Bone Research最新文献

{"title":"A phase 2 trial of burosumab for treatment of fibroblast growth factor-23-mediated hypophosphatemia in children and adults with fibrous dysplasia","authors":"Olivia de Jong, Zubeyir Hasan Gun, Afua Asante-Otoo, Ibrahim I Elbashir, Xiaobai Li, Babak Saboury, Vardit Kram, Luis F. de Castro, Vivian MacDonald, Alison M. Boyce","doi":"10.1038/s41413-026-00523-7","DOIUrl":"https://doi.org/10.1038/s41413-026-00523-7","url":null,"abstract":"Fibrous dysplasia (FD) is a rare disorder associated with fractures and deformities. FD lesions produce excess phosphaturic hormone fibroblast growth factor 23 (FGF23), leading to hyperphosphaturia in most patients, and hypophosphatemia in those with high FD burden. Skeletal complications are associated with both low-normophosphatemia and frank hypophosphatemia. Burosumab is approved for other forms of FGF23 excess, but there is little evidence to inform use in FD. A phase 2 study investigated the safety and efficacy of burosumab in patients with FD. The primary endpoint was the proportion of participants achieving phosphate levels within the mid to upper part of the normal range (age and sex-adjusted Z-score –1 to +2). 12 participants (7 children, 5 adults) received burosumab for 48 weeks. Median phosphate Z-score increased from −2.88 (1.65) to 0.22 (1.37), meeting the target in 100% of participants. Alkaline phosphatase levels were elevated at baseline in 8 participants [median 846 U/L (464)] and declined by 49% at week 48, representing a median decline of −364 (244.5) U/L. PROMIS questionnaires showed trends toward improvements in all domains in children; adult scores showed no identifiable trends. Two children experienced transformational mobility gains, including advancement from full-time wheelchair use to independent ambulation. Lesion biopsies showed no changes in cellularity or composition, and 18F-NaF PET/CT scans showed no changes in tracer uptake, suggesting burosumab did not adversely impact lesional activity. Adverse events were mild, and none resulted in treatment withdrawal. Burosumab treatment in patients with FD was well-tolerated, restored phosphate homeostasis, and reduced alkaline phosphatase levels. Burosumab has the potential to lead to functional improvements and ambulation gains in severely affected patients and is a valuable tool to reduce the impact of FD-related disability.","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"133 1","pages":""},"PeriodicalIF":12.7,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147751796","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":"Osteoblastic sclerostin loop3-LRP4 interaction required by sclerostin to inhibit bone formation.","authors":"Luyao Wang,Xiaohui Tao,Hewen Jiang,Shijian Ding,Ning Zhang,Xin Yang,Shenghang Wang,Yihao Zhang,Nanxi Li,Haitian Li,Zhanghao Li,Xiaoxin Wen,Meiheng Sun,Chuanxin Zhong,Heiwa So,Jin Liu,Yuanyuan Yu,Hua Yue,Xianghang Luo,Péter Ferdinandy,Tao Zhang,Shu Zhang,Zhenlin Zhang,Aiping Lu,Baoting Zhang,Ge Zhang","doi":"10.1038/s41413-026-00511-x","DOIUrl":"https://doi.org/10.1038/s41413-026-00511-x","url":null,"abstract":"Sclerostin negatively regulates bone formation. The marketed antibody against sclerostin loop2 promoted bone formation but may have caused severe cardiovascular events in clinical use. In our published studies, sclerostin loop3 was found to be involved in inhibitory effects of sclerostin on bone formation, whereas cardiovascular protective effects of sclerostin in mice were independent of loop3. It is necessary to investigate how sclerostin loop3 participates in the inhibitory effects of sclerostin on bone formation to facilitate developing precise strategies that promote bone formation without increasing cardiovascular risk. In this study, sclerostin loop3 was identified to bind to LRP4, thereby facilitating binding of sclerostin to LRP6 in osteoblasts. Blockade of sclerostin loop3-LRP4 interaction by both Lrp4 mutation (Lrp4m) and blocking peptide (LRP4-Pep) diminished the antagonistic effect of sclerostin on Wnt/β-catenin signaling in osteoblasts in vitro. Consistently, Lrp4m promoted bone formation in Lrp4m mice in vivo. Mechanistically, osteoblast-conditional correction of Lrp4m to wild-type Lrp4 resulted in significantly lower bone formation than Lrp4m