Bone最新文献

{"title":"Comment on “Impact of baseline PINP on the BMD increase with romosozumab, teriparatide, and denosumab in treatment-naïve primary osteoporosis: A retrospective cohort study”","authors":"Daquan Liao , Xuezheng Zhu , Shiye Huang , Yubin Feng , Ziye Zhuang","doi":"10.1016/j.bone.2025.117667","DOIUrl":"10.1016/j.bone.2025.117667","url":null,"abstract":"","PeriodicalId":9301,"journal":{"name":"Bone","volume":"202 ","pages":"Article 117667"},"PeriodicalIF":3.6,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145260095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The “Last Mile” of ResNet50-based osteoporosis screening on chest radiographs: Standardization, federated learning, and interpretability","authors":"Siyi Liu","doi":"10.1016/j.bone.2025.117677","DOIUrl":"10.1016/j.bone.2025.117677","url":null,"abstract":"","PeriodicalId":9301,"journal":{"name":"Bone","volume":"202 ","pages":"Article 117677"},"PeriodicalIF":3.6,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145264525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Skin Advanced Glycation End Products (AGEs) are not associated with bone mineral density longitudinally: The Rotterdam Study","authors":"Mengyuan Cai ,&nbsp;Jinluan Chen ,&nbsp;Jiawei Li ,&nbsp;Katerina Trajanoska ,&nbsp;Evert F.S. van Velsen ,&nbsp;M. Carola Zillikens","doi":"10.1016/j.bone.2025.117676","DOIUrl":"10.1016/j.bone.2025.117676","url":null,"abstract":"<div><h3>Background</h3><div>Advanced glycation end products (AGEs), formed through non-enzymatic glycation of, e.g., proteins in collagen have been associated with prevalent fractures, but their relation with bone mineral density (BMD) and trabecular bone score (TBS) is unclear.</div></div><div><h3>Objectives</h3><div>To assess the association of skin AGEs with BMD and TBS changes over time.</div></div><div><h3>Methods</h3><div>In the Rotterdam Study, skin AGEs were assessed as skin autofluorescence (SAF) using the AGE Reader®. Total body (TB), femoral neck (FN) and lumbar spine (LS) BMD were assessed using dual-energy X-ray absorptiometry (DXA). SAF was analyzed with baseline and follow-up BMD and TBS, employing a linear mixed effects model adjusted for clinical and lifestyle confounders, with interaction analysis for sex, prevalent type 2 diabetes mellitus (T2DM), chronic kidney disease, and bisphosphonate use.</div></div><div><h3>Results</h3><div>Longitudinal analyses between SAF and TB BMD were performed in 2553 participants (mean follow-up time 4.9 years), and between SAF and LS BMD, FN BMD and TBS in 851 participants (mean follow-up 5.6 years). SAF was not associated with BMD nor with TBS changes over time. Significant interactions were observed with sex (TB and FN BMD) and with diabetes (FN BMD), but stratified analysis revealed no significant associations.</div></div><div><h3>Conclusion</h3><div>We did not observe a longitudinal association between SAF and BMD at multiple sites or TBS, which is consistent with our earlier findings that associations of SAF with prevalent fractures were not explained by BMD or TBS. Other aspects of bone quality or muscle characteristics including fall risk may be involved.</div></div>","PeriodicalId":9301,"journal":{"name":"Bone","volume":"202 ","pages":"Article 117676"},"PeriodicalIF":3.6,"publicationDate":"2025-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145240659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Piezo1-mediated mechanotransduction regulates diabetic osteoporosis and hyperglycemia via low-intensity pulsed ultrasound","authors":"Mengshu Cao ,&nbsp;Fang Pang ,&nbsp;Xueyou Duan ,&nbsp;Lijun Sun ,&nbsp;Xiushan Fan ,&nbsp;Liang Tang ,&nbsp;Dean Ta","doi":"10.1016/j.bone.2025.117664","DOIUrl":"10.1016/j.bone.2025.117664","url":null,"abstract":"<div><div>This study investigates the effects and mechanism by which low-intensity pulsed ultrasound (LIPUS) regulates osteoporosis and hyperglycemia in mice with type 1 diabetes mellitus (T1DM). The mice were randomly divided into four groups: normal control (NC), T1DM mice (DM), T1DM mice treated with insulin (DM + INS), and T1DM mice treated with LIPUS (DM + LIPUS). The DM + INS group served as a positive control for the study. The DM + LIPUS group received LIPUS treatment (80 mW cm⁻², 20 min daily) on the quadriceps femoris for 6 weeks. The results show that LIPUS improves