of underlying causes essential. Bone mineral density (BMD) and fracture risk are influenced by sex-specific patterns of skeletal growth and age-related bone loss, with men typically exhibiting greater cortical thickness, larger bone size, and trabecular thinning rather than loss of trabecular number. Although randomized controlled trials in men are fewer than in postmenopausal women, bisphosphonates, denosumab, teriparatide, abaloparatide, and romosozumab have all been shown to significantly increase BMD. Fracture outcome data remain limited; however, reductions in vertebral fracture risk have been demonstrated for zoledronate, alendronate, risedronate, denosumab, and teriparatide. Treatment should be individualized according to fracture risk, comorbidities, and patient preferences. In men at very high fracture risk, osteoanabolic therapy should be considered as first-line treatment, followed by antiresorptive therapy to consolidate and maintain BMD gains. Goal-directed (treat-to-target) management, including long-term maintenance therapy, and careful discontinuation strategies, particularly following denosumab, is essential for optimizing long-term skeletal health. This narrative review and position statement by The ECTS Clinical Action Group provides an updated overview of current and emerging treatment options and offers practical, evidence-based recommendations for the long-term management of osteoporosis in men.</p>","PeriodicalId":185,"journal":{"name":"Journal of Bone and Mineral Research","volume":" ","pages":""},"PeriodicalIF":6.5,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149101775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Children with X-linked hypophosphatemia have hypertension and left ventricular hypertrophy associated with obesity.","authors":"Chelsey Grimbly, Leanne M Ward, Anna Ryabets-Lienhard, Irene Chen, Sreya Molakalapalli, Lily Lin, Piush J Mandhane, R Todd Alexander","doi":"10.1093/jbmr/zjag142","DOIUrl":"https://doi.org/10.1093/jbmr/zjag142","url":null,"abstract":"<p><strong>Introduction: </strong>X-linked Hypophosphatemia (XLH) is a genetic condition of renal phosphate wasting with multisystem complications. Children and adults with XLH have increased frequency of obesity, a risk factor for hypertension. We evaluated hypertension and left ventricular hypertrophy in children with XLH, and their relationship with XLH treatment (phosphate/active vitamin D vs burosumab).</p><p><strong>Methods: </strong>Blood pressure and hypertension were combined and analyzed from four datasets: prospective data from the 301 burosumab vs conventional therapy randomized active-controlled trial (301 RCT, NCT02915705) and the XLH Disease Monitoring Program (NCT03651505), and retrospective clinical data from two tertiary centers. Hypertension was defined as three or more blood pressures ≥95th percentile for children 1-13 years of age or systolic blood pressure >130 or diastolic blood pressure >80 for children ≥13 years of age, obtained at separate clinical visits. Echocardiograms were conducted for safety monitoring in a subset of patients in the 301 RCT and these data were analyzed to assess left ventricular mass and left ventricular hypertrophy. Generalized estimating equations were used to assess the association of clinical factors and blood pressure or left ventricular hypertrophy.</p><p><strong>Results: </strong>1,555 blood pressure readings from 252 children were evaluated. Hypertension was identified in 42/252 (17%) children and overweight/obesity was present in 51% of the cohort at baseline. 50 children underwent 310 echocardiograms, of which 22% (11/50) at baseline had left ventricular mass that met criteria for left ventricular hypertrophy. On multivariable analysis, obesity was associated with increased systolic blood pressure (Coeff 8.2, 95%CI [4.4, 12.1], p <0.001) and left ventricular hypertrophy (Coeff 2.2, 95%CI [1.0, 3.4], p<0.001).</p><p><strong>Conclusion: </strong>Children with XLH have increased frequency of obesity, hypertension and left ventricular hypertrophy. Obesity was the main factor associated with hypertension or left ventricular hypertrophy. Longer follow-up studies are needed to assess the impact of burosumab on cardiovascular outcomes.