mice, indicating that the promotive effects of Lrp4m on bone formation acted in osteoblasts in vivo. Moreover, re-expression of sclerostin dramatically inhibited bone formation in sost-/- mice, whilst the inhibitory effects of sclerostin were significantly weaker in sost-/-.Lrp4m mice. Pharmacologically, LRP4-Pep diminished the inhibitory effects of sclerostin on bone formation in SOSTki mice. Taken together, osteoblastic sclerostin loop3-LRP4 interaction, as an anchor, was required by sclerostin to bind to LRP6, thereby inhibiting bone formation. Translationally, blockade of sclerostin loop3-LRP4 interaction in osteoblasts would provide precise therapeutic strategies to promote bone formation without increasing cardiovascular risk.","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"9 1","pages":""},"PeriodicalIF":12.7,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147739076","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":"Neural regulation of bone: from central neural circuits to peripheral innervation of the skeletal stem cell niche.","authors":"Zihan Chen,Zhengqiong Luo,Matthew B Greenblatt,Zuoxing Wu,Ren Xu","doi":"10.1038/s41413-026-00534-4","DOIUrl":"https://doi.org/10.1038/s41413-026-00534-4","url":null,"abstract":"The nervous system has emerged as a multi-scale regulator of bone biology, integrating central neural circuits with peripheral innervation to control skeletal homeostasis and repair. While bone remodeling is classically described as being governed by coupling between bone formation and resorption, neural signaling provides an additional hierarchical layer that links organism-level cues to local skeletal stem/progenitor cell niches. This review presents a mechanistic framework for the neuro-bone regulatory network across three hierarchical levels. First, we examine central regulation, in which hypothalamic circuits integrate hormonal and metabolic signals via circumventricular organs to modulate endocrine outputs such as parathyroid hormone (PTH), thereby establishing circadian rhythms and systemic control of bone metabolism. Second, we analyze peripheral neural communication, where sensory inputs triggered by injury or inflammation, along with autonomic efferent signaling, including β-adrenergic pathways, directly influence osteolineage and stromal cells. These signals recalibrate cellular metabolic states, differentiation programs, and regenerative responses, linking pain perception with tissue repair mechanisms. Third, we investigate the bone marrow niche, where distinct subtypes of nerve fibers release a diverse array of neurotransmitters and or neuromodulators that shape the microenvironment of skeletal stem and progenitor cells (SSPCs) as well as downstream osteoprogenitors, thereby regulating proliferation, lineage commitment, and quiescence. Collectively, these findings delineate an integrated model of neural regulation of bone spanning central, peripheral, and local niche levels, providing a foundation for testable hypotheses in neuro-osteobiology.","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"1 1","pages":""},"PeriodicalIF":12.7,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147731485","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":"Identification of a new population of Tnn+ progenitors to form tendon enthesis fibrocartilage.","authors":"Tao Zhang,Lin Zhang,Ziyang Yuan,Linfeng Wang,Jianzhong Hu,Thomas Skutella,Hongbin Lu","doi":"10.1038/s41413-026-00519-3","DOIUrl":"https://doi.org/10.1038/s41413-026-00519-3","url":null,"abstract":"Elucidating the identity of enthesis-resident progenitors is critical for advancing regenerative strategies, particularly in the context of the long-standing question of how is fibrocartilage formed at tendon enthesis (bone-tendon interface) under mechanical loading. To address the question of cellular origins of entheseal fibrocartilage, we first employed spatial transcriptional and single cell sequencing to identify a novel population of Tnn⁺ progenitor cells and delineate their lineage trajectories across developmental stages. Subsequently, we used a diphtheria toxin mediated ablation model targeting these Tnn⁺ progenitors and demonstrated their functional importance, as ablation resulted in hypoplastic phenotypes characterized by impaired fibrocartilage