Calcified Tissue International最新文献

{"title":"Anti-osteoporotic Pharmacotherapy and Muscle Outcomes in Osteosarcopenia: a Source-Verified Translational Evidence Map.","authors":"Dong-Ju Lim, Min Kue Kang","doi":"10.1007/s00223-026-01608-5","DOIUrl":"https://doi.org/10.1007/s00223-026-01608-5","url":null,"abstract":"<p><p>Anti-osteoporotic drugs are increasingly discussed as candidate dual bone-muscle therapies in osteosarcopenia, yet clinical claims often conflate biological plausibility, observational signals, and randomized efficacy. We conducted a source-verified scoping evidence map and translational review, updated through 25 July 2026 using PubMed/MEDLINE, Europe PMC, and citation tracking. Evidence was classified as primary randomized evidence, secondary randomized analysis, observational human evidence, mechanistic/preclinical rationale, or review-level context; quantitative pooling was avoided because no drug-outcome pair had a sufficiently homogeneous randomized evidence base. Denosumab has the most coherent translational rationale through RANKL/RANK/NF-kB signaling, but randomized long-term-care data were neutral for muscle mass, strength, and performance despite bone mineral density improvement. Long-term-care context may reduce anabolic reserve, but a drug-by-exercise interaction remains unproven. Early pamidronate data in severe pediatric burns support prevention of resorption-linked muscle catabolism rather than reversal of established age-related sarcopenia. Bisphosphonates and teriparatide have preclinical or secondary signals; romosozumab and abaloparatide lack direct clinical muscle-efficacy evidence. Nandrolone is retained only as a historical positive control. Future trials should distinguish prevention from reversal and use factorial or rigorously standardized exercise designs with prespecified strength, muscle-mass, physical-performance, and pathway endpoints.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149001402","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}

{"title":"Associations Between Peripheral Blood Inflammatory and Immune Markers and Osteoporotic and Fragility Fractures: A Systematic Review and Meta-Analysis.","authors":"Chenyang Li, Chenbing Zhao, Ruhui Fu, Shangkun Zhong, Qiang Yuan, Peifeng Li, Yanan Fan, Ying Zhang","doi":"10.1007/s00223-026-01606-7","DOIUrl":"10.1007/s00223-026-01606-7","url":null,"abstract":"<p><p>Chronic low-grade inflammation and osteoimmune dysregulation may contribute to skeletal fragility, but evidence across circulating markers and fracture outcomes remains heterogeneous. We evaluated associations between peripheral blood inflammatory or immune markers and osteoporotic or fragility fractures. This PRISMA 2020-compliant systematic review and meta-analysis was registered in PROSPERO (CRD420261441126). Five databases were searched from inception to 25 June 2026. Eligible observational studies evaluated serum, plasma, or whole-blood inflammatory or immune markers in relation to observed osteoporotic, fragility, low-energy, or site-specific fractures. Reported ratio estimates were synthesized within marker-outcome-contrast units using random-effects models, with effect-type sensitivity analyses. Evidence certainty was assessed using GRADE. Forty-eight studies were included. C-reactive protein/high-sensitivity C-reactive protein-related (CRP/hsCRP-related) exposures were associated with hip fracture (pooled ratio estimate 1.39, 95% CI 1.17-1.67) and vertebral fracture (2.16, 95% CI 1.47-3.18). Interleukin-6 was associated with hip fracture (1.40, 95% CI 1.15-1.71), as were tumor necrosis factor-alpha or soluble TNF receptors (1.81, 95% CI 1.34-2.44). Certainty was low. Findings for blood-count-derived indices were less stable, and temporally unclear studies could support only associations with fracture status. Observational evidence supports marker- and site-specific associations, but heterogeneity in design, temporality, populations, bone mineral density adjustment, and covariates precludes causal or established predictive interpretation. These markers should not replace established fracture-risk assessment.Trial registration PROSPERO, CRD420261441126.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149001317","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}