the mechanical properties, morphological characteristics, and bone microstructure and alleviate hyperglycemia in the T1DM mice. In addition, knockout of Piezo1 using CRISPR-Cas9 was performed in MC3T3-E1 cells (Piezo1^−/−) to verify the role of LIPUS during treatment. The cell experiments showed that LIPUS improved proliferation, osteogenic differentiation capabilities, and cytoskeletal morphology, while significantly reducing the extracellular glucose level of MC3T3-E1 cells in a high glucose medium. All these results indicate that Piezo1-mediated mechanotransduction is closely related to the alleviation of osteoporosis and hyperglycemia in T1DM mice treated with LIPUS. LIPUS showed comparable efficacy to insulin in reducing the severity of osteoporosis and lowering hyperglycemia in T1DM mice. This therapy effectively alleviated symptoms (including osteoporosis and hyperglycemia) in T1DM mice without insulin injections. These findings suggest that LIPUS therapy could serve as an adjunct method to conventional diabetes treatment in T1DM.</div></div>","PeriodicalId":9301,"journal":{"name":"Bone","volume":"202 ","pages":"Article 117664"},"PeriodicalIF":3.6,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145234479","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decreased bone strength in skeletally mature female mice with T2D is associated with changes in OLCN and spatially compromised architecture","authors":"Carlos A. Urrego ,&nbsp;Benjamin S. Sexton ,&nbsp;David H. Kohn","doi":"10.1016/j.bone.2025.117665","DOIUrl":"10.1016/j.bone.2025.117665","url":null,"abstract":"<div><div>Women with Type-2 diabetes (T2D) have a higher incidence of fractures and associated mortality compared to men. However, most animal models for studying diabetes-induced bone effects use males and the impact of T2D on bone quality in skeletally mature females remains unknown. We developed a mouse model to determine the effect of T2D on female bone quality. T2D was induced in 16-week-old female C57BL/6J mice using a High-Fat Diet and Streptozotocin (HFD + STZ), controls received a Low-Fat Diet and sham injections (LFD + VEH). The diabetic group displayed hyperglycemia, hypoinsulinemia, and increased body fat. T2D altered bone architecture spatially, the T2D group displayed decreased cortical and trabecular bone volume (BV) and total volume (TV) with varying magnitude at specific locations compared to the control. T2D also reduced bone yield and ultimate loads under four-point bending, without affecting tissue-level properties. Moreover, changes in TV with T2D explained up to 70 % of the variance in bone strength, suggesting that the weakening effect of T2D on female bone strength is architecture-driven. Compromised architecture with T2D was associated with changes in the Osteocyte Lacuno-Canalicular Network (OLCN). T2D decreased canalicular density, the total number of nodes and increased lacunae surface area. These changes in the OLCN with T2D explained up to 37 % of bone architecture variance. In summary, our novel T2D female mouse model displayed a bone phenotype with compromised OLCN associated to impaired architecture, which led to decreased bone strength. These outcomes suggest that the effect of T2D on female bone strength is architecture-driven rather than material-driven.</div></div>","PeriodicalId":9301,"journal":{"name":"Bone","volume":"202 ","pages":"Article 117665"},"PeriodicalIF":3.6,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145234496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FGF8 induces bone and joint regeneration at digit amputation wounds in neonate mice","authors":"Ling Yu ,&nbsp;Mingquan Yan ,&nbsp;Sarah M. Wolff ,&nbsp;Joseph D. Knue ,&nbsp;Hannah M. Smith ,&nbsp;Connor P. Dolan ,&nbsp;Ken Muneoka ,&nbsp;Selim Romero ,&nbsp;James J. Cai ,&nbsp;Carissa Yun ,&nbsp;Devon J. Boland ,&nbsp;Regina Brunauer ,&nbsp;Lindsay A. Dawson","doi":"10.1016/j.bone.2025.117663","DOIUrl":"10.1016/j.bone.2025.117663","url":null,"abstract":"<div><div>Due to increases in vascular diseases, the incidence of limb loss is predicted to more than double in the next quarter century. Therefore, developing a greater understanding of the latent regenerative capacity in mammals is a significant and growing goal. Mammals, including humans and mice, have limited regenerative capacity following limb