JBMR Plus最新文献

{"title":"Fracture discrimination capability of ulnar flexural rigidity measured via cortical bone mechanics technology: study protocol for the Stronger study","authors":"Stuart J Warden, Andrew Dick, Janet E Simon, Todd M. Manini, David W. Russ, Charalampos Lyssikatos, Leatha A. Clark, Brian C. Clark","doi":"10.1093/jbmrpl/ziad002","DOIUrl":"https://doi.org/10.1093/jbmrpl/ziad002","url":null,"abstract":"\u0000 Osteoporosis is characterized by low bone mass and structural deterioration of bone tissue, leading to bone fragility (i.e., weakness) and an increased risk for fracture. The current standard for assessing bone health and diagnosing osteoporosis is dual-energy x-ray absorptiometry (DXA), which quantifies areal bone mineral density (BMD), typically at the hip and spine. However, DXA-derived BMD assesses only one component of bone health and is notably limited in evaluating bone strength, a critical factor in fracture resistance. Although multifrequency vibration analysis can quickly and painlessly assay bone strength, there has been limited success in advancing a device of this nature. Recent progress has resulted in the development of Cortical Bone Mechanics Technology (CBMT), which conducts a dynamic 3-point bending test to assess the flexural rigidity (EI) of ulnar cortical bone. Data indicates that ulnar EI accurately estimates ulnar whole bone strength and provides unique and independent information about cortical bone compared to DXA-derived BMD. Consequently, CBMT has the potential to address a critical unmet need: better identification of patients with diminished bone strength who are at high risk of experiencing a fragility fracture. However, the clinical utility of CBMT-derived EI has not yet been demonstrated. We have designed a clinical study to assess the accuracy of CBMT-derived ulnar EI in discriminating post-menopausal women who have suffered a fragility fracture from those who have not. These data will be compared to DXA-derived peripheral and central measures of BMD obtained from the same subjects. In this article, we describe the study protocol for this multi-center fracture discrimination study (The STRONGER Study).","PeriodicalId":14611,"journal":{"name":"JBMR Plus","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139450579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparison of physiological and behavioural nutrition-related factors in people with and without adolescent idiopathic scoliosis, from cohort data at 8 to 20 years","authors":"Phoebe T T Ng, Kylie Tucker, Farah Zahir, M. Izatt, Leon Straker, Andrew Claus","doi":"10.1093/jbmrpl/ziad013","DOIUrl":"https://doi.org/10.1093/jbmrpl/ziad013","url":null,"abstract":"\u0000 \u0000 \u0000 Nutrition-related variables including lower body mass index (BMI), lower bone mineral density (BMD), altered body composition and hormone levels have been reported in adolescent idiopathic scoliosis (AIS).\u0000 \u0000 \u0000 \u0000 To determine if physiological and behavioural nutrition-related factors differ between people with and without AIS, and to quantify their relationship with AIS, in unbiased cohort sample.\u0000 \u0000 \u0000 \u0000 BMI, presence of an eating disorder, leptin, adiponectin, BMD, vitamin D, lean mass and fat mass were compared between those with and without AIS at ages 8, 10, 14, 17 and 20 years, and multiple logistic regression was performed between these variables and AIS.\u0000 \u0000 \u0000 \u0000 Lower total body BMD (median 1.0 g/cm2 vs 1.1 g/cm2, p = 0.03) and lean mass (median 38.8 kg vs 46.0 kg, p = 0.04) at age 20 years were observed in those with AIS compared to those without scoliosis. At age 20, the odds of AIS were 3.23 times higher for adolescents with an eating disorder compared to those with no eating disorder (95%CI[1.02, 8.63)) when adjusted for BMI. Every 1 kg/m2 increase in BMI decreased the odds of AIS by 0.88 times (95%CI[0.76 to 0.98]) after adjusting for eating disorder diagnosis.