{"title":"Health-Related Quality of Life in Children with X-Linked Hypophosphatemia Treated with Burosumab: Real-World Data from a German-Swiss Study.","authors":"Ineke Böckmann, Martin Klein, Helena Mutze, Mirko Rehberg, Giuseppina Spartà, Katrina Evers, Karl Peter Schlingmann, Markus J Kemper, Annette Richter-Unruh, Dorothee Schmidt, Olaf Hiort, Karina Grohmann-Held, Carmen Schröder, Ute Derichs, Clemens Freiberg, Marcus Weitz, Desiree Dunstheimer, Elmar Schmid, Ulrike John-Kroegel, Oliver Metzing, Sabine Heger, Norbert Jorch, Hagen Staude, Ludwig Patzer, Elke Wühl, Carl-Joachim Partsch, Angela Hübner, Michaela Marx, Christof Land, Norbert Albers, Jens Banzer, Inka Baus, Frauke Wilkening, Kristina Möller, Verena Wagner, Gabriele Krauch, Michaela Gessner, Alexandra Goischke, Maren Leifheit-Nestler, Miroslav Zivicnjak, Dirk Schnabel, Dieter Haffner","doi":"10.1007/s00223-026-01602-x","DOIUrl":"10.1007/s00223-026-01602-x","url":null,"abstract":"<p><p>Burosumab is effective in improving rickets in children with X-linked hypophosphatemia (XLH). Predictors of health-related quality of life (HRQoL) in pediatric XLH patients treated with burosumab are unknown. In this cross-sectional analysis of a prospective binational observational study, we investigated HRQoL in 64 pediatric XLH patients (36 female) on burosumab treatment, using the KIDSCREEN-52 questionnaire and qualitative interviews. Associations between HRQoL and clinical findings were analysed using multiple regression and receiver operating characteristics (ROC) curve analyses. Median age at investigation and duration of burosumab treatment were 13.1 (IQR 10.4; 14.8) and 2.8 (IQR 1.4; 3.8) years, respectively; 54.7% of patients received secondary burosumab treatment following prior active vitamin D and phosphate. Overall, HRQoL scores were comparable to national reference values. Caregivers rated Physical Well-Being, Moods & Emotions, and Bullying lower than the patients themselves. Burosumab dose was significantly associated with Physical Well-Being, Psychological Well-Being, and Self-Perception in self-report, and with total T-values and Physical Well-Being in proxy questionnaires. The duration of prior treatment with active vitamin D and phosphate was significantly associated with the dimension of Autonomy in self-report and proxy reports. A burosumab dosage above 0.6 mg/kg was associated with a good Physical Well-Being (above the mean of the general population) with a sensitivity and specificity of 75% and 70% in self-report, and 67% and 70% in proxy questionnaires, respectively. In this real-world study, HRQoL in burosumab-treated children with XLH was comparable to that of the general population and associated with burosumab dosage.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13582184/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148982047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of Serum Parathyroid Hormone Levels with All-Cause and Cause-Specific Mortality Among U.S. Adults, with a Focus on the Parathyroid Hormone Levels Within the Normal Range: a Population-Based Cohort Study from NHANES 2003-2006.","authors":"Xiao-Chun Cheng, Li-Yuan Mu, Ze Wang, Hao Li, Xiu-Quan Qu, Dong-Li Liu, Shu Li, Bai-Qing Peng, Pu Qiu, Zhi-Yu Jiang, Zhao-Xing Li, Yuan-Yin Xi, Yu-Xuan Huang, Xi-Rui Li, Ling-Quan Kong","doi":"10.1007/s00223-026-01604-9","DOIUrl":"https://doi.org/10.1007/s00223-026-01604-9","url":null,"abstract":"<p><p>This study investigated the correlation between serum parathyroid hormone (PTH) levels and the risks of all-cause and cause-specific mortality, with specific focus on the association between serum PTH levels within the normal range and mortality risk. This prospective cohort study included 6633 non-hypoparathyroid participants (aged ≥ 20 years) from the National Health and Nutrition Examination Survey 2003-2006. We employed restricted cubic splines to depict the dose-response relationship between serum PTH and the risks of mortality. Multivariate Cox proportional hazards models were used to calculate the hazard ratios (HR) and 95% confidence intervals (95%CI). Among the 6633 participants, 1309 died during follow-up, including 437 cardiovascular deaths, 316 cancer-related deaths, and 556 non-cardiovascular-non-cancer deaths. Restricted cubic splines suggested that ideal outcomes were observed with serum PTH at the lower level of the normal range (18-41 pg/ml). Compared with participants in the low-normal PTH range (18-41 pg/ml), those in the high-normal range (42-74 pg/ml, accounting for 40.4% of the entire normal range) had 22% (HR:1.22,95%CI 1.02-1.46) and 66% (HR:1.66,95%CI 1.20-2.30) increased risks of all-cause and cardiovascular mortality. Similarly, participants in the high PTH range (> 74 pg/ml) had 34% (HR:1.34,95%CI 1.08-1.68), 59% (HR:1.59,95%CI 1.03-2.46) and 44% (HR:1.44,95%CI 1.02-2.04) increased risks of all-cause, cardiovascular and non-cardiovascular-non-cancer mortality. Among U.S. adults, high-normal and high PTH levels were both associated with higher risks of all-cause and cardiovascular mortality. Further studies are needed to evaluate the clinical implications of screening and management for this high-risk population, especially those with high-normal PTH levels, who account for a substantial proportion of the normal-range population but are usually receiving insufficient clinical attention.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148982101","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}