amputation, with regenerative responses restricted to amputations transecting the distal digit tip (P3). Unlike P3, amputations of the adjacent skeletal segment, the middle phalanx, P2, are non-regenerative and result in bone truncation and soft tissue scar formation. As such, P2 amputation is a simple yet powerful model to test strategies for inducing mammalian musculoskeletal regeneration from an otherwise non-regenerative amputation plane. Here, we report that Fibroblast Growth Factor 8 (FGF8) drives synovial joint regeneration at P2 amputation wounds in neonate mice. This response is characterized by the regeneration of a synovial cavity, a skeletal nodule lined with articular cartilage, and tendon and ligament regeneration. FGF8 also induces cartilage formation on the P2 stump that serves as a template for partial P2 bone regeneration, thus FGF8 drives the composite regeneration of stump and joint tissues. FGF8-induced joint regeneration is associated with the upregulation of several, but not all, genes that characterize joint development, and is morphologically distinct from digit joint development. Lineage tracing studies demonstrate that cells at the amputation wound contribute to the regenerated joint structures. These studies provide evidence that the otherwise non-regenerative P2 amputation wound possesses tremendous regenerative capacity that is dormant under normal circumstances.</div></div>","PeriodicalId":9301,"journal":{"name":"Bone","volume":"202 ","pages":"Article 117663"},"PeriodicalIF":3.6,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145227672","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A deep intronic PHEX variant in a large Danish family with hereditary hypophosphatemia and a milder skeletal, but more severe dental phenotype","authors":"Jenny Blechingberg ,&nbsp;Kristian Alsbjerg Skipper ,&nbsp;Signe Sparre Beck-Nielsen ,&nbsp;Pernille Axél Gregersen","doi":"10.1016/j.bone.2025.117666","DOIUrl":"10.1016/j.bone.2025.117666","url":null,"abstract":"<div><div>Hereditary hypophosphatemia (HH) are rare diseases, characterized by excessive renal phosphate wasting, rickets and osteomalacia in growing children, and osteomalacia in adults. There are several types of HH caused by pathogenic variants in a number of different genes. We present a large Danish family consisting of 19 family members with clinically and biochemically hypophosphatamia caused by a previously unreported deep intronic splice variant in <em>PHEX</em>: c.1080-687 A &gt; G (p.?). The affected family members displayed a milder HH phenotype compared with a larger group of individuals with other disease causing <em>PHEX</em> variants. We were able to genetically confirm a diagnosis of X-linked hypophosphatemia (XLH) by genome sequencing intron analysis and in vitro analysis consisting of an exon trapping assay. Our findings emphasize the phenotypic variability of XLH, where this family in general displays a milder phenotype. Furthermore, our findings demonstrate that XLH can be caused by intron variants in <em>PHEX</em>.</div></div>","PeriodicalId":9301,"journal":{"name":"Bone","volume":"202 ","pages":"Article 117666"},"PeriodicalIF":3.6,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145226488","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of frailty with incident fractures and the mediating effect of inflammatory biomarkers: a prospective cohort study from the UK Biobank","authors":"Yi Zhang ,&nbsp;Kai Zhang ,&nbsp;Weizheng Kong ,&nbsp;Xiaolin Hu ,&nbsp;Lirong Chai ,&nbsp;Weijing Wang ,&nbsp;Dongfeng Zhang ,&nbsp;Junning Fan","doi":"10.1016/j.bone.2025.117662","DOIUrl":"10.1016/j.bone.2025.117662","url":null,"abstract":"<div><h3>Background</h3><div>Limited evidence exists regarding the association of frailty with fractures of different types and the potential mediating factors. This study investigated the prospective associations of frailty status with incident fracture risk and potential mediating role of inflammatory biomarkers.</div></div><div><h3>Methods</h3><div>This prospective cohort study utilized the UK Biobank data (median follow-up: 13.6 years). Frailty status was assessed using the frailty index (FI) and Fried's phenotype (FP). The outcomes of interest were any, vertebral, hip, and non-hip non-vertebral (NHNV) fractures. Cox regression models were employed to estimate association between frailty and fracture outcomes. Subgroup analyses by age, sex, and body mass index were conducted. Additionally, mediation analyses were performed to explore whether and quantify the extent to which inflammation may mediate the frailty-fracture association.