Bone最新文献

{"title":"Higher carboxylated osteocalcin is an independent predictor of improved femoral bone strength: A cross-sectional study","authors":"Deepti K. Sharma ,&nbsp;Rebecca Bahnisch ,&nbsp;Christopher G. Schultz ,&nbsp;Manuela Rogers ,&nbsp;Chloe Furst ,&nbsp;Lucian Bogdan Solomon ,&nbsp;Stuart A. Callary ,&nbsp;Boopalan Ramasamy","doi":"10.1016/j.bone.2025.117610","DOIUrl":"10.1016/j.bone.2025.117610","url":null,"abstract":"<div><div>Carboxylated osteocalcin (cOC), produced during post-translational modification of osteocalcin (OC) in a vitamin K-dependent pathway, has a high affinity for calcium and hydroxyapatite. Despite the observed link between vitamin K deficiency and fracture risk, supplementation studies have not consistently demonstrated improvements in bone mineral density (BMD) or bone microarchitecture, though studies have reported improvement in cOC status. We hypothesise that these inconsistent findings are due to the lack of knowledge on the mechanisms by which cOC affects bone health. Hence, the aim of this study was to investigate the relationship between cOC and bone turnover markers, cortical and trabecular bone microarchitecture and strength. Forty-five patients who underwent hip arthroplasty for hip osteoarthritis were prospectively recruited. Patients with conditions or medications that could affect bone outcomes were excluded and intra-operative bloods and bone biopsies were collected. Cortical thickness and hip strength was measured with dual-energy X-ray absorptiometry and micro-computed tomography was used to determine trabecular bone microarchitecture. Cortical thickness, cross-sectional area, cross-sectional moment of inertia, femoral neck width and section modulus correlated positively with cOC (<em>p</em> &lt; 0.05, all). There was no association between partially or fully un-carboxylated fractions and hip strength variables. Further, cOC was found to be an independent predictor of bone alkaline phosphastase while the partially or fully un-carboxylated OC predicted c-terminal telopeptide of type 1 collagen. In conclusion, higher cOC concentrations were associated with improved femoral bone strength, and the effect is possibly mediated through higher bone mineralisation, independent of age, parathyroid hormone, kidney function, BMD and physical activity.</div></div>","PeriodicalId":9301,"journal":{"name":"Bone","volume":"200 ","pages":"Article 117610"},"PeriodicalIF":3.6,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144908297","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":"Biological age acceleration predicts osteoporosis and reduced longevity in a large prospective cohort","authors":"Rui Zhang ,&nbsp;Wanyang Zhong ,&nbsp;Yuelan Gao ,&nbsp;Xingxiang Duan ,&nbsp;Qingsong Ye","doi":"10.1016/j.bone.2025.117609","DOIUrl":"10.1016/j.bone.2025.117609","url":null,"abstract":"<div><h3>Background</h3><div>Osteoporosis is a major age-related musculoskeletal condition, yet chronological age does not fully capture individual risk. Biological age acceleration (BAA), as a biomarker of systemic aging, may offer greater predictive value for osteoporosis and lifespan loss.</div></div><div><h3>Methods</h3><div>We analyzed data from 293,224 participants in the UK Biobank cohort who were free of osteoporosis at baseline. BAA was estimated using two validated models—Klemera-Doubal Method Biological Age (KDM-BA) and PhenoAge. Polygenic risk scores (PRS) were used to account for genetic susceptibility. Multivariable Cox models examined associations of BAA and PRS with incident osteoporosis and all-cause mortality.</div></div><div><h3>Results</h3><div>Over a median follow-up of 8.5 years, 9780 participants developed osteoporosis. Each one standard deviation (SD) increase in KDM-BA and PhenoAge acceleration was associated with a 22.6 % (95 % CI: 1.11, 1.36) and 19.3 % (95 % CI: 1.12, 1.36) higher risk of osteoporosis, respectively. Participants in the highest tertile of BAA had a 38–43 % increased risk compared to those in the lowest tertile. Individuals with both high BAA and high PRS had nearly threefold higher osteoporosis risk, indicating a strong additive effect. Accelerated aging was also linked to a 1.3–1.8-year reduction in life expectancy at age 45, independent of osteoporosis status.