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Fracture discrimination capability of ulnar flexural rigidity measured via cortical bone mechanics technology: study protocol for the Stronger study 通过皮质骨力学技术测量尺骨挠曲刚度的骨折辨别能力:"更强大 "研究的研究方案
IF 3.8 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-01-04 DOI: 10.1093/jbmrpl/ziad002
Stuart J Warden, Andrew Dick, Janet E Simon, Todd M. Manini, David W. Russ, Charalampos Lyssikatos, Leatha A. Clark, Brian C. Clark
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).
骨质疏松症的特点是骨量低和骨组织结构退化,导致骨质脆弱(即软弱无力)和骨折风险增加。目前评估骨骼健康和诊断骨质疏松症的标准是双能 X 射线吸收测量法(DXA),它可以量化骨矿密度(BMD),通常是髋关节和脊柱的骨矿密度。然而,DXA 导出的 BMD 仅能评估骨骼健康的一个组成部分,在评估骨强度(抗骨折的一个关键因素)方面具有明显的局限性。虽然多频振动分析可以快速、无痛地检测骨强度,但在推广此类设备方面取得的成功却很有限。最近的进展是开发出了皮质骨力学技术(CBMT),该技术可进行动态三点弯曲测试,以评估尺骨皮质骨的弯曲刚度(EI)。数据表明,尺骨 EI 能准确估算尺骨整体强度,与 DXA 导出的 BMD 相比,它能提供独特而独立的皮质骨信息。因此,CBMT 有可能满足一项关键的未满足需求:更好地识别骨强度减弱且有发生脆性骨折高风险的患者。然而,CBMT 衍生 EI 的临床实用性尚未得到证实。我们设计了一项临床研究,以评估 CBMT 导出的尺骨 EI 在区分绝经后脆性骨折妇女和未发生脆性骨折妇女方面的准确性。这些数据将与从同一受试者身上获得的 DXA 导出的外周和中心 BMD 测量值进行比较。在本文中,我们将介绍这项多中心骨折鉴别研究(STRONGER 研究)的研究方案。
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引用次数: 0
Pten knockout in mouse preosteoblasts leads to changes in bone turnover and strength 小鼠前成骨细胞中的 Pten 基因敲除导致骨转换和骨强度发生变化
IF 3.8 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-01-04 DOI: 10.1093/jbmrpl/ziad016
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
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. 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. 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. 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.
骨骼的发育和重塑受磷酸肌醇-3-激酶(Pi3k)信号通路的控制。我们研究了下调磷酸酶和天丝蛋白同源物(Pten)的影响,Pten是Pi3k信号传导的负调控因子。我们的目的是找出参与调节骨转换并与骨疾病相关的机制。我们将从 Osterix/Sp7 表达骨生成细胞中条件性缺失 Pten(Pten cKO)的小鼠体内分离出的股骨、胫骨和骨髓基质细胞(BMSCs)与 Cre 阴性对照组进行了比较。通过μCT测量、骨组织形态测量、骨转换标记物CTX和P1NP定量以及三点弯曲试验对骨表型进行了分析。BMSCs 的增殖通过细胞核计数和 Ki-67 染色细胞进行测量。在体外,通过ALP染色和检测成骨标志物的基因表达来确定成骨分化能力。Pten cKO 小鼠的 BMSCs 在功能上与对照组 BMSCs 不同。Pten cKO 小鼠的 BMSCs 中成骨细胞标志物增加,而 Pten 蛋白表达降低,Akt 磷酸化增加。我们在 Pten cKO 小鼠骨骼中检测到较高的骨小梁体积和改变的皮质骨形态,骨和组织矿物质密度逐渐降低。Pten cKO骨骼的每个骨小梁表面显示出较少的破骨细胞和较多的成骨细胞(p = 0.00095),骨小梁骨形成率较高。生物力学分析表明,Pten cKO 股骨的骨强度(男性 p = 0.00012)和弹性明显更高。在细胞水平上,与对照组相比,Pten cKO BMSCs 的增殖和成骨分化能力均显著提高。我们的研究结果表明,骨生成细胞中的Pten基因敲除可通过增加骨小梁质量来提高骨的稳定性和弹性,并导致骨髓基质细胞的增殖和成骨分化能力增强。
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引用次数: 0
Staphylococcus aureus Panton-Valentine Leukocidin worsens acute implant-associated osteomyelitis in humanized BRGSF mice 金黄色葡萄球菌潘通-瓦伦丁白细胞介素会加重人源化 BRGSF 小鼠急性植入物相关骨髓炎的病情
IF 3.8 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-01-04 DOI: 10.1093/jbmrpl/ziad005
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
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. 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.