{"title":"Sigma Anti-bonding Calcium Attenuates Ovariectomy-Induced Bone Loss by Preserving Trabecular Microarchitecture and Suppressing Osteoclastogenesis.","authors":"Yena Oh, Byong Chul Yoo, Sohee Moon, Sun Moo Rhee, Ha Jin Noh, Donghoon Yoon, Paul K Lee, Alex Lee, Jaehong Lee, Server Bozdogan, Joko Waluyo Saputro, Jong Y Park, Jongsung Lee, Ji Hye Kim, Jae Youl Cho","doi":"10.1007/s00223-026-01605-8","DOIUrl":"https://doi.org/10.1007/s00223-026-01605-8","url":null,"abstract":"<p><p>Estrogen deficiency-induced osteoporosis is characterized by increased bone resorption and progressive deterioration of trabecular microarchitecture, leading to skeletal fragility. This study investigated the effects of sigma anti-bonding calcium (SAC), a formulation designed to enhance ion release, in an ovariectomized (OVX) mouse model and in RANKL-induced osteoclastogenesis in vitro. Female mice underwent OVX and received oral SAC (100 or 200 mg/kg/day) for 13 weeks following surgery. Body and major organ weights were monitored during the experimental period. SAC administration did not significantly affect body or major organ weights under the conditions examined. Micro-computed tomography demonstrated that SAC attenuated OVX-induced trabecular deterioration, as evidenced by preservation of bone mineral density (BMD), partial restoration of trabecular number, and reduction of structural model index, whereas trabecular thickness and separation were minimally affected. Histological analysis further confirmed preservation of trabecular bone area in SAC-treated mice, whereas marrow adiposity assessed by Oil Red O staining was not markedly altered. Serum analysis revealed that SAC significantly reduced OVX-induced elevation of C-terminal telopeptide of type I collagen (CTX), while formation-associated markers did not show consistent recovery. In vitro, SAC suppressed RANKL-induced osteoclast differentiation in RAW264.7 cells without significantly affecting cell viability at the concentrations examined. SAC dose-dependently reduced the mRNA expression of osteoclast-related genes, including TRAP, NFATc1, Ctsk, and Atp6v0d2, and attenuated NFATc1 protein induction. SAC treatment was associated with reduced RANKL-stimulated p38 phosphorylation without changes in total p38 expression and with decreased MITF protein expression. Collectively, these findings indicate that SAC attenuates estrogen deficiency-associated trabecular bone deterioration and suppresses osteoclast differentiation, accompanied by changes in p38 phosphorylation and NFATc1 and MITF expression. These findings support further investigation of SAC as a potential adjunctive approach for attenuating estrogen deficiency-associated bone loss; however, comparative studies with conventional calcium formulations are required to determine whether the observed effects are specific to SAC.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148982052","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}

{"title":"The Liver-Bone Axis in Steatotic Liver Disease.","authors":"Krzysztof Łupina, Adrian Nowak, Anna Romac, Paulina Jaskulska, Weronika Stępień, Aleksandra Kalisz, Kamil Jończyk, Jakub Janczura","doi":"10.1007/s00223-026-01603-w","DOIUrl":"https://doi.org/10.1007/s00223-026-01603-w","url":null,"abstract":"<p><p>Steatotic liver disease (SLD) encompasses a spectrum of conditions, including metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction and alcohol-related liver disease (MetALD), and alcohol-related liver disease (ALD), all of which may have consequences extending beyond the liver. Growing evidence suggests that SLD is associated with impaired skeletal health through a complex liver-bone axis. This review summarizes current evidence linking SLD with reduced bone mineral density, impaired bone quality, osteoporosis, and fracture risk. In MASLD, skeletal vulnerability appears to be heterogeneous and may largely reflect shared metabolic risk factors, fibrosis severity, and sarcopenia rather than hepatic steatosis alone. In contrast, alcohol-related cirrhosis is more consistently associated with clinically important increases in fracture risk and post-fracture mortality. Chronic viral hepatitis may also contribute to adverse bone outcomes, while the mechanisms of coexisting steatosis differ between hepatitis C virus (HCV), particularly genotype 3 infection, and hepatitis B virus (HBV). Several molecular mediators have been implicated in liver-bone interactions, although much of the evidence remains experimental or associative. Clinically, risk-based bone-health assessment may be appropriate in patients with advanced liver disease or additional osteoporosis risk factors. Lifestyle interventions, nutritional support, alcohol cessation, and standard osteoporosis treatment remain central, while therapies simultaneously targeting SLD and skeletal fragility require further prospective evaluation.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148982106","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}