\u0000 \u0000 \u0000 \u0000 Lower BMI in mid-adolescence and presence of eating disorder outcomes, lower BMD and lower lean mass in late adolescence were associated with the presence of AIS. Current data do not explain the mechanisms for these associations, but suggest that serum leptin, adiponectin and vitamin D are unlikely to be contributing factors. Conclusive determination of the prevalence of eating disorders in AIS will require further studies with larger sample sizes.\u0000","PeriodicalId":14611,"journal":{"name":"JBMR Plus","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139385396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bone-turnover variability via progenitor feedback","authors":"Young Kwan Kim, Yoshitaka Kameo, Sakae Tanaka, Taiji Adachi","doi":"10.1093/jbmrpl/ziad003","DOIUrl":"https://doi.org/10.1093/jbmrpl/ziad003","url":null,"abstract":"\u0000 Bone turnover markers (BTMs) are commonly used in osteoporosis treatment as indicators of cell activities of bone-resorbing osteoclasts and bone-forming osteoblasts. The wide variability in their values due to multiple factors, such as aging and diseases, makes it difficult for physicians to utilize them for clinical decision-making. The progenitors of osteoclasts and osteoblasts are indispensable for a comprehensive interpretation of the variability in BTM values because these upstream progenitors strongly regulate the downstream cell activities of bone turnover. However, understanding the complex interactions among the multiple populations of bone cells is challenging. In this study, we aimed to gain a fundamental understanding of the mechanism by which the progenitor dynamics affect the variability in bone turnover through in silico experiments by exploring the cell dynamics with aging effects on osteoporosis. Negative feedback control driven by the consumptive loss of progenitors prevents rapid bone loss due to excessive bone turnover, and through feedback regulation, aging effects on osteoclast differentiation and osteoclast progenitor proliferation cause variability in the osteoclast and osteoblast activity balance and its temporal transition. By expressing the variability in the bone turnover status, our model describes the individualities of patients based on their clinical backgrounds. Therefore, our model could play a powerful role in assisting tailored treatment and has the potential to resolve the various health problems associated with osteoporosis worldwide.","PeriodicalId":14611,"journal":{"name":"JBMR Plus","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139450676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pten knockout in mouse preosteoblasts leads to changes in bone turnover and strength","authors":"J. Lorenz, Sandy Richter, Anna S. Kirstein, Florentien Kolbig, Michèle Nebe, Marco Schulze, Wieland Kiess, Ingo Spitzbarth, Nora Klöting, D. Le Duc, Ulrike Baschant, A. Garten","doi":"10.1093/jbmrpl/ziad016","DOIUrl":"https://doi.org/10.1093/jbmrpl/ziad016","url":null,"abstract":"\u0000 Bone development and remodeling are controlled by the phosphoinositide-3-kinase (Pi3k) signaling pathway. We investigated the effects of downregulation of phosphatase and tensin homolog (Pten), a negative regulator of Pi3k signaling, in a mouse model of Pten deficiency in preosteoblasts. We aimed to identify mechanisms that are involved in the regulation of bone turnover and are linked to bone disorders.\u0000 Femora, tibiae, and bone marrow stromal cells (BMSCs) isolated from mice with a conditional deletion of Pten (Pten cKO) in Osterix/Sp7 expressing osteoprogenitor cells were compared to Cre negative controls. Bone phenotyping was performed by μCT measurements, bone histomorphometry, quantification of bone turnover markers CTX and P1NP and 3-point bending test. Proliferation of BMSCs was measured by counting nuclei and Ki-67-stained cells. In vitro, osteogenic differentiation capacity was determined by ALP staining, as well as by detecting gene expression of osteogenic markers.