</div></div><div><h3>Conclusion</h3><div>Accelerated biological aging is an independent predictor of osteoporosis and premature mortality. Integration of BAA into clinical assessment could enhance early identification of at-risk individuals and support aging-targeted interventions for skeletal health.</div></div>","PeriodicalId":9301,"journal":{"name":"Bone","volume":"200 ","pages":"Article 117609"},"PeriodicalIF":3.6,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144852727","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":"Mortality and fracture risk in children with osteogenesis imperfecta: Results from the French nationwide hospital discharge database","authors":"Cécile Philippoteaux ,&nbsp;Christine Lefevre ,&nbsp;Chloé Saint-Dizier ,&nbsp;Julien Paccou ,&nbsp;Emmanuel Chazard","doi":"10.1016/j.bone.2025.117607","DOIUrl":"10.1016/j.bone.2025.117607","url":null,"abstract":"<div><h3>Introduction</h3><div>Osteogenesis imperfecta (OI) is a rare genetic disorder causing bone fragility and recurrent fractures. Few studies have assessed its burden using health claims data. This study evaluated immediate and long-term mortality and fracture risk in children with OI.</div></div><div><h3>Methods</h3><div>This historical cohort included children with a first inpatient stay recording an OI diagnosis, from the French nationwide hospital discharge database (2014–2022). Children born before 2014 were excluded. Based on age at index stay, patients were classified as newborns (≤1 month), infants (&gt;1–&lt;24 months), or children (≥2 years). Immediate mortality (during the index stay or after same-day transfer) and long-term mortality were analyzed along with fracture risk using descriptive statistics, Kaplan-Meier estimates, and Cox models.</div></div><div><h3>Results</h3><div>A total of 658 patients (5849 stays) were included (mean age 1.59 years): 30.2 % were newborns, 18.1 % infants, and 51.7 % children. Seventy-nine children (12.0 %) died, with immediate mortality higher in newborns (30.2 %) than infants (8.4 %) and children (0.9 %) (<em>p</em> &lt; 0.001). Stillbirth accounted for 69.9 % of deaths. Six-month survival for newborns was 68.3 % (95 % CI [62.2–75.1]). At index stay, 146 patients (22.2 %) had fractures, mainly femoral (50.7 %). During follow-up, 17.9 % presented a high fracture rate (&gt;0.5/year). 46.9 % of patients were high care users (≥1 stay/year).</div></div><div><h3>Conclusion</h3><div>Newborns with OI face significantly higher immediate and long-term in-hospital mortality than infants and children, and 126 times higher than that of the general population. Mortality remained stable post-2017 despite national guidelines. A quarter of patients had fractures at index stay, half of which involved the femur.</div></div>","PeriodicalId":9301,"journal":{"name":"Bone","volume":"200 ","pages":"Article 117607"},"PeriodicalIF":3.6,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144842833","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":"Corrigendum to “Transforming growth factor, beta-2 gene mutation causes autosomal dominant Camurati-Engelmann disease, type 2 (OMIM % 606631)” [Bone 197 (2025) 117477]","authors":"Steven Mumm ,&nbsp;José L. Paz-Ibarra ,&nbsp;Philippe M. Campeau ,&nbsp;Elizabeth Garrido-Carrasco ,&nbsp;Jonathan C. Baker ,&nbsp;Ethel Pino-Nina ,&nbsp;Shenghui Duan ,&nbsp;William H. McAlister ,&nbsp;Michael P. Whyte","doi":"10.1016/j.bone.2025.117573","DOIUrl":"10.1016/j.bone.2025.117573","url":null,"abstract":"","PeriodicalId":9301,"journal":{"name":"Bone","volume":"200 ","pages":"Article 117573"},"PeriodicalIF":3.6,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144801230","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":"An underdiagnosed manifestation: Mandibular bone loss in primary hyperparathyroidism","authors":"Burcak Cavnar Helvaci ,&nbsp;Meltem Horoz ,&nbsp;Ceren Karacalik Unver ,&nbsp;Aysegul Cavnar ,&nbsp;Sema Hepsen ,&nbsp;Burcu Candemir ,&nbsp;Bekir Ucan ,&nbsp;Huseyin Demirci ,&nbsp;Erman Cakal","doi":"10.1016/j.bone.2025.117598","DOIUrl":"10.1016/j.bone.2025.117598","url":null,"abstract":"<div><h3>Introduction</h3><div>Primary hyperparathyroidism (PHPT) is a metabolic bone disorder characterized by elevated parathyroid hormone (PTH) levels, leading to decreased bone mineral density and increased risk of osteoporosis. While oral manifestations are frequently reported, mandibular bone loss and its relationship with systemic bone health remain inadequately characterized. This study aimed to investigate mandibular bone loss in PHPT patients and its association with osteoporosis.