</div></div><div><h3>Results</h3><div>Among 418,700 participants aged 38–72 years, frailty significantly increased risk of incident fracture, taking the frailty index as an example, with hazard ratios (HRs) and 95 % confidence intervals (CIs) of 1.53 (1.45–1.60) for any fractures, 2.33 (2.04–2.66) for vertebral fractures, 1.74 (1.55–1.95) for hip fractures, and 1.43 (1.35–1.52) for NHNV fractures. The FI-any fracture association was stronger in participants aged ≥60 years compared to younger participants (<em>P</em> _interaction = 0.0414); FP exhibited more pronounced associations with any fractures in men than women (<em>P</em> _interaction = 0.0001). Moreover, three inflammatory biomarkers - C-reactive protein, neutrophils, and platelets - significantly mediated 0.86–2.20 % of the frailty-fracture relationships.</div></div><div><h3>Conclusion</h3><div>Frailty was independently linked to increased risks of incident fracture, partially mediated through inflammatory biomarkers. These findings underscore the clinical importance of frailty screening in fracture prevention settings.</div></div>","PeriodicalId":9301,"journal":{"name":"Bone","volume":"201 ","pages":"Article 117662"},"PeriodicalIF":3.6,"publicationDate":"2025-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145202531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Management of osteoporosis in Parkinson's disease: A scoping review","authors":"Lyan Abdul Wadood ,&nbsp;Victoria McHugh ,&nbsp;Kristin K. Clemens ,&nbsp;Mary E. Jenkins ,&nbsp;Jeffrey D. Holmes ,&nbsp;Jamie L. Fleet","doi":"10.1016/j.bone.2025.117646","DOIUrl":"10.1016/j.bone.2025.117646","url":null,"abstract":"<div><h3>Background</h3><div>Parkinson's Disease (PD) is a progressive neurodegenerative disorder that primarily affects the dopaminergic neurons in the basal ganglia. It leads to a range of motor symptoms such as tremors, bradykinesia, rigidity, and gait instability. A significant, but often overlooked, sequela of PD is osteoporosis, which contributes to a higher incidence of fractures. This risk is exacerbated by both PD itself as well as the medications used to manage PD. Despite the heightened risk of fragility fractures, osteoporosis in PD is frequently under-recognized and inadequately managed.</div></div><div><h3>Objective</h3><div>This review aimed to explore the current literature on osteoporosis management strategies specifically for individuals with PD.</div></div><div><h3>Methods</h3><div>MEDLINE, Scopus, and EMBASE were searched from database inception to August 10, 2025.</div></div><div><h3>Results</h3><div>Following a two-stage review process conducted by two independent reviewers, 18 relevant articles were identified. Of these, 17 were review articles and one was an interventional study. The literature most commonly identified lifestyle modifications, pharmacological treatments, and surgical interventions as management strategies for osteoporosis in PD. However, most of the recommendations were based on research conducted in the general population, raising concerns about their effectiveness for individuals with PD, who may have unique clinical needs.</div></div><div><h3>Conclusions</h3><div>We note a significant gap in research focused on osteoporosis management in PD patients. Research efforts should prioritize developing tailored strategies to manage osteoporosis in individuals with PD.</div></div>","PeriodicalId":9301,"journal":{"name":"Bone","volume":"202 ","pages":"Article 117646"},"PeriodicalIF":3.6,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145182393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structural challenges in using Japanese claims databases for real-world evidence in osteoporosis research","authors":"Hiroshi Kawaguchi","doi":"10.1016/j.bone.2025.117661","DOIUrl":"10.1016/j.bone.2025.117661","url":null,"abstract":"","PeriodicalId":9301,"journal":{"name":"Bone","volume":"201 ","pages":"Article 117661"},"PeriodicalIF":3.6,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145155738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}