JBMR Plus最新文献

{"title":"Is direct oxidative damage of bone collagen associated with poor human cortical bone tissue fracture resistance?","authors":"Daniel Y Dapaah, Shoutaro Arakawa, Gwennyth A Carroll, Yiran Wang, Stewart McLachlin, Mitsuru Saito, Thomas L Willett","doi":"10.1093/jbmrpl/ziag152","DOIUrl":"10.1093/jbmrpl/ziag152","url":null,"abstract":"<p><p>The limitations of clinical X-ray-based tools and fracture risk assessment tools, such as FRAX, particularly for disease groups, including type 2 diabetes (T2D) and CKD, suggest that important determinants of bone fracture resistance are not assessed. One such determinant is the bone collagen network, whose nativity and connectivity contribute to cortical bone fracture resistance, but whose degradation mechanisms remain unclear. Oxidative damage to the collagen network, driven by oxidative stress, has been proposed as a contributing factor. Two pathways are recognized: an indirect pathway involving glycoxidation and advanced glycation end-product formation, examined in a precursor study, and a direct pathway, examined herein, involving protein fragmentation and amino acid side chain modifications, such as carbonylation. To investigate the direct pathway, bulk collagen carbonyl content (measured using a fluorescence-based assay and normalized to collagen content) and intact collagen α-chain content (the opposite of α-chain fragmentation and measured via α-chain band intensities using gel electrophoresis) were quantified ex vivo using cortical bone specimens from 80 human donors with and without T2D and/or CKD. Relationships with fracture toughness and other bone quality measures from a precursor study were assessed using Spearman correlations and multiple linear regression. Bulk collagen carbonyl content was not directly associated with collagen network connectivity or cortical bone fracture toughness. In contrast, intact collagen α-chain content emerged as an independent explanatory variable for stable crack-growth fracture toughness measures (adj-<i>R</i> ² = 46.3%, <i>p</i> = .028) and was negatively associated with bulk collagen carbonyl content (<i>r</i> = -0.37, <i>p</i> < .001). These findings suggest that collagen α-chain integrity may provide insight into variation in cortical bone fracture resistance, whereas bulk collagen carbonyl content did not support the hypothesized direct oxidative damage pathway in this donor cohort.</p>","PeriodicalId":14611,"journal":{"name":"JBMR Plus","volume":"10 10","pages":"ziag152"},"PeriodicalIF":3.0,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13615536/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149060914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Response to Letter to the Editor on \"Romosozumab for the treatment of thalassemia-associated osteoporosis in two female patients\".","authors":"Maria P Yavropoulou, Maria-Evangelia Koloutsou, Polyxeni Delaporta, Polyzois Makras, Athanasios D Anastasilakis, Eva Kassi, Antonis Kattamis, Paraskevi Xekouki","doi":"10.1093/jbmrpl/ziag109","DOIUrl":"10.1093/jbmrpl/ziag109","url":null,"abstract":"","PeriodicalId":14611,"journal":{"name":"JBMR Plus","volume":"10 9","pages":"ziag109"},"PeriodicalIF":3.0,"publicationDate":"2026-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13455606/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148706660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histological and molecular characterization of bone integrity in osteogenesis imperfecta: a case series across genetic subtypes.","authors":"Zhiming Wu, Suzanne den Haan, Helen E King, Wouter H Nijhuis, Harrie Weinans, Anne J Spaans, Ralph Sakkers, Kelly Warmink","doi":"10.1093/jbmrpl/ziag111","DOIUrl":"10.1093/jbmrpl/ziag111","url":null,"abstract":"<p><p>Osteogenesis imperfecta (OI) is a genetically heterogeneous skeletal disorder characterized by bone fragility and variable clinical severity. However, how molecular defects translate into alterations of bone microstructure and composition across OI subtypes remains incompletely understood. In this case series, we systematically evaluated cortical bone integrity in patients with OI types 1, 3, 4, 6, 8, and 14 using histological and molecular approaches, including Raman spectroscopy, and compared findings with non-OI controls. Histological analyses revealed case-specific disruption of bone architecture across OI cases, where the severity of bone disorganization increased progressively from OI type 1 to types 3, 6, 8, and 14. In addition osteocyte