</div></div><div><h3>Materials and methods</h3><div>In this single-center, case-control study, 226 participants (111 PHPT patients and 115 age- and sex-matched healthy controls) were enrolled. Clinical, laboratory, and imaging data were collected, including panoramic radiographs to assess mandibular bone loss using the Parathyroid Mandibular Index (PMI) and the Klemetti Index (KI). Dual-energy X-ray absorptiometry (DXA) was used to assess bone mineral density and diagnose osteoporosis. Correlation and logistic regression analyses were performed to explore associations between mandibular indices and osteoporosis.</div></div><div><h3>Results</h3><div>PHPT patients had significantly lower PMI values and more advanced KI categories compared to controls, indicating greater mandibular bone loss. Also, in the PHPT group, patients with osteoporosis had worse PMI and KI values than those without osteoporosis. Correlation analysis showed that PMI scores positively correlate with skeleton t scores. Multivariate logistic regression analysis identified PMI as an independent predictor for osteoporosis in PHPT patients.</div></div><div><h3>Conclusion</h3><div>Mandibular bone loss, particularly indicated by lower PMI values, is a potential early marker for osteoporosis in PHPT patients. To our knowledge, our study is one of the first to highlight the significance of mandibular bone loss in PHPT patients and its correlation with osteoporosis. Routine panoramic radiographs, commonly obtained in dental practice, could provide valuable adjunctive information for osteoporosis risk assessment in this population.</div></div>","PeriodicalId":9301,"journal":{"name":"Bone","volume":"200 ","pages":"Article 117598"},"PeriodicalIF":3.6,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144779993","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":"Prevalent vertebral fracture is associated with incident cardiovascular disease events in older individuals referred for bone densitometry","authors":"John T. Schousboe ,&nbsp;Barret A. Monchka ,&nbsp;J. Michael Davidson ,&nbsp;Douglas Kimelman ,&nbsp;Syed Zulqarnain Gilani ,&nbsp;Zaid Ilyas ,&nbsp;Siobhan Reid ,&nbsp;Joshua R. Lewis ,&nbsp;William D. Leslie","doi":"10.1016/j.bone.2025.117601","DOIUrl":"10.1016/j.bone.2025.117601","url":null,"abstract":"<div><h3>Background</h3><div>It is unknown if prevalent vertebral fracture (PVFx) captured on bone density vertebral fracture assessment (VFA) images predicts incident CVD events.</div></div><div><h3>Methods</h3><div>11,760 individuals (mean [SD] age 75.7 [6.8] years, 94 % female) had VFA contemporaneously with bone densitometry in Manitoba, Canada, between February 2010 and December 2017, of whom 1919 (16.3 %) had ≥1 PVFx. This cohort was followed over a mean (SD) 3.8 (2.3) years for Major Adverse Cardiovascular Events (MACE, composite of hospitalization for myocardial infarction, non-hemorrhagic stroke, or all-cause mortality) and other CVD events (hospitalization for coronary artery disease, congestive heart failure, peripheral vascular disease, or coronary bypass/stenting). Proportional hazards models were used to estimate hazard ratios (HR) for incident MACE and other CVD events in those with compared to those without PVFx.</div></div><div><h3>Results</h3><div>Adjusted for age and sex, those with PVFx had HR for incident MACE of 1.34 (95 % C·I. 1.19, 1.51), hospitalization for myocardial infarction (HR 1.35, 95 % C.I. 1.02, 1.79), all-cause mortality (HR 1.36, 95 % C.I, 1.19, 1.56), and other CVD events (HR 1.40, 95 % C.I. 1.21, 1.61). These associations were only slightly attenuated with further adjustment for prior CVD disease and additional CVD risk factors.</div></div><div><h3>Conclusion</h3><div>Prevalent vertebral fracture identified on VFA images in routine clinical practice is robustly associated with incident MACE, independent of other risk factors including AAC which can be simultaneously ascertained on the same images. VFA may have utility for prediction of fractures and CVD outcomes via ascertainment of both prevalent vertebral fracture and AAC.