maturation. Furthermore, comparative single-cell profiling between unloaded entheses and normal entheses revealed that tendon unloading significantly diminished both the abundance and chondrogenic potential of Tnn⁺ progenitors. Collectively, these findings resolve fundamental questions regarding enthesis morphogenesis and provide mechanistic insights into how mechanical loading orchestrates this critical developmental process.","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"65 1","pages":""},"PeriodicalIF":12.7,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147725635","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":"Dasatinib and quercetin senolytic treatment delays early onset intervertebral disc degeneration in SM/J mice.","authors":"Emanuel J Novais, Olivia K Ottone, Sanjana Jagannath, Esther Jesutofunmi Akande, Ruteja A Barve, Makarand V Risbud","doi":"10.1038/s41413-026-00526-4","DOIUrl":"10.1038/s41413-026-00526-4","url":null,"abstract":"<p><p>Genetic background is a major determinant of disc degeneration, a leading cause of chronic back pain and disability. Herein, we demonstrate that premature disc cell senescence contributes to early-onset degeneration in SM/J mice and test two systemic senotherapeutic strategies to mitigate it: Navitoclax (Nav.) and a cocktail of Dasatinib and Quercetin (DQ). While Nav. treatment did not improve severe degeneration in SM/J mice or senescence status, DQ-treated mice showed lower grades of degeneration and a decreased abundance of senescence markers, including p19ARF, p21, and the senescence-associated secretory phenotype (SASP). DQ improved disc cell viability and phenotype retention and retarded fibrosis of the nucleus pulposus tissue. Transcriptomic analysis revealed tissue-specific effects of the treatment, with cell cycle regulation and JNK signaling being commonly affected across different tissue types. A comparison of SM/J data with DQ-mediated aging-dependent amelioration of disc degeneration in C57BL/6 N mice identified Junb and Zfp36l1 signaling as shared DQ targets in the mouse disc. Notably, the in vitro inhibition studies of the JUN pathway in human degenerated NP cells mimicked the benefits of DQ, namely, a reduction in senescence and SASP. This study reinforces the efficacy of senolytic treatment in ameliorating local senescence and intervertebral disc fibrosis.</p>","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"14 1","pages":""},"PeriodicalIF":20.1,"publicationDate":"2026-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13076796/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147670419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ubiquitin-specific protease 26 facilitates endochondral ossification by driving chondrocyte hypertrophy and mineralization.","authors":"Changwei Li,Yiming Xu,Li Zhou,Leilei Chang,Zhou Dan,Yunhe Jiang,Chao Wang,Lianfu Deng,Guoqing Tang","doi":"10.1038/s41413-026-00517-5","DOIUrl":"https://doi.org/10.1038/s41413-026-00517-5","url":null,"abstract":"Chondrocyte hypertrophy and mineralization are essential for endochondral ossification; however, the mechanisms underlying these processes remain incompletely understood. In this study, we have identified the facilitated role of ubiquitin-specific protease 26 (USP26) in endochondral ossification by stimulating chondrocyte hypertrophy and mineralization. Ultimately, this promotes skeletal development, bone fracture healing, and the occurrence of osteoarthritis. Mechanistically, USP26 decreases FBP2 undergoing K63-linked ubiquitination, leading to a reduction in the protein level of FBP2. This reduction promotes mitochondrial biogenesis and oxidative phosphorylation, thus facilitating chondrocyte hypertrophy and mineralization and aiding in the process of endochondral ossification. Furthermore, our study found that compression loading induces USP26 to initiate chondrocyte hypertrophy and mineralization through the phosphorylation of estrogen receptor-α at serine 118. These findings suggest that USP26, acting as a mechanosensor, facilitates chondrocyte hypertrophy and mineralization by maintaining mitochondrial biogenesis through the reduction of FBP2. Identifying USP26 as a potential therapeutic target for physiological skeletal growth, bone fracture healing, and