金黄色葡萄球菌是导致植入相关骨髓炎的最常见病原体,这是一种临床上无法治愈的疾病。金黄色葡萄球菌依靠各种机制躲避免疫,以便在骨龛中生存,其中包括分泌白细胞毒素,如潘顿-瓦伦丁白细胞介素(PVL)。PVL 是一种孔隙形成毒素,对中性粒细胞、单核细胞和巨噬细胞上的 C5a 受体(C5aR1 和 C5aR2)具有选择性的人类趋附性。PVL 是肺部、皮肤和软组织感染的重要毒力决定因素。关于 PVL 在骨感染过程中参与金黄色葡萄球菌致病机理的研究尚未广泛开展。为了研究这个问题,我们用社区获得性耐甲氧西林金黄色葡萄球菌(CA-MRSA)USA300野生型菌株(WT)、缺乏lukF/S-PV的同源突变体(Δpvl)或互补突变体(Δpvl+pvl)对人源化BALB/c Rag2-/-Il2rg-/-SirpaNODFlk2-/-(huBRGSF)小鼠进行了经胫骨植入相关性骨髓炎试验。手术后三天,与 WT 感染的小鼠相比,Δpvl 感染的 huBRGSF 小鼠的感染程度较轻,其特点是:1)临床结果有所改善;2)体内外细菌骨负荷较低;3)骨髓中没有葡萄球菌脓肿群落(SAC);4)MRSA 向内脏(肝、肾、脾、心脏)的扩散受到影响。有趣的是,与 WT 感染的小鼠相比,Δpvl 感染的 huBRGSF 小鼠骨龛中的人类髓系细胞、中性粒细胞和 HLA-DR+ 单核细胞较少。因此,在感染了Δpvl 的 huBRGSF 动物中,凋亡的人髓系细胞的比例也较小。综上所述,我们的研究强调了 PVL 在人源化小鼠急性植入物相关骨髓炎中的关键作用。
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引用次数: 0
Bone-turnover variability via progenitor feedback 通过祖先反馈实现骨转换的可变性
IF 3.8 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-01-04 DOI: 10.1093/jbmrpl/ziad003
Young Kwan Kim, Yoshitaka Kameo, Sakae Tanaka, Taiji Adachi
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.
骨转换标志物(BTMs)是骨质疏松症治疗中常用的骨吸收破骨细胞和骨形成成骨细胞的细胞活性指标。由于受衰老和疾病等多种因素的影响,这些指标的数值变化很大,因此医生很难将其用于临床决策。要全面解释 BTM 值的变化,破骨细胞和成骨细胞的祖细胞是不可或缺的,因为这些上游祖细胞对骨转换的下游细胞活动有很强的调控作用。然而,要了解骨细胞多个种群之间复杂的相互作用具有挑战性。在本研究中,我们旨在通过探索衰老对骨质疏松症影响的细胞动态,通过硅学实验从根本上了解祖细胞动态影响骨转换变化的机制。由祖细胞消耗性丢失驱动的负反馈控制可防止骨转换过度导致的骨量快速丢失,而通过反馈调节,衰老对破骨细胞分化和破骨细胞祖细胞增殖的影响会导致破骨细胞和成骨细胞活性平衡及其时间转换的变异性。通过表达骨转换状态的变异性,我们的模型可以根据患者的临床背景描述其个性。因此,我们的模型可在辅助定制治疗方面发挥强大作用,并有可能解决全球与骨质疏松症相关的各种健康问题。
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引用次数: 0
Assessment of bovine cortical bone fracture behavior using impact microindentation as a surrogate of fracture toughness. 用冲击微压痕法评估牛皮质骨的断裂行为,作为断裂韧性的替代方法。
IF 3.4 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-01-04 eCollection Date: 2024-02-01 DOI: 10.1093/jbmrpl/ziad012
Babak Jahani, Rachana Vaidya, James M Jin, Donald A Aboytes, Kaitlyn S Broz, Siva Krothapalli, Bhanuteja Pujari, Walee M Baig, Simon Y Tang

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 (n = 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 (KIC) 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 KIC (P < .0001) and the average BMSi (P < .0001), leading to impaired resistance of bone to crack propagation. Remarkably, the average BMSi exhibited a high correlation with KIC (r = 0.86; P < .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.