</div></div>","PeriodicalId":9301,"journal":{"name":"Bone","volume":"200 ","pages":"Article 117601"},"PeriodicalIF":3.6,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144779994","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":"Comparison of in vitro and ex vivo osteogenic efficacy of fucoidans extracted from three brown macroalgae of the Pacific Ocean","authors":"Jessica S. Landeros-Juárez ,&nbsp;Brenda Iduarte-Frias ,&nbsp;Enrique Hernández-Garibay ,&nbsp;Eréndira Olvera Félix ,&nbsp;Rodrigo Beas-Luna ,&nbsp;M. Nomura ,&nbsp;Pierrick G.J. Fournier ,&nbsp;Patricia Juárez","doi":"10.1016/j.bone.2025.117606","DOIUrl":"10.1016/j.bone.2025.117606","url":null,"abstract":"<div><div>Brown macroalgae possesses bioactive compounds including fucoidan, a sulfated polysaccharide that can affect bone cells based on its origin and composition. This study examined the potential of fucoidan isolated from three macroalgal species — <em>Macrocystis pyrifera</em>, <em>Sargassum muticum</em>, and <em>Undaria pinnatifida</em> — to modulate the bone remodeling process and evaluated their comparative effectiveness. Fucoidans were extracted under acidic media, and chemically and structurally characterized before comparing their bioactivity on bone cells at different stages. Fucoidans moderately decreased the survival of progenitor cells in a concentration-dependent manner, demonstrating their minimal toxicity to the cells. All fucoidans enhanced the mineralization of preosteoblast MC3T3-E1 or mouse bone marrow cells (BMCs), particularly at higher concentrations. While low concentrations of fucoidans stimulated osteoclastogenesis, higher concentrations inhibited osteoclast formation which could be due to a reduction in the RANKL/OPG ratio as indicated by gene expression analysis. Furthermore, in a 3D <em>ex vivo</em> calvaria culture, fucoidans increased the new bone formation area in a concentration-dependent manner. Although all three fucoidans showed comparable bioactivities, the fucoidan from <em>U. pinnatifida</em> was the most effective.</div><div>We found that fucoidans from marine algae can enhance bone growth and osteoclastogenesis depending on concentration. These findings suggest a dual biological activity in bone remodeling and highlight the need for <em>in vivo</em> studies to confirm their therapeutic potential for bone-loss diseases.</div></div>","PeriodicalId":9301,"journal":{"name":"Bone","volume":"200 ","pages":"Article 117606"},"PeriodicalIF":3.6,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144801229","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":"Osteoclasts in osteoradionecrosis: Pathogenic mechanisms and emerging therapies","authors":"Feng Li ,&nbsp;Xinyuan Liu ,&nbsp;Anne-Laure Vandevelde ,&nbsp;Yao Gao ,&nbsp;Jeroen Van Dessel ,&nbsp;Yi Sun ,&nbsp;Robin Willaert","doi":"10.1016/j.bone.2025.117605","DOIUrl":"10.1016/j.bone.2025.117605","url":null,"abstract":"<div><div>Osteoradionecrosis (ORN) is a severe complication of radiation therapy characterized by impaired bone repair and regeneration, disrupting the delicate balance between osteoclast-mediated bone resorption and osteoblast-driven bone formation. Despite significant research, the intricate pathological mechanisms underlying ORN remain incompletely understood. Notably, while radiation therapy generally inhibits the function of most cells in bone tissue, its specific activation of osteoclasts is a key feature of ORN. Recent findings emphasize the pivotal role of excessive osteoclast activity in driving ORN progression.</div><div>This review provides a comprehensive exploration of osteoclast adaptations within the unique bone microenvironment of ORN, shaped by hypoxia, immune dysfunction, and bacterial infections. It delves into the cellular stress responses—including oxidative stress, metabolic reprogramming, autophagy, and iron regulation—that further influence osteoclast function in ORN. By integrating these insights, we evaluate current therapeutic approaches and propose innovative osteoclast-targeted strategies to mitigate ORN. Through this synthesis of emerging evidence, the review sheds light on the complex interplay of factors contributing to ORN pathogenesis and highlights promising avenues for prevention and treatment, offering hope for improved clinical outcomes.