{"title":"Potential Role for the Ubiquitin Ligase SIAH2 in Modulating Bone Morphology and Adiposity.","authors":"Matthew C Scott, Bhaswati Ghosh, Gail Kilroy, Beata Lecka-Czernik, Z Elizabeth Floyd","doi":"10.1007/s00223-026-01596-6","DOIUrl":"10.1007/s00223-026-01596-6","url":null,"abstract":"<p><p>Marrow adipose expansion, with obesity or ageing, increases fracture risk. Skeletal stem cells can commit to osteoblast or adipocyte endpoints, an inverse relationship influenced by peroxisome proliferator-activated receptor gamma (PPARγ). Seven in absentia homologue 2 (SIAH2) is a ubiquitin ligase that acts in peripheral adipose tissue stromal progenitors, promoting PPARγ activity and adipogenesis. The pivotal role of PPARγ in bone marrow adipose tissue accumulation prompted us to evaluate SIAH2's role in the balance between osteogenesis and adipogenesis. Using adherent skeletal stem and/or progenitor cells (SSPCs) isolated from the marrow of wild-type (WT) and Siah2^-/- mice, we assessed in vitro osteogenic and adipogenic capacity. Bone morphology and adiposity were assessed, in vivo, using WT and Siah2^-/- mice in the context of dietary, high-fat diet, and pharmacological, rosiglitazone, PPARγ stimulation. We hypothesized increased osteogenesis in Siah2^-/- SSPCs and expected Siah2^-/- mice would be resistant to the effects of PPARγ activation on trabecular morphology and marrow fat expansion. Our results show that Siah2^-/- SSPCs display increased capacity for both osteogenesis and adipogenesis in vitro. Further, exploratory experiments in vivo indicate Siah2^-/- mice have fewer, yet thicker, trabeculae on a low fat diet, while Siah2^-/- mice on a high-fat diet paired with rosiglitazone trend toward more marrow adipose, decreased bone mass and increased trabecular spacing compared to WT. Our results suggest SIAH2 moderates both osteogenic and adipogenic commitment as the absence of SIAH2 results in progenitor cells that will more readily commit to either outcome. These observations underscore SIAH2's context-specific modulatory effects on PPARγ activities determined by tissue, nutrients and pharmacological cues.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13569602/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148944186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SERPINE1/PAI-1 in Skeletal Degeneration: A Proposed Context-Dependent Framework for Bone Remodeling Regulation.","authors":"Hang Liu, Dengbo Yao, Yu Wang, Qingquan Kong","doi":"10.1007/s00223-026-01598-4","DOIUrl":"https://doi.org/10.1007/s00223-026-01598-4","url":null,"abstract":"<p><p>SERPINE1 encodes plasminogen activator inhibitor-1 (PAI-1), a key inhibitor of tissue-type and urokinase-type plasminogen activators. Beyond fibrinolysis, PAI-1 participates in extracellular matrix remodeling, cellular senescence, inflammatory amplification, fibrosis-like repair, metabolic stress responses, and bone-cell coupling. These processes are central to osteoporosis, osteoarthritis, and intervertebral disc degeneration, yet the role of SERPINE1/PAI-1 in skeletal tissues is highly context dependent. In osteoporosis, excessive PAI-1 activity is mainly associated with impaired osteogenesis, osteoblast-lineage senescence, defective repair, and bone loss. In osteoarthritis, PAI-1 shows a context-dependent role: persistent elevation may promote chondrocyte senescence and maladaptive matrix remodeling, whereas experimental loss-of-function studies suggest that PAI-1 may protect cartilage in specific settings by restraining excessive plasmin-MMP-mediated degradation. In intervertebral disc degeneration, emerging evidence links SERPINE1 expression and PAI-1 activity to nucleus pulposus cell senescence, fibrosis-like extracellular matrix remodeling, oxidative/metabolic stress, and matrix dysregulation. This review synthesizes current evidence and proposes a testable conceptual framework in which SERPINE1/PAI-1 may function as a stress-responsive remodeling rheostat rather than as a uniformly pathogenic or protective factor. From a translational perspective, SERPINE1/PAI-1 is unlikely to serve as a stand-alone diagnostic biomarker or a target for uniform systemic inhibition. Instead, its clinical value may lie in molecular stratification, identification of disease-stage- and compartment-specific endotypes, and locally targeted modulation of pathogenic downstream programs. Future studies should integrate spatial multi-omics, time-resolved disease models, human cohort validation, and tissue-specific delivery strategies to determine when SERPINE1/PAI-1 is therapeutically actionable in skeletal degeneration.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148944162","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}