</p>","PeriodicalId":185,"journal":{"name":"Journal of Bone and Mineral Research","volume":" ","pages":""},"PeriodicalIF":6.5,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149101795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Muscle-Bone Unit in Children and Adolescents: Insights from the Canadian Health Measures Survey.","authors":"Oliver Li, Leanne M Ward, Lauren E Griffith, Laura N Anderson, Andy Kin On Wong, Jonathan D Adachi, Jinhui Ma, Frank Rauch","doi":"10.1093/jbmr/zjag143","DOIUrl":"https://doi.org/10.1093/jbmr/zjag143","url":null,"abstract":"<p><p>Muscle and bone are closely related during growth and development. We sought to identify determinants of the muscle-bone relationship using peripheral quantitative computed tomography (pQCT) at the distal lower extremity and jumping mechanography among Canadian children. Data were obtained from the Canadian Health Measures Survey (CHMS), a national, cross-sectional, population-based study. 3,225 participants (aged 6 to 19.9 years) were included. Calf muscle cross-sectional area (CSA; 66% site) z-score was used as a surrogate measure of muscle strength, bone mineral content (BMC) z-score of the tibia shaft cross-section (38% site) was used as a surrogate measure of bone strength. Maximum jumping power (Pmax) z-score from the single two-legged jump test was assessed as a mediator between muscle CSA and BMC z-scores using path analysis. Peripheral QCT and Pmax z-scores were calculated using CHMS data. Height, weight, and body mass index (BMI) z-scores were calculated using Centers for Disease Control reference data. We found a strong positive association between muscle CSA z-score and tibia BMC z-score (β = 0.64, 95% confidence interval [CI]: 0.62 to 0.67). Calf subcutaneous fat CSA (β = -0.04, 95% CI: -0.07 to -0.01) and muscle density (β = 0.08, 95% CI: 0.03 to 0.13) z-scores were weak determinants, and weight (β = 0.10, 95% CI: 0.05 to 0.15) and BMI (β = 0.14, 95% CI: 0.07 to 0.21) z-scores were strong determinants of the association between muscle CSA z-score and BMC z-score. Self-reported moderate-to-vigorous physical activity and serum total calcium, 25-hydroxy-vitamin D3, and parathyroid hormone were not determinants. Pmax z-score was a partial mediator of the association between muscle CSA and BMC z-scores. In conclusion, we found that the effect of muscle size on bone mass was in part mediated by muscle power. Subcutaneous fat, muscle density, weight, and BMI were determinants of the muscle-bone relationship.</p>","PeriodicalId":185,"journal":{"name":"Journal of Bone and Mineral Research","volume":" ","pages":""},"PeriodicalIF":6.5,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149056655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatic Selenoprotein P Impairs Bone Formation via Osteoblastic IGF-1 Resistance.","authors":"Kiyo-Aki Ishii, Hiroaki Takayama, Cynthia M Galicia-Medina, Hein Ko Oo, Guzel Gafiyatullina, Yoshiro Saito, Hiroyuki Tsuchiya, Hiroyuki Nakamura, Toshinari Takamura","doi":"10.1093/jbmr/zjag139","DOIUrl":"https://doi.org/10.1093/jbmr/zjag139","url":null,"abstract":"<p><p>Bone fragility is increasingly recognized as a complication of metabolic dysfunction, but endocrine mechanisms linking hepatic stress to impaired bone formation remain incompletely defined. We tested whether selenoprotein P, a hepatokine elevated in metabolic disease, suppresses osteoblast function and skeletal integrity. In mice fed a high-fat, high-sucrose diet, whole-body Selenop deficiency preserved trabecular bone mass, bone formation, bone stiffness, and cortical bone defect repair. Hepatocyte-specific Selenop deficiency also preserved trabecular bone mass. Histomorphometry showed that selenoprotein P primarily suppressed osteoblast activation without materially altering osteoclast indices. In calvaria-derived osteoblast cultures, purified human plasma-derived selenoprotein P inhibited IGF-1-induced phosphorylation of IGF-1 receptor, IRS-1, PI3K, PDK1, and Akt, reduced alkaline phosphatase activity, matrix mineralization, and osteogenic gene expression, and blunted receptor-proximal ROS generation. LRP1 was the predominant candidate receptor during osteogenic differentiation. Osteoblast cultures derived from Osx-Cre/+ Lrp1fl/fl mice showed reduced cell-associated human selenoprotein P, and the inhibitory effects of selenoprotein P on IGF-1 signaling and osteoblast maturation were absent in these cultures. In vivo, pharmacologic blockade of IGF-1 receptor signaling eliminated the skeletal protection conferred by Selenop deficiency, supporting a requirement for intact IGF-1 receptor signaling in this pathway. In a cross-sectional analysis of a general population cohort, serum selenoprotein P was not significantly associated with OSI across the full cohort, whereas exploratory analyses in the highest quintile suggested an inverse association between high circulating selenoprotein P and bone mass. Together, these findings identify hepatic selenoprotein P as a negative regulator of bone formation and define a hepato-osteogenic reductive stress axis that links metabolic stress to impaired skeletal integrity.