osteoarthritis.","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"19 1","pages":""},"PeriodicalIF":12.7,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147641744","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":"Periosteal mitochondria DNA structures drive aging-associated poor skeletal repair.","authors":"Yanlin Wu,Chuyi Han,Xue Yang,Yitian Wang,Weidong Tian,Quan Yuan,Hui Wang,Haisheng Wang,Bei Yin,Ling Ye,Feifei Li,Fanyuan Yu","doi":"10.1038/s41413-026-00524-6","DOIUrl":"https://doi.org/10.1038/s41413-026-00524-6","url":null,"abstract":"Insufficient skeletal repair is the primary threat of health span and lifespan in elders with increasingly vast global burden; yet, to date, the knowledge of resolving this crisis remains limited. In this study, we addressed the specific mechanisms underlying aging-associated poor bone repair, which are driven by the mitochondrial DNA structures mitochondrial G-quadruplex (mtG4). We found that mtG4 is spatiotemporal-wisely accumulated within Pdgfra+ periosteal mesenchymal stromal/stem cells (PPM) both in healthy and premature aging, which substantially increases cellular senescence and the degenerative alterations of PPM. By utilizing transgenic lineage tracking, PPM organoids formation, mitochondrial transgenic mutation, organoids transplantation, and serial cellular molecular investigations, we reveal that mtG4 in PPM restricts vital mitochondrial genes' transcription to cause mitochondrial dysfunction, which utterly leads to severe mitophagy and cell senescence. These senescent PPM demonstrates impaired stemness and disrupted fate determination, finally phenocopying aging-associated poor bone repair. This study decodes the mitochondrial genomic reasons for insufficient bone repair during aging, which offers insights for developing cell-type- and disease-specific senolytic therapies in the future.","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"5 1","pages":""},"PeriodicalIF":12.7,"publicationDate":"2026-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147630406","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":"Bone adhesive with temporally-synchronized degradation for enhanced osteointegration.","authors":"Jun-Ting Gu,Zhi-Ting Li,Yu-Zhu Wang,Dong-Xiao Hao,Gao-Peng Dang,Xiao-Qing Cao,Franklin R Tay,Ji-Hua Chen,Conrado Aparicio,Kai Jiao,Li-Na Niu","doi":"10.1038/s41413-026-00522-8","DOIUrl":"https://doi.org/10.1038/s41413-026-00522-8","url":null,"abstract":"Bone adhesives have emerged as promising alternatives for complex fracture fixation. However, discrepancies between material degradation rates and the physiological timeline of bone healing remain a critical limitation. Here, a polyurethane-based adhesive (TNC) was developed, synthesized from trimeric hexamethylene diisocyanate, nano-hydroxyapatite, and type I collagen. The TNC demonstrates strong initial adhesion to both wet and blood-contaminated bone surfaces and exhibits excellent biocompatibility. A distinguishing feature of TNC is its capacity to synchronize degradation with the stages of bone healing. During degradation, TNC forms a mineralized surface layer that releases calcium ions. The calcium ions activate cathepsin K, an enzyme integral to bone remodeling. This calcium-mediated mechanism accelerates TNC degradation by 1.9-fold during the remodeling phase compared to the initial phase. In a rat skull fracture model, TNC supported effective fracture stabilization and achieved favorable bone regeneration at 8 weeks after implantation. These findings demonstrate that TNC combines early mechanical stability with phase-specific degradability to facilitate bone regeneration in a temporally-controlled manner. The present work provides a framework for the development of bio-responsive bone adhesives that synchronize degradation behavior with healing phases for orthopedic applications.","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"6 1","pages":""},"PeriodicalIF":12.7,"publicationDate":"2026-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147630402","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":"ADAR2 induces the differentiation of osteosarcoma cells by editing activity on IGFBP7: new implications for therapy.","authors":"Michela Rossi,Federica Scotto di Carlo,Jacopo Di Gregorio,Sharon Russo,Laura Di