骨骼的断裂行为对于评估其机械性能和抗断裂能力至关重要。断裂韧性是一种内在的材料属性,可量化材料在受控条件下承受裂纹扩展的能力。然而,正确进行断裂韧性测试需要使用校准过的机械载荷框架和对骨骼样本进行破坏性测试,因此断裂韧性测试在临床上并不实用。冲击微压痕在某些方面模仿了断裂韧性测量,但其与断裂韧性的关系仍不清楚。在这项研究中,我们旨在比较新鲜牛骨和煮沸牛骨的缺口断裂韧性测量值和冲击微压痕测量值。我们制备了骨骼成熟的牛骨标本(n = 48),其中一半通过煮沸使有机基质变性,另一半在冷冻条件下保存。所有样本都进行了缺口断裂韧性测试,以确定其抗开裂性(KIC),并使用 OsteoProbe 进行了冲击微压痕测试,以获得骨材料强度指数(BMSi)。沸煮骨样本会增加变性胶原蛋白的含量,而矿物质密度和孔隙率则不受影响。沸煮后的骨骼还显示出 KIC(P < .0001)和平均 BMSi(P < .0001)的显著降低,导致骨骼抗裂纹扩展的能力减弱。值得注意的是,平均 BMSi 与 KIC 呈高度相关性(r = 0.86;P < .001)。排序差异分析证实了这两种测量方法之间的极佳一致性。这项研究首次证明了冲击微压痕可作为骨断裂行为的替代测量方法。冲击微压痕法可以在尽量不破坏样本的情况下评估骨断裂阻力,无需使用笨重的测试设备和破坏样本,因此可以为了解骨骼健康状况提供有价值的信息。
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引用次数: 0
JBMR Plus Reviewer list 2023 2023 年 JBMR Plus 评审员名单
IF 3.8 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2023-12-19 DOI: 10.1002/jbm4.10844
<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
ASBMR 和期刊编辑非常感谢审稿人自愿抽出时间担任同行评审这一重要的指导角色。以下人员在过去一年中为《JBMR Plus》进行了审稿,并提供了宝贵的反馈意见,帮助改进所提交的论文。Annette AdamsRiad AkhundovHenry AkinbiAhmed Al Saedi*Imranul AlamMatt AllenCatherine AmbroseNatasha Appelman- DijkstraJohn AsplerDijkstraJohn Asplin*Reggie AuroraUgur AyturkYangjin BaeChelsea BahneyJeannie BaileyRafal BartoszewskiKristen BeaversSanjay BhadadaHarry BlairRobert Blank**Elizabeth BradleyMikkel BrentJacques Brown*Lucas BrunBjoern BuehringEllish BurkeDavid B. Burke.布尔*比约恩-布塞Jay J. Cao达娜-卡彭特Alesandra Carriero詹姆斯-卡萨特Naibedya Chattopadhyay陈建良*陈进然Je-Yong Choi克里斯蒂安娜-西普里安Brian C.ClarkMartine Cohen-SolalAdi Cohen**Mary ColeKelsey CollinsFabio Vasconcellos ComimTim CootesSabrina CorbettaNicola CrabtreeApril CraftCarolyn CrandallJames Cray*Laura CreemersSouadDaamouchRafael de MolonSusan DiemNaomi DirckxSinee DisthabanchongPaola Divieti Pajevic*Kate DuchownyEmma DuncanFlorent ElefteriouKlaus EngelkeDaniel EvansPeterPerFabianAlberto Falchetti*Charles FarberVirginia FergusonAníbal FerreiraTrine Elisabeth FinnesAntonella Forlino*Andrea FoxMorten FrostSeiji Fukumoto**Dana GaddyGustavo GarletDamian Genetos**Samuel GhatanCharles GinsbergNeil GittoesDavid GoldhamerCorinna GrasemannMatthew Greenblatt*Jennifer GregoryAnne Grethe JurikYaodong Gu*Scott