\u0000 BMSCs from Pten cKO mice were functionally different from control BMSCs. Osteogenic markers were increased in BMSCs derived from Pten cKO mice, while Pten protein expression was lower and Akt phosphorylation was increased. We detected a higher trabecular bone volume and an altered cortical bone morphology in Pten cKO bones with a progressive decrease in bone and tissue mineral density. Pten cKO bones displayed fewer osteoclasts and more osteoblasts (p = 0.00095) per trabecular bone surface and a higher trabecular bone formation rate. Biomechanical analysis revealed a significantly higher bone strength (p = 0.00012 for males) and elasticity of Pten cKO femora. On the cellular level, both proliferation and osteogenic differentiation capacity of Pten cKO BMSCs were significantly increased compared to controls.\u0000 Our findings suggest that Pten knockout in osteoprogenitor cells increases bone stability and elasticity by increasing trabecular bone mass and leads to increased proliferation and osteogenic differentiation of bone marrow stromal cells.","PeriodicalId":14611,"journal":{"name":"JBMR Plus","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139384597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Staphylococcus aureus Panton-Valentine Leukocidin worsens acute implant-associated osteomyelitis in humanized BRGSF mice","authors":"Marloes I. Hofstee, C. Siverino, Motoo Saito, Himanshu Meghwani, James Tapia-Dean, Samson Arveladze, M. Hildebrand, Javier Rangel-Moreno, M. Riool, S. Zeiter, S. Zaat, T. F. Moriarty, G. Muthukrishnan","doi":"10.1093/jbmrpl/ziad005","DOIUrl":"https://doi.org/10.1093/jbmrpl/ziad005","url":null,"abstract":"\u0000 Staphylococcus aureus is the most common pathogen that causes implant-associated osteomyelitis, a clinically incurable disease. Immune evasion of S. aureus relies on various mechanisms to survive within the bone niche, including the secretion of leukotoxins such as Panton-Valentine leukocidin (PVL). PVL is a pore-forming toxin exhibiting selective human tropism for C5a receptors (C5aR1 and C5aR2) on neutrophils, monocytes, and macrophages. PVL is an important virulence determinant in lung, skin and soft tissue infections. The involvement of PVL in S. aureus pathogenesis during bone infections has not been studied extensively yet.\u0000 To study this, humanized BALB/c Rag2−/−Il2rg−/−SirpaNODFlk2−/− (huBRGSF) mice were subjected to transtibial implant-associated osteomyelitis with community-acquired methicillin-resistant S. aureus (CA-MRSA) USA300 wild type strain (WT), an isogenic mutant lacking lukF/S-PV (Δpvl), or complemented mutant (Δpvl+pvl). Three days post-surgery, Δpvl-infected huBRGSF mice had a less severe infection compared to WT-infected animals as characterized by 1) improved clinical outcomes, 2) lower ex vivo bacterial bone burden, 3) absence of staphylococcal abscess communities (SACs) in their bone marrow, and 4) compromised MRSA dissemination to internal organs (liver, kidney, spleen, heart). Interestingly, Δpvl-infected huBRGSF mice had fewer human myeloid cells, neutrophils, and HLA-DR+ monocytes in the bone niche compared to WT-infected animals. Expectedly, a smaller fraction of human myeloid cells were apoptotic in the Δpvl-infected huBRGSF animals. Taken together, our study highlights the pivotal role of PVL during acute implant-associated osteomyelitis in humanized mice.","PeriodicalId":14611,"journal":{"name":"JBMR Plus","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139386487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessment of bovine cortical bone fracture behavior using impact microindentation as a surrogate of fracture toughness.","authors":"Babak Jahani, Rachana Vaidya, James M Jin, Donald A Aboytes, Kaitlyn S Broz, Siva Krothapalli, Bhanuteja Pujari, Walee M Baig, Simon Y Tang","doi":"10.1093/jbmrpl/ziad012","DOIUrl":"10.1093/jbmrpl/ziad012","url":null,"abstract":"<p><p>The fracture behavior of bone is critically important for evaluating its mechanical competence and ability to resist fractures. Fracture toughness is an intrinsic material property that quantifies a material's ability to withstand crack propagation under controlled conditions. However, properly conducting fracture toughness testing requires the access to calibrated mechanical load frames and the destructive testing of bone samples, and therefore fracture toughness tests are clinically impractical. Impact microindentation mimicks certain aspects of fracture toughness measurements, but