lacunar area (Ot.Lc.Ar) was increased specifically in OI subtypes 1, 6, 8, and 14 bones, while osteocyte lacunar appearance was heterogeneous in size, shape, alignment, and spatial distribution in OI types 3, 6, 8, and 14, underscoring the case-specific alterations. Consistently, polarized light microscopy demonstrated increased green birefringence under polarized light microscopy in OI types 1 and 14 and reduced lamellar thickness in OI types 1, 6, and 8. At the molecular level, Raman spectroscopic analyses showed reduced mineral and organic matrix signals in OI bone, specifically OI type 3, indicating compromised mineralization and altered bone matrix composition. Together, these findings illustrate the potential that OI bone phenotype illustrates potential subtype-specific trends in bone microarchitecture, collagen disorganization, impaired lamellar bone formation, and deficits in bone mineral and matrix composition. This integrative analysis links genetic defects in collagen-related and non-collagen genes to multiscale alterations in bone tissue, providing mechanistic insight into OI pathophysiology and highlighting potential structural targets for individualized therapeutic strategies.</p>","PeriodicalId":14611,"journal":{"name":"JBMR Plus","volume":"10 8","pages":"ziag111"},"PeriodicalIF":3.0,"publicationDate":"2026-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13411277/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148619965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigating the interrelationship of vitamin K and vitamin D status on bone density: results from the VITamin D and OmegA-3 TriaL.","authors":"Sharon H Chou, Sarah L Booth, Nancy R Cook, Eunjung Kim, Gregory Kotler, Xueyan Fu, Julie E Buring, JoAnn E Manson, Meryl S LeBoff","doi":"10.1093/jbmrpl/ziag110","DOIUrl":"10.1093/jbmrpl/ziag110","url":null,"abstract":"<p><p>Sufficient intake of both vitamin D and K may be necessary for bone health. Although the synthesis of osteocalcin (OC) is stimulated by vitamin D, OC needs to be carboxylated, or activated, by vitamin K to deposit calcium into bone. In the VITamin D and OmegA-3 TriaL (VITAL), there were no differences in 2-yr changes in areal BMD (aBMD) at the spine, hip, or whole body in 771 U.S. participants (687 with follow-up data) randomized to supplemental vitamin D₃ (2000 IU/d) vs placebo. In this ancillary study, we investigated whether baseline vitamin K status was associated with changes in bone density and structure and whether baseline vitamin K status modified the effects of supplemental vitamin D on aBMD changes. Higher baseline vitamin K status, as assessed by blood levels of phylloquinone, percent undercarboxylated OC, and dephosphorylated undercarboxylated matrix Gla protein, was not associated with favorable 2-yr changes in aBMD at the spine, hip, or whole body as assessed by DXA, trabecular bone score, or volumetric BMD (vBMD) and bone architecture outcomes at the radius and tibia as assessed by peripheral QCT. The effects of supplemental vitamin D on aBMD were not modified by baseline measures of vitamin K. In VITAL, higher vitamin K status, even when accompanied by supplemental vitamin D, did not prevent bone loss. Clinical Trial Registration No.: NCT04573946 (ClinicalTrials.gov).</p>","PeriodicalId":14611,"journal":{"name":"JBMR Plus","volume":"10 8","pages":"ziag110"},"PeriodicalIF":3.0,"publicationDate":"2026-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13411269/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148620019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intensive, interdisciplinary pain treatment in fibrous dysplasia/McCune-Albright syndrome.","authors":"Camryn Berry, Edin Randall, Julie Shulman, Shealyn O'Donnell, Catherine E Stewart, Jen Christofferson, Kevin Zirko, Ana Gallotto, Eleanor Powell, Zachary S Peacock, Amanda Cao, Ella Trumper, Boyu Ren, Michael Mannstadt, Ingrid A Holm, Navil Sethna, Jaymin Upadhyay","doi":"10.1093/jbmrpl/ziag107","DOIUrl":"10.1093/jbmrpl/ziag107","url":null,"abstract":"<p><p>Pain in fibrous dysplasia/McCune-Albright syndrome (FD/MAS) remains inadequately treated. The pilot study was aimed to determine the feasibility (ie, completion, retention, and acceptability) and to explore the effectiveness of an intensive interdisciplinary pain treatment (IIPT) using a biopsychosocial approach in patients with FD/MAS. Five patients (4 females and 1 male; 22-30 yr old) with FD/MAS, with baseline pain severity of 4+ (0-10 scale) were enrolled. A 