A..GuelcherAnyonya GunturMelanie Haffner-LuntzerDieter HaffnerMark HamrickSarah Hardcastle****Nan HatchAlberto Hidalgo-BravoKevin HoffsethHironori HojoNilsson HolguinMichael HolickKara Holloway-KewKuo-Chin HuangJulie HughesSteven Ing*Alex IrelandCarlos Isales**M.Kassim JavaidKarl JepsenEijiro JimiFjola Johannesdottir*Mark JohnsonHiroshi KajiLamya KarimKurt KennelHa-Neui Kim*Keunyoung KimFrank Ko**Joyce S.B.KohYoshihiro KomatsuSung Hye KongSusan KrumTakuo KubotaLisa LangsetmoChristine LaryMichael LaurentCarole Le Henaff*Maarit LeinonenWilliam LeslieMichael LevineHuiqi LiMichael T.C..LiangCesar LebanatiEva LiuHuan LiuJulian LuiGuillaume MabilleauHeather MacdonaldJay MagazinerOuti Makitie*KimManskyClaudio MarcocciTakamitsu MaruyamaYuki MatsumuraTakehiko MatsushitaYukiGherardo MazziottiGabriel MbalavieleMichael McClungMeghan McGee-Lawrence**Donal McNallyRobert MeertensDaniela Merlotti*LisaK.MicklesfieldSalvivier*MicklesfieldSalvivier*LisaK.MicklesfieldSalvatore Minisola*Takeshi MiyamotoSharonMoePierre MoffattSubburaman MohanRebecca MoonRoy MorelloKendall Moseley*Katherine MotylChristian MuschitzSandesh NagamaniMark NanesThomas NickolasKeizo NishikawaRobert NissensonJeffry S.NymanMícheál Ó BreasailRalf OheimCatherine OmosuleNoriaki Ono*Wanida OnoBenjamin OsipovMiguel OteroNeil PaloianSerk In ParkEleftherios Paschalis*Erwin PauwsJohn PettiforMarcelo PinheiroLilian Plotkin**IgnacioPortales CastilloSudhaker RaoAlexander RauchFrank RauchMartina RaunerRevit RegevIan ReidR.RevueltaIniestaYumie RheeAmy RibetAlexander RodriguezTim RolvienGenevieve RomanowiczTamara RozentalMishaela RubinEric RushDanielle RuxNithin SKhashayar SakhaeeAmy SatoDominik SaulMitchell SchafflerErica SchellerInez SchoenmakersAnn Schwartz*Peter SchwarzDavid S
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Burr*&lt;/p&gt;&lt;p&gt;Bjoern Busse&lt;/p&gt;&lt;p&gt;Jay J. Cao&lt;/p&gt;&lt;p&gt;Dana Carpenter&lt;/p&gt;&lt;p&gt;Alesandra Carriero&lt;/p&gt;&lt;p&gt;James Cassat&lt;/p&gt;&lt;p&gt;Naibedya Chattopadhyay&lt;/p&gt;&lt;p&gt;Chien-Liang Chen*&lt;/p&gt;&lt;p&gt;Jin-RanChen&lt;/p&gt;&lt;p&gt;Je-Yong