its relationship with fracture toughness remains unknown. In this study, we aimed to compare measurements of notched fracture toughness and impact microindentation in fresh and boiled bovine bone. Skeletally mature bovine bone specimens (<i>n</i> = 48) were prepared, and half of them were boiled to denature the organic matrix, while the other half remained preserved in frozen conditions. All samples underwent a notched fracture toughness test to determine their resistance to crack initiation (K_IC) and an impact microindentation test using the OsteoProbe to obtain the Bone Material Strength index (BMSi). Boiling the bone samples increased the denatured collagen content, while mineral density and porosity remained unaffected. The boiled bones also showed significant reduction in both K_IC (<i>P</i> < .0001) and the average BMSi (<i>P</i> < .0001), leading to impaired resistance of bone to crack propagation. Remarkably, the average BMSi exhibited a high correlation with K_IC (<i>r</i> = 0.86; <i>P</i> < .001). A ranked order difference analysis confirmed the excellent agreement between the 2 measures. This study provides the first evidence that impact microindentation could serve as a surrogate measure for bone fracture behavior. The potential of impact microindentation to assess bone fracture resistance with minimal sample disruption could offer valuable insights into bone health without the need for cumbersome testing equipment and sample destruction.</p>","PeriodicalId":14611,"journal":{"name":"JBMR Plus","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10945719/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140174718","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":"JBMR Plus Reviewer list 2023","authors":"","doi":"10.1002/jbm4.10844","DOIUrl":"10.1002/jbm4.10844","url":null,"abstract":"<p>The ASBMR and the journal Editors are incredibly thankful for the reviewers who volunteer their time for the vital mentoring role of peer reviewer. The following individuals have reviewed for JBMR Plus in the past year and have provided invaluable feedback to help improve submitted papers.</p><p>Data through November 14, 2022 – October 25, 2023.</p><p>*Indicates 3 or more reviews completed.</p><p>**Indicates 5 or more reviews completed.</p><p>Annette Adams</p><p>Riad Akhundov</p><p>Henry Akinbi</p><p>Ahmed Al Saedi*</p><p>Imranul Alam</p><p>Matt Allen</p><p>Catherine Ambrose</p><p>Natasha Appelman-Dijkstra</p><p>John Asplin*</p><p>Reggie Aurora</p><p>Ugur Ayturk</p><p>Yangjin Bae</p><p>Chelsea Bahney</p><p>Jeannie Bailey</p><p>Rafal Bartoszewski</p><p>Kristen Beavers</p><p>Sanjay Bhadada</p><p>Harry Blair</p><p>Robert Blank**</p><p>Elizabeth Bradley</p><p>Mikkel Brent</p><p>Jacques Brown*</p><p>Lucas Brun</p><p>Bjoern Buehring</p><p>Ellish Burke</p><p>David B. Burr*</p><p>Bjoern Busse</p><p>Jay J. Cao</p><p>Dana Carpenter</p><p>Alesandra Carriero</p><p>James Cassat</p><p>Naibedya Chattopadhyay</p><p>Chien-Liang Chen*</p><p>Jin-RanChen</p><p>Je-Yong Choi</p><p>Cristiana Cipriani</p><p>Brian C. Clark</p><p>Martine Cohen-Solal</p><p>Adi Cohen**</p><p>Mary Cole</p><p>Kelsey Collins</p><p>Fabio Vasconcellos Comim</p><p>Tim Cootes</p><p>Sabrina Corbetta</p><p>Nicola Crabtree</p><p>April Craft</p><p>Carolyn Crandall</p><p>James Cray*</p><p>Laura Creemers</p><p>Souad Daamouch</p><p>Rafael de Molon</p><p>Susan Diem</p><p>Naomi Dirckx</p><p>Sinee Disthabanchong</p><p>Paola Divieti Pajevic*</p><p>Kate Duchowny</p><p>Emma Duncan</p><p>Florent Elefteriou</p><p>Klaus Engelke</p><p>Daniel Evans</p><p>Peter Fabian</p><p>Alberto Falchetti*</p><p>Charles Farber</p><p>Virginia Ferguson</p><p>Aníbal Ferreira</p><p>Trine Elisabeth Finnes</p><p>Antonella Forlino*</p><p>Andrea Fox</p><p>Morten Frost</p><p>Seiji Fukumoto**</p><p>Dana Gaddy</p><p>Gustavo Garlet</p><p>Damian Genetos**</p><p>Samuel Ghatan</p><p>Charles Ginsberg</p><p>Neil Gittoes</p><p>David Goldhamer</p><p>Corinna Grasemann</p><p>Matthew Greenblatt*</p><p>Jennifer Gregory</p><p>Anne Grethe Jurik</p><p>Yaodong Gu*</p><p>Scott A. Guelcher</p><p>Anyonya Guntur</p><p>Melanie Haffner-Luntzer</p><p>Dieter Haffner</p><p>Mark Hamrick</p><p>Sarah Hardcastle**</p><p>Nan