</p>","PeriodicalId":185,"journal":{"name":"Journal of Bone and Mineral Research","volume":" ","pages":""},"PeriodicalIF":6.5,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149056626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction of: Isosorbide Mononitrate Increases Bone Formation and Decreases Bone Resorption in Postmenopausal Women: A Randomized Trial.","authors":"","doi":"10.1093/jbmr/zjag108","DOIUrl":"10.1093/jbmr/zjag108","url":null,"abstract":"","PeriodicalId":185,"journal":{"name":"Journal of Bone and Mineral Research","volume":" ","pages":"1149"},"PeriodicalIF":6.5,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148617571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Goal-directed therapy is not as simple as it seems.","authors":"Nelson B Watts","doi":"10.1093/jbmr/zjag080","DOIUrl":"10.1093/jbmr/zjag080","url":null,"abstract":"<p><p>A case is discussed of a postmenopausal woman started on alendronate treatment based on a low T-score in the total hip (TH). Three years later, her TH score remains below -2.5, the target set by the ASBMR task force on goal-directed therapy.1 The important question at this juncture is whether she should change to a different treatment that might result in better improvement in TH bone mineral density (BMD) or if she should continue treatment with alendronate.</p>","PeriodicalId":185,"journal":{"name":"Journal of Bone and Mineral Research","volume":" ","pages":"1056-1059"},"PeriodicalIF":6.5,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147925060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circadian regulator PER1 inhibits osteoclastogenesis by activating inflammatory genes.","authors":"Nobuko Katoku-Kikyo, Elizabeth K Vu, Samuel Mitchell, Ismael Y Karkache, Elizabeth W Bradley, Nobuaki Kikyo","doi":"10.1093/jbmr/zjag025","DOIUrl":"10.1093/jbmr/zjag025","url":null,"abstract":"<p><p>Disruption of circadian rhythms predisposes shift workers to many chronic conditions, including osteoporosis. However, the effects of disrupted circadian rhythms on bone remodeling remain largely unknown. Here, we show that one of the core circadian regulators PER1 inhibits osteoclastogenesis by upregulating genes involved in inflammation. Conditional knockout (KO) of Per1 in osteoclasts and related cells resulted in decreased bone mass in the femurs of mice, along with increased osteoclasts and decreased osteoblasts. Osteoclastogenesis was also promoted by Per1 depletion in vitro with 16 downregulated inflammatory genes. Seven of these genes were known to promote or inhibit osteoclastogenesis depending on the stage of osteoclastogenesis and the presence or absence of infection. Knockdown of Nlrp3, Tlr8, or Tlr9 in the group of genes promoted osteoclastogenesis, mirroring the effects of Per1 KO and offering a mechanistic explanation for the Per1-mediated inhibition of osteoclastogenesis. These results were not observed following the KO of a paralog Per2. Per1 KO mice maintain general circadian rhythms, unlike arrhythmic Per1;Per2 double KO mice. This gives credence to Per1 as a selective target for therapeutic interventions without disrupting the circadian rhythms. This study uncovered a molecular link between a circadian regulator and osteoclastogenesis in the broader context of inflammatory reactions. Our findings may be mechanistically relevant to inflammatory bone diseases influenced by circadian rhythms, such as rheumatoid arthritis and osteoarthritis, as well as other bone diseases predisposed by chronic circadian disruption.</p>","PeriodicalId":185,"journal":{"name":"Journal of Bone and Mineral Research","volume":" ","pages":"1136-1148"},"PeriodicalIF":6.5,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146123093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}