3-wk intervention (4 d/wk; 3-4 h/d) integrating psychological, physical, and occupational therapies was administered to patients. Study measures included patient-reported outcomes at treatment admission (week 0), discharge (week 3), and follow-up (week 15). Physician Global Assessments (PGA) at weeks 0 and 3 were also collected. All 5 patients completed the 3-wk intervention and follow-up assessment and reported a high degree of acceptability, appropriateness, and feasibility of the intervention. Average pain severity decreased after treatment, with mean changes of -3.0 and -3.2 points at weeks 3 and 15, respectively. Patients demonstrated improvements in pain interference, external pain expression (measured with the pain behavior scale), and pain catastrophizing. Trends of decreased anxiety and depression were observed. Overall health-related quality of life improved at treatment discharge, which was consistent with the PGA (ie, +2 to +3) scores. This pilot study demonstrates that IIPT was feasible and showed initial clinical benefit across multiple dimensions in a small cohort of patients with FD/MAS. Larger-scale, controlled trials are needed for further validation.</p>","PeriodicalId":14611,"journal":{"name":"JBMR Plus","volume":"10 8","pages":"ziag107"},"PeriodicalIF":3.0,"publicationDate":"2026-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13395099/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148578717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bone anabolic effects of tibial loading in combination with dual sclerostin and Dkk1 antibodies in aged mice.","authors":"Lisa Y Lawson, Christopher J Chermside-Scabbo, Michael D Brodt, Nicole Migotsky, John T Shuster, Evan G Buettmann, Matthew J Silva","doi":"10.1093/jbmrpl/ziag106","DOIUrl":"10.1093/jbmrpl/ziag106","url":null,"abstract":"<p><p>Aging is associated with decreased bone formation and bone mass and increased fracture risk. Wnt pathway activation by mechanical loading is a potent strategy to improve bone mass; however, load-induced bone formation is diminished with aging. Neutralizing antibody (Ab) therapies targeting Wnt pathway inhibitors sclerostin (Scl) and Dickkopf-related protein 1 (Dkk1) have proven successful in preclinical and clinical osteoporotic conditions. We asked whether treatment combining Scl-Ab and Dkk1-Ab can increase load-induced bone formation in a preclinical model of osteoporosis. Aged (22-mo) C57BL/6N female mice underwent combination Scl-Ab plus Dkk1-Ab therapy (15 mg/kg each; s.c.; 2×/wk; saline control) for 2 wk, concomitant with tibial loading (-2200 me, 1200 cycles/d, 5 d/wk). Based on serial micro-CT, dual-antibody treatment had a significant, positive effect on bone morphology, independent of loading. For example, from day 0 to day 15 cancellous BV/TV increased by 50% and cortical area by 25% in non-loaded limbs of antibody-treated mice, while vehicle-treated mice had no change. However, antibody treatment did not enhance the effects of tibial loading on bone morphology, which was not significant. On the other hand, antibody treatment and loading each increased periosteal bone formation indices and together had a synergistic effect. For example, periosteal BFR/BS was 10-fold higher in loaded limbs of antibody- vs vehicle-treated mice. Gene expression analysis showed that antibody treatment and loading synergistically upregulated <i>Wnt1</i> expression in bone, which may have contributed to the synergistic effect on bone formation. These results confirm the potent anabolic effect of combination Scl plus Dkk1 antibody treatment. Moreover, they show that antibody treatment and skeletal loading may be more effective at increasing periosteal bone formation in aged mice than either treatment alone. Longer term studies are needed to determine if combination treatment leads to a similar synergistic effect on bone morphology and bone strength.