Choi&lt;/p&gt;&lt;p&gt;Cristiana Cipriani&lt;/p&gt;&lt;p&gt;Brian C. Clark&lt;/p&gt;&lt;p&gt;Martine Cohen-Solal&lt;/p&gt;&lt;p&gt;Adi Cohen**&lt;/p&gt;&lt;p&gt;Mary Cole&lt;/p&gt;&lt;p&gt;Kelsey Collins&lt;/p&gt;&lt;p&gt;Fabio Vasconcellos Comim&lt;/p&gt;&lt;p&gt;Tim Cootes&lt;/p&gt;&lt;p&gt;Sabrina Corbetta&lt;/p&gt;&lt;p&gt;Nicola Crabtree&lt;/p&gt;&lt;p&gt;April Craft&lt;/p&gt;&lt;p&gt;Carolyn Crandall&lt;/p&gt;&lt;p&gt;James Cray*&lt;/p&gt;&lt;p&gt;Laura Creemers&lt;/p&gt;&lt;p&gt;Souad Daamouch&lt;/p&gt;&lt;p&gt;Rafael de Molon&lt;/p&gt;&lt;p&gt;Susan Diem&lt;/p&gt;&lt;p&gt;Naomi Dirckx&lt;/p&gt;&lt;p&gt;Sinee Disthabanchong&lt;/p&gt;&lt;p&gt;Paola Divieti Pajevic*&lt;/p&gt;&lt;p&gt;Kate Duchowny&lt;/p&gt;&lt;p&gt;Emma Duncan&lt;/p&gt;&lt;p&gt;Florent Elefteriou&lt;/p&gt;&lt;p&gt;Klaus Engelke&lt;/p&gt;&lt;p&gt;Daniel Evans&lt;/p&gt;&lt;p&gt;Peter Fabian&lt;/p&gt;&lt;p&gt;Alberto Falchetti*&lt;/p&gt;&lt;p&gt;Charles Farber&lt;/p&gt;&lt;p&gt;Virginia Ferguson&lt;/p&gt;&lt;p&gt;Aníbal Ferreira&lt;/p&gt;&lt;p&gt;Trine Elisabeth Finnes&lt;/p&gt;&lt;p&gt;Antonella Forlino*&lt;/p&gt;&lt;p&gt;Andrea Fox&lt;/p&gt;&lt;p&gt;Morten Frost&lt;/p&gt;&lt;p&gt;Seiji Fukumoto**&lt;/p&gt;&lt;p&gt;Dana Gaddy&lt;/p&gt;&lt;p&gt;Gustavo Garlet&lt;/p&gt;&lt;p&gt;Damian Genetos**&lt;/p&gt;&lt;p&gt;Samuel Ghatan&lt;/p&gt;&lt;p&gt;Charles Ginsberg&lt;/p&gt;&lt;p&gt;Neil Gittoes&lt;/p&gt;&lt;p&gt;David Goldhamer&lt;/p&gt;&lt;p&gt;Corinna Grasemann&lt;/p&gt;&lt;p&gt;Matthew Greenblatt*&lt;/p&gt;&lt;p&gt;Jennifer Gregory&lt;/p&gt;&lt;p&gt;Anne Grethe Jurik&lt;/p&gt;&lt;p&gt;Yaodong Gu*&lt;/p&gt;&lt;p&gt;Scott A. Guelcher&lt;/p&gt;&lt;p&gt;Anyonya Guntur&lt;/p&gt;&lt;p&gt;Melanie Haffner-Luntzer&lt;/p&gt;&lt;p&gt;Dieter Haffner&lt;/p&gt;&lt;p&gt;Mark Hamrick&lt;/p&gt;&lt;p&gt;Sarah Hardcastle**&lt;/p&gt;&lt;p&gt;Nan Hatch&lt;/p&gt;&lt;p&gt;Alberto Hidalgo-Bravo&lt;/p&gt;&lt;p&gt;Kevin Hoffseth&lt;/p&gt;&lt;p&gt;Hironori Hojo&lt;/p&gt;&lt;p&gt;Nilsson Holguin&lt;/p&gt;&lt;p&gt;Michael Holick&lt;/p&gt;&lt;p&gt;Kara Holloway-Kew&lt;/p&gt;&lt;p&gt;Kuo-Chin Huang&lt;/p&gt;&lt;p&gt;Julie Hughes&lt;/p&gt;&lt;p&gt;Steven