Hatch</p><p>Alberto Hidalgo-Bravo</p><p>Kevin Hoffseth</p><p>Hironori Hojo</p><p>Nilsson Holguin</p><p>Michael Holick</p><p>Kara Holloway-Kew</p><p>Kuo-Chin Huang</p><p>Julie Hughes</p><p>Steven Ing*</p><p>Alex Ireland</p><p>Carlos Isales**</p><p>M. Kassim Javaid</p><p>Karl Jepsen</p><p>Eijiro Jimi</p><p>Fjola Johannesdottir*</p><p>Mark Johnson</p><p>HiroshiKaji</p><p>Lamya Karim</p><p>Kurt Kennel</p><p>Ha-Neui Kim*</p><p>Keunyoung Kim</p><p>Frank Ko**</p><p>Joyce S.B. Koh</p><p>Yoshihiro Komatsu</p><p>Sung Hye Kong</p><p>Susan Krum</p><p>Takuo Kubota</p><p>Lisa Langsetmo</p><p>Christine Lary</p><p>Michael Laurent</p><p>Carole Le Henaff*</p><p>Ma","PeriodicalId":14611,"journal":{"name":"JBMR Plus","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2023-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://asbmr.onlinelibrary.wiley.com/doi/epdf/10.1002/jbm4.10844","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138822476","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":"Corneal and Coronary Calcification in Maintenance Hemodialysis: The Face Is No Index to the Heart","authors":"Maria Beatriz C. N. Pessoa,&nbsp;Ruth Miyuki Santo,&nbsp;Aline A. de Deus,&nbsp;Eduardo J Duque,&nbsp;Shirley F. Crispilho,&nbsp;Vanda Jorgetti,&nbsp;Maria Aparecida Dalboni,&nbsp;Carlos Eduardo Rochitte,&nbsp;Rosa M. A. Moyses,&nbsp;Rosilene M. Elias","doi":"10.1002/jbm4.10823","DOIUrl":"10.1002/jbm4.10823","url":null,"abstract":"<p>Although the eyes are the main site of metastatic calcification in patients with chronic kidney disease (CKD), corneal and conjunctival calcification (CCC) is poorly evaluated in this population. Whether CCC correlates with coronary artery calcification remains unknown since studies so far have relied on methods with low sensitivity. Our objective was to test the relationship between CCC and coronary calcification based on tomography. This was a cross-sectional study that included patients on maintenance dialysis. Clinical, demographic, and biochemical data (calcium, phosphorus, parathormone, alkaline phosphatase, and 25(OH)-vitamin D) were recorded. Hyperparathyroidism was defined as parathyroid hormone (PTH) &gt; 300 pg/mL. CCC was evaluated by anterior segment optical coherence tomography (AS-OCT), and coronary calcium scores (Agatston method) were assessed by computed tomography. We compared no/mild with moderate/severe CCC. Twenty-nine patients were included (49.6 ± 15.0 years, 62.1% female, on hemodialysis for 5.7 [2.7–9.4] years, 17.2% with diabetes mellitus, 75.9% with hyperparathyroidism). CCC was found in 82.7% of patients, with median scores of 9 (3, 14.5), ranging from 0 to 16. CCC was classified as absent/mild, moderate, and severe in 27.6%, 20.7%, and 51.7%, respectively. Coronary calcification was found in 44.8% of patients, with median scores of 11 (0, 464), varying from 0 and 6456. We found no significant correlation between coronary calcium scores and CCC (<i>r</i> = 0.203, <i>p</i> = 0.282). Hyperphosphatemia was more frequent in patients with moderate/severe CCC than in those with absent/mild CCC. We concluded that CCC was frequent in patients with CKD on dialysis and did not correlate with coronary calcium scores. Hyperphosphatemia appears to contribute to CCC. © 2023 The Authors. <i>JBMR Plus</i> published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research.</p>","PeriodicalId":14611,"journal":{"name":"JBMR Plus","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2023-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://asbmr.onlinelibrary.wiley.com/doi/epdf/10.1002/jbm4.10823","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138822416","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":"The Dietary Fiber Inulin Slows Progression of Chronic Kidney Disease–Mineral Bone Disorder (CKD-MBD) in a Rat Model of CKD","authors":"Annabel Biruete,&nbsp;Neal X. Chen,&nbsp;Corinne E. Metzger,&nbsp;Shruthi Srinivasan,&nbsp;Kalisha O'Neill,&nbsp;Paul B. Fallen,&nbsp;Austin Fonseca,&nbsp;Hannah E. Wilson,&nbsp;Henriette de Loor,&nbsp;Pieter Evenepoel,&nbsp;Kelly S. Swanson,&nbsp;Matthew R. Allen,&nbsp;Sharon