</p>","PeriodicalId":14611,"journal":{"name":"JBMR Plus","volume":"10 8","pages":"ziag106"},"PeriodicalIF":3.0,"publicationDate":"2026-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13384640/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148603250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bioelectrical phase angle predicts sarcopenia in older adults with type 2 diabetes mellitus.","authors":"Methavee Poochanasri, Kasidid Lawongsa, Thanapat Limpaarayakul, Jiranon Pirapattanapong, Thawee Songpatanasilp, Nattapol Sathavarodom, Apussanee Boonyavarakul, Parinya Samakkarnthai","doi":"10.1093/jbmrpl/ziag099","DOIUrl":"10.1093/jbmrpl/ziag099","url":null,"abstract":"<p><p>Sarcopenia is common among older adults with type 2 diabetes mellitus (T2DM) and is associated with increased risks of functional decline and adverse health outcomes. Phase angle (PhA), derived from bioelectrical impedance analysis, has emerged as a potential marker of muscle health. This cross-sectional study aimed to evaluate the predictive value of PhA for detecting sarcopenia in older adults with T2DM and to determine sex-specific cutoff values for sarcopenia screening. A total of 390 patients aged ≥60 yr with T2DM were included. Sarcopenia was defined according to the Asian Working Group for Sarcopenia 2019 criteria. Lower PhA values were significantly associated with sarcopenia, and PhA showed good discriminatory performance for detecting sarcopenia. Sex-specific cutoff values improved the diagnostic accuracy of PhA for sarcopenia screening. These findings suggest that PhA may serve as a practical and noninvasive tool for identifying sarcopenia in older adults with T2DM. Further longitudinal studies are warranted to confirm its prognostic value.</p>","PeriodicalId":14611,"journal":{"name":"JBMR Plus","volume":"10 8","pages":"ziag099"},"PeriodicalIF":3.0,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13372094/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148455868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of an automated landmarking tool for the femur in dual-energy X-ray absorptiometry scans using contour-based image analysis.","authors":"Edward M Chu, Jonathan D Adachi, Cheryl E Quenneville","doi":"10.1093/jbmrpl/ziag103","DOIUrl":"10.1093/jbmrpl/ziag103","url":null,"abstract":"<p><p>Osteoporosis is a skeletal disease that significantly increases fracture risk and imposes a growing public health and economic burden. Notably, hip fractures are associated with high mortality, long-term disability, and loss of independence. When evaluating osteoporosis and estimating fracture risk, DXA is commonly used to determine the BMD. To capture geometrical morphology from these DXA scans as factors in fracture risk prediction, landmarking around the femur is conducted manually around the ROI. However, this process is labor-intensive and prone to variability. This study presents the development of a fully automated femoral landmarking tool that integrates a U-Net convolutional neural network for femur contour segmentation with a geometric algorithm for consistent landmark placement. A heterogeneous dataset of 555 DXA scans was used to train and evaluate the U-Net model, achieving a pixel-wise accuracy of 97.55%, an Intersection over Union of 91.55%, and a Dice coefficient of 95.56% on the test set. When incorporated into a statistical shape and appearance modeling (SSAM) framework for fracture risk prediction, predictions using the automatically generated landmarks achieved a test AUC of 0.831 (95% CI: 0.698-0.965), compared with 0.780 (95% CI: 0.635-0.925) for manual landmarks; a paired DeLong test showed no significant difference (<i>p</i> = .53), indicating a comparable performance. The proposed pipeline produces anatomically relevant, reproducible landmarks, and supports fracture prediction performance similar to manual methods. It presents a scalable and objective solution for morphometric analysis in DXA imaging.</p>","PeriodicalId":14611,"journal":{"name":"JBMR Plus","volume":"10 8","pages":"ziag103"},"PeriodicalIF":3.0,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13367575/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148446739","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular mechanisms of ANKH function and regulation in skeletal mineralization.","authors":"Nuwanthika Wathuliyadde, Katherine E Willmore, Gregory M Kelly","doi":"10.1093/jbmrpl/ziag100","DOIUrl":"10.1093/jbmrpl/ziag100","url":null,"abstract":"<p><p>Progressive ankylosis homolog (ANKH) is a transmembrane protein essential for regulating bone mineralization through the export of nucleoside triphosphates, primarily adenosine triphosphate (ATP), and citrate into the extracellular matrix. Exported ATP is hydrolyzed by ectonucleotide pyrophosphatase/phosphodiesterase 1 into AMP and inorganic pyrophosphate (PPi). Progressive ankylosis homolog is widely expressed across tissues, where it limits ectopic mineralization of tissues and other roles. Its functional role is particularly prominent in mineralizing cells such as osteoblasts and chondrocytes that maintain the