{"title":"Dietary Protein and the Risk of Mortality in Adults with Low Bone Mineral Density: A Longitudinal Study.","authors":"Si-Qi Liu, Bing Wang, Hong Wei, Hong-Zhen Du, Jing Yang, Qi Zeng, An-Qi Fu, Zeng-Ning Li, Li-Qiang Qin, Khemayanto Hidayat","doi":"10.1007/s00223-026-01592-w","DOIUrl":"https://doi.org/10.1007/s00223-026-01592-w","url":null,"abstract":"<p><p>Low bone mineral density (BMD) is common in older adults and is associated with increased mortality risk. Although higher protein intake is recommended for skeletal health, it remains unclear whether total protein intake or protein source is more relevant for mortality risk. We examined associations of dietary protein quantity and source with mortality risk among adults with low BMD. Data from 4148 adults aged ≥ 40 years with osteopenia or osteoporosis who participated in six National Health and Nutrition Examination Survey cycles from 2007 to 2008 through 2017-2018 were analyzed. Survey-weighted estimates indicated a mean age of 58.1 years, a female proportion of 65.0%, and mean total protein intake, animal protein density, and plant protein density of 1.04 g/kg/day, 18.5 g/1000 kcal, and 6.0 g/1000 kcal, respectively. Protein intake was assessed using two 24-hour dietary recalls. Total protein was expressed as g/kg/day, and animal and plant protein as energy-adjusted densities (g/1000 kcal). Mortality outcomes were ascertained via linkage to the National Death Index. Associations with all-cause and cause-specific mortality risk were estimated using survey-weighted Cox proportional hazards models. Cross-sectional associations with BMD were also evaluated. Over a median follow-up of 6.7 years, 578 deaths occurred. Total protein intake was not associated with the risk of all-cause mortality (HR per 0.1 g/kg/day: 1.00; 95% CI 0.96-1.05). Higher plant protein density was associated with a lower risk of all-cause mortality (HR per 10 g/1000 kcal: 0.72; 95% CI 0.55-0.95), whereas animal protein density was not (HR: 0.94; 95% CI 0.84-1.06). Plant protein density also showed evidence of an inverse association with the risk of cardiovascular mortality, but not with the risk of cancer mortality. Cross-sectionally, both animal and plant protein densities were positively associated with femoral neck BMD, whereas no association was observed for lumbar spine BMD. In adults with low BMD, mortality risk differed by protein source rather than total intake, with higher plant protein density associated with lower risk of all-cause mortality and showing evidence of an inverse association with the risk of cardiovascular mortality.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148886019","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}

{"title":"AI for Opportunistic Identification of BMD and Bone Microarchitecture: A Narrative Review.","authors":"Katharina Ziegeler, Sharmila Majumdar","doi":"10.1007/s00223-026-01597-5","DOIUrl":"https://doi.org/10.1007/s00223-026-01597-5","url":null,"abstract":"<p><p>Artificial intelligence (AI) has rapidly transformed the potential for opportunistic assessment of bone mineral density (BMD) and bone microarchitecture from routinely acquired imaging. This narrative review synthesizes recent advances across radiography, computed tomography (CT), and magnetic resonance imaging (MRI), focusing on AI-driven methods for automatic extraction of bone quality markers. In radiography, convolutional and transformer-based architectures achieve near-DXA precision by integrating regional texture and clinical features. In CT, deep learning pipelines combining segmentation and end-to-end regression now enable scalable volumetric BMD and trabecular texture analysis, with correlations of approximately 0.8-0.9 versus reference techniques and near-perfect agreement with dedicated quantitative CT. MRI-based methods, leveraging fat-water signal ratios and textural radiomics, increasingly provide surrogate markers of bone integrity. Barriers to clinical translation include interoperability with existing systems, lack of reimbursement frameworks, and limited explainability of black-box models. Emerging foundation models (e.g., SAM, BiomedCLIP) and synthetic imaging networks promise cross-modality generalization. Future work must focus on regulatory validation, model drift surveillance, and equitable deployment to ensure AI-based opportunistic osteoporosis screening improves outcomes across diverse populations.</p>","PeriodicalId":9601,"journal":{"name":"Calcified Tissue International","volume":"117 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148879011","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}