M. Moe","doi":"10.1002/jbm4.10837","DOIUrl":"10.1002/jbm4.10837","url":null,"abstract":"<p>Chronic kidney disease (CKD)–mineral bone disorder (CKD-MBD) leads to fractures and cardiovascular disease. Observational studies suggest beneficial effects of dietary fiber on both bone and cardiovascular outcomes, but the effect of fiber on CKD-MBD is unknown. To determine the effect of fiber on CKD-MBD, we fed the Cy/+ rat with progressive CKD a casein-based diet of 0.7% phosphate with 10% inulin (fermentable fiber) or cellulose (non-fermentable fiber) from 22 weeks to either 30 or 32 weeks of age (~30% and ~15% of normal kidney function; CKD 4 and 5). We assessed CKD-MBD end points of biochemistry, bone quantity and quality, cardiovascular health, and cecal microbiota and serum gut-derived uremic toxins. Results were analyzed by two-way analysis of variance (ANOVA) to evaluate the main effects of CKD stage and inulin, and their interaction. The results showed that in CKD animals, inulin did not alter kidney function but reduced the increase from stage 4 to 5 in serum levels of phosphate and parathyroid hormone, but not fibroblast growth factor-23 (FGF23). Bone turnover and cortical bone parameters were similarly improved but mechanical properties were not altered. Inulin slowed progression of aorta and cardiac calcification, left ventricular mass index, and fibrosis. To understand the mechanism, we assessed intestinal microbiota and found changes in alpha and beta diversity and significant changes in several taxa with inulin, together with a reduction in circulating gut derived uremic toxins such as indoxyl sulfate and short-chain fatty acids. In conclusion, the addition of the fermentable fiber inulin to the diet of CKD rats led to a slowed progression of CKD-MBD without affecting kidney function, likely mediated by changes in the gut microbiota composition and lowered gut-derived uremic toxins. © 2023 The Authors. <i>JBMR Plus</i> published by Wiley Periodicals LLC. on behalf of American Society for Bone and Mineral Research.</p>","PeriodicalId":14611,"journal":{"name":"JBMR Plus","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2023-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://asbmr.onlinelibrary.wiley.com/doi/epdf/10.1002/jbm4.10837","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138591935","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":"Correction to Osteoclast microRNA Profiling in Rheumatoid Arthritis to Capture the Erosive Factor","authors":"","doi":"10.1002/jbm4.10845","DOIUrl":"10.1002/jbm4.10845","url":null,"abstract":"<p>Nguyen HD, Lortie A, Mbous Nguimbus L, et al. Osteoclast microRNA profiling in rheumatoid arthritis to capture the erosive factor. <i>JBMR Plus</i>. 2023;7:e10776. https://doi.org/10.1002/jbm4.10776</p><p>In the originally published version of the article, the author's names were inadvertently transposed. The correct author list appears below. The online version of this article has been corrected accordingly.</p><p>We apologize for this error.</p><p>Hoang Dong Nguyen,¹ Audrey Lortie,² Léopold Mbous Nguimbus,² Javier Marrugo,² Hugues Allard-Chamard,² Luigi Bouchard,¹,³ Gilles Boire,² Michelle S Scott,¹ and Sophie Roux ².</p><p>¹Department of Biochemistry and Functional Genomics, University of Sherbrooke and Research Centre of the Centre Intégré Universitaire de Santé et Services Sociaux de l'Estrie – Centre Hospitalier Universitaire de Sherbrooke (CIUSSSE-CHUS), Sherbrooke, Canada.</p><p>²Division of Rheumatology, Department of Medicine, Faculty of Medicine and Health Sciences, University of Sherbrooke and Research Centre of the Centre Intégré Universitaire de Santé et Services Sociaux de l'Estrie – Centre Hospitalier Universitaire de Sherbrooke (CIUSSSE-CHUS), Sherbrooke, Canada.</p><p>³Department of Medical Biology, CIUSS du Saguenay-Lac-Saint-Jean Hôpital Universitaire de Chicoutimi, Saguenay, Canada.</p>","PeriodicalId":14611,"journal":{"name":"JBMR Plus","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://asbmr.onlinelibrary.wiley.com/doi/epdf/10.1002/jbm4.10845","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138617175","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}