</div></div>","PeriodicalId":9301,"journal":{"name":"Bone","volume":"200 ","pages":"Article 117605"},"PeriodicalIF":3.6,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144796312","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":"Corrigendum to “Metabolism-epigenetic interaction-based bone and dental regeneration: From impacts and mechanisms to treatment potential” [Bone 192 (2025) 117382]","authors":"Xinyi Chen ,&nbsp;Xiaoyuan Huang ,&nbsp;Xiatong Zhang ,&nbsp;Zhuo Chen","doi":"10.1016/j.bone.2025.117602","DOIUrl":"10.1016/j.bone.2025.117602","url":null,"abstract":"","PeriodicalId":9301,"journal":{"name":"Bone","volume":"200 ","pages":"Article 117602"},"PeriodicalIF":3.6,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144769449","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":"Moderate-intensity exercise attenuates bone loss in hyperuricemic nephropathic mice","authors":"Liang Chen ,&nbsp;Rong Xie ,&nbsp;Zuxi Cen ,&nbsp;Jun Zou ,&nbsp;Buping Liu ,&nbsp;Gang Liu ,&nbsp;Ying Zhang ,&nbsp;Yu Yuan ,&nbsp;Lin Yang","doi":"10.1016/j.bone.2025.117603","DOIUrl":"10.1016/j.bone.2025.117603","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Hyperuricemia (HUA) is an independent risk factor for chronic kidney disease (CKD) and can lead to hyperuricemic nephropathy (HN) with skeletal disorders and bone loss. Exercise, as a non-pharmacologic intervention, has potential value in improving bone health and slowing disease progression. However, the protective effect of exercise on HN-induced bone loss and its mechanism has not been clarified. This study aims to investigate the effects of moderate-intensity exercise on renal injury and bone microstructure in HN mice.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Method&lt;/h3&gt;&lt;div&gt;Thirty-two 5-week-old C57BL/6 mice were randomly divided into blank control (CON), model (HUA), exercise blank control (EX-CON), and exercise model (EX-HUA) groups. The HN model was induced by gavage of potassium oxalate (300 mg/kg) and adenine (75 mg/kg) in the HUA and EX-HUA groups. The EX-CON and EX-HUA groups were subjected to 8 weeks of moderate-intensity exercise. At the end of the experiment, serum levels of uric acid, creatinine, and urea nitrogen, as well as inflammatory factors and uric acid excretion factors in renal tissues, were detected, and then the pathological changes in the kidneys were assessed by HE staining, and the microstructures of the bones were assessed and analyzed by micro-CT, HE staining and TRAP staining. The expression of osteogenic factors (ALP, RUNX2) and bone resorption factors (MMP9, NFATC1) were detected by qPCR, Western blotting, and immunofluorescence.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Result&lt;/h3&gt;&lt;div&gt;Compared with the CON group, mice in the HUA group showed significantly higher serum uric acid levels, lower levels of creatinine and urea nitrogen, and pathological changes in the kidneys, such as vacuolar degeneration, nuclear detachment, and tubular atrophy. After the exercise intervention, the uric acid level of the EX-HUA group was significantly reduced, the renal function indexes were improved, and the renal pathological damage was reduced. Micro-CT results showed that the bone quality, bone density, trabecular tissue volume, trabecular number, trabecular connectivity, and trabecular thickness of the HUA group were significantly decreased, and trabecular separation was increased, whereas the exercise intervention significantly improved these bone microstructural parameters. In addition, the mRNA and protein expression levels of bone-forming factors (ALP, RUNX2) were significantly reduced in the HUA group, while the expression levels of bone resorption factors (MMP9, NFATC1) were significantly increased, and exercise intervention reversed these changes.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusion&lt;/h3&gt;&lt;div&gt;hyperuricemic nephropathy leads to deterioration of bone microarchitecture, dysregulation of the balance between bone formation and bone resorption, and consequent bone loss. In contrast, moderate-intensity exercise improves renal function and regulates the balance of osteogenic-osteoclastogenic cytokines, thereby attenuating renal injury and bone lo","PeriodicalId":9301,"journal":{"name":"Bone","volume":"200 ","pages":"Article 117603"},"PeriodicalIF":3.6,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144757983","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}