balance between mineral formation and inhibition required for healthy skeletal function. Mutations in ANKH cause 2 main mineralization disorders: craniometaphyseal dysplasia, characterized by progressive craniofacial bone thickening, and calcium pyrophosphate deposition disease (CPPD), marked by crystal deposits causing arthritis-like joint symptoms. Functionally, ANKH operates within a coordinated regulatory axis with ectonucleotide pyrophosphatase/phosphodiesterase 1 and tissue-nonspecific alkaline phosphatase (TNAP) that governs extracellular PPi homeostasis. Although TNAP-mediated PPi hydrolysis contributes negligibly to extracellular inorganic phosphate (Pi) levels, this process remains essential for clearing PPi to prevent excessive inhibition of mineral deposition, thereby preserving the Pi/PPi ratio required for physiological mineralization. Emerging evidence also implicates ANKH in citrate export, influencing bone matrix composition, and mechanical integrity. Further, ANKH expression and function are regulated by multiple signaling pathways including Wnt, tumor necrosis factor-alpha, and FGF, as well as by post-transcriptional modifications, although these regulatory mechanisms remain poorly characterized. Current mouse models, primarily knock-in lines carrying craniometaphyseal dysplasia-associated mutations, only partially recapitulate human phenotypes while comparable models for CPPD-associated mutations remain unavailable. Addressing these gaps by elucidating mutation-specific mechanisms, signaling networks, and developing improved animal models will be critical to advance targeted therapies for ANKH-related mineralization disorders and improve patient outcomes.</p>","PeriodicalId":14611,"journal":{"name":"JBMR Plus","volume":"10 8","pages":"ziag100"},"PeriodicalIF":3.0,"publicationDate":"2026-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13356900/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148430131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypertension worsens bone loss and weakens bone in aged ovariectomized mice.","authors":"Elizabeth M Hennen, Sasidhar Uppuganti, Santosh Thapa, Néstor de la Visitación, Priya Mathiy, Gabriel Ramirez, Elizabeth Rendina-Ruedy, David G Harrison, Jeffry S Nyman","doi":"10.1093/jbmrpl/ziag101","DOIUrl":"10.1093/jbmrpl/ziag101","url":null,"abstract":"<p><p>The occurrence of both hypertension and osteoporosis increases after menopause, and fracture risk is higher in adults with hypertension than in adults without this chronic disease. We hypothesized that ovariectomy (OVX)-induced estrogen-deficiency and angiotensin (Ang) II-hypertension together cause a greater decline in bone strength than OVX alone. Ovaries were removed (OVX) or remained intact (Sham) in 12-mo-old, C57BL/6J mice. Four weeks after surgery, mice received either an infusion of vehicle or angiotensin II at 490 ng/kg/min for 6 wk to induce hypertension. We monitored blood pressure (BP) and areal BMD (aBMD) before surgery, before infusion, and before euthanasia. OVX augmented the increase in BP in hypertensive mice. OVX, not hypertension, decreased whole-body aBMD. Nonetheless, hypertension lowered cortical bone area and thickness of the femur mid-diaphysis in only the OVX group. As determined by the ultimate force that the femur mid-diaphysis endured during 3-point bending, OVX lowered the strength of cortical bone when mice were hypertensive; and hypertension did the same when mice were estrogen deficient. Hypertension and OVX independently affected trabecular bone, such that reductions in trabecular thickness and tissue mineral density were additive with the lowest mean observed in the OVX-hypertension group. OVX significantly lowered the compressive ultimate force of the lumbar vertebra when controlling for hypertension group. Although hypertension did not significantly affect vertebral strength, OVX-hypertension significantly reduced this parameter. The addition of hypertension to OVX in 12-mo-old female mice weakened bone beyond either effect alone. Thus, hypertension, which commonly occurs after menopause or ovarian loss, increases the likelihood of osteoporosis, and thus indicates a high-risk population.</p>","PeriodicalId":14611,"journal":{"name":"JBMR Plus","volume":"10 8","pages":"ziag101"},"PeriodicalIF":3.0,"publicationDate":"2026-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13349054/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148421164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}