Giuseppe,Giulia Battafarano,Sara Terreri,Olivia Pagliarosi,Domenico Alessandro Silvestris,Marco Corona,Adriano Barra,Marco Pezzullo,Cristiano De Stefanis,Simone Pelle,Pier Francesco Costici,Salvatore Minisola,Jessica Pepe,Franco Locatelli,Fernando Gianfrancesco,Angela Gallo,Andrea Del Fattore","doi":"10.1038/s41413-026-00516-6","DOIUrl":"https://doi.org/10.1038/s41413-026-00516-6","url":null,"abstract":"Osteosarcoma is a highly malignant bone tumor which primarily affects the juvenile population and is characterized by high rate of recurrence and metastasis. RNA editing has emerged as a key process in cancer progression. Herein, we investigated the role of RNA editing enzyme ADAR2 (Adenosine Deaminase Acting on RNA 2) in osteosarcoma. We demonstrated that ADAR2 expression increases during osteoblast differentiation and inversely correlates with the aggressiveness of osteosarcoma cells. Interestingly, the overexpression of ADAR2 in osteosarcoma cell lines reduces their tumoral properties and promotes their differentiation in osteoblast-like cells, as shown by gene expression analysis and mineralization assays. These results were also confirmed by in vivo experiments; indeed, intratibial injection of ADAR2-overexpressing osteosarcoma cells in NSG mice resulted in less aggressive tumors compared to mice injected with pEmpty or pInactive ADAR2 E/A vector-transfected cells. To elucidate the mechanisms by which ADAR2 overexpression induces osteogenic terminal differentiation of osteosarcoma cells, we performed RNA-seq analysis of Saos-2 cells and identified IGFBP7 (Insulin-like Growth Factor Binding Protein 7) as the most highly edited transcript in ADAR2-overexpressing cells. We showed that the editing activity of ADAR2 on IGFBP7 abolishes its proliferative effect on osteosarcoma cells and triggers terminal differentiation. Overall, our results indicate that ADAR2 acts as a tumor suppressor in osteosarcoma and may represent a novel therapeutic target for this aggressive pediatric tumor.","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"195 1","pages":""},"PeriodicalIF":12.7,"publicationDate":"2026-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147599330","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":"Radiomics identifies distinct cortical bone texture alterations in patients with CKD using HR-pQCT","authors":"Youngjun Lee, Seokkyoon Hong, Miran Lee, Choongbeom Seo, Sangjun Park, Kenneth J. Lim, Sharon M. Moe, Stuart J. Warden, Rachel K. Surowiec","doi":"10.1038/s41413-026-00515-7","DOIUrl":"https://doi.org/10.1038/s41413-026-00515-7","url":null,"abstract":"Standard clinical imaging metrics perform poorly in predicting skeletal fragility in chronic kidney disease (CKD), particularly due to the complex and heterogeneous cortical deterioration that characterizes advanced disease. Here, this study aimed to identify radiomic features derived from high-resolution peripheral quantitative computed tomography (HR-pQCT) in tibial cortical bone that distinguish CKD-related differences and may serve as markers of subtle cortical alterations undetected by conventional imaging. HR-pQCT image stacks were obtained from 72 participants (38 non-CKD and 34 with CKD stage 5D) at 7.3% (distal) and 30% (diaphyseal) proximally from the tibial endplate, resulting in a total of 24 192 slices. In non-CKD cases, features were largely derived from first-order statistics, while complex features from higher-order statistics were more prominent in CKD cases. Although conventional HR-pQCT outcomes, such as volumetric bone mineral density, showed limited ability to differentiate CKD from non-CKD cortical bone in our population of stage 5D patients, the top features, such as Minimum and Strength, provided a significant distinction between the two groups (P < 0.001, Effect size r = from 0.813 to 0.856). Our findings demonstrate that radiomic analysis identifies cortical bone differences associated with CKD that were not distinguished by conventional HR-pQCT metrics, highlighting its potential to improve bone quality assessment in this high-risk population.","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"17 1","pages":""},"PeriodicalIF":12.7,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147585937","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}