Ing*&lt;/p&gt;&lt;p&gt;Alex Ireland&lt;/p&gt;&lt;p&gt;Carlos Isales**&lt;/p&gt;&lt;p&gt;M. Kassim Javaid&lt;/p&gt;&lt;p&gt;Karl Jepsen&lt;/p&gt;&lt;p&gt;Eijiro Jimi&lt;/p&gt;&lt;p&gt;Fjola Johannesdottir*&lt;/p&gt;&lt;p&gt;Mark Johnson&lt;/p&gt;&lt;p&gt;HiroshiKaji&lt;/p&gt;&lt;p&gt;Lamya Karim&lt;/p&gt;&lt;p&gt;Kurt Kennel&lt;/p&gt;&lt;p&gt;Ha-Neui Kim*&lt;/p&gt;&lt;p&gt;Keunyoung Kim&lt;/p&gt;&lt;p&gt;Frank Ko**&lt;/p&gt;&lt;p&gt;Joyce S.B. Koh&lt;/p&gt;&lt;p&gt;Yoshihiro Komatsu&lt;/p&gt;&lt;p&gt;Sung Hye Kong&lt;/p&gt;&lt;p&gt;Susan Krum&lt;/p&gt;&lt;p&gt;Takuo Kubota&lt;/p&gt;&lt;p&gt;Lisa Langsetmo&lt;/p&gt;&lt;p&gt;Christine Lary&lt;/p&gt;&lt;p&gt;Michael Laurent&lt;/p&gt;&lt;p&gt;Carole Le Henaff*&lt;/p&gt;&lt;p&gt;Ma","PeriodicalId":14611,"journal":{"name":"JBMR Plus","volume":"7 12","pages":""},"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}
引用次数: 0
Corneal and Coronary Calcification in Maintenance Hemodialysis: The Face Is No Index to the Heart 维持性血液透析中的角膜和冠状动脉钙化:脸不是心脏的索引
IF 3.8 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2023-12-13 DOI: 10.1002/jbm4.10823
Maria Beatriz C. N. Pessoa, Ruth Miyuki Santo, Aline A. de Deus, Eduardo J Duque, Shirley F. Crispilho, Vanda Jorgetti, Maria Aparecida Dalboni, Carlos Eduardo Rochitte, Rosa M. A. Moyses, Rosilene M. Elias

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) > 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 (r = 0.203, p = 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. JBMR Plus published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research.

虽然眼睛是慢性肾脏病(CKD)患者转移性钙化的主要部位,但对这一人群的角膜和结膜钙化(CCC)评估却很少。CCC 是否与冠状动脉钙化相关仍是未知数,因为迄今为止的研究都依赖于灵敏度较低的方法。我们的目的是根据断层扫描检测 CCC 与冠状动脉钙化之间的关系。这是一项包括维持性透析患者在内的横断面研究。研究记录了临床、人口统计学和生化数据(钙、磷、副甲状腺激素、碱性磷酸酶和 25(OH)-vitamin D)。甲状旁腺功能亢进的定义是甲状旁腺激素(PTH)超过 300 pg/mL。CCC通过前段光学相干断层扫描(AS-OCT)进行评估,冠状动脉钙化评分(Agatston法)通过计算机断层扫描进行评估。我们将无/轻度 CCC 与中度/重度 CCC 进行了比较。共纳入 29 名患者(49.6 ± 15.0 岁,62.1% 为女性,血液透析 5.7 [2.7-9.4] 年,17.2% 患有糖尿病,75.9% 患有甲状旁腺功能亢进)。82.7%的患者发现了 CCC,中位数为 9(3,14.5)分,范围从 0 到 16。分别有27.6%、20.7%和51.7%的患者将CCC分为无/轻度、中度和重度。44.8%的患者发现冠状动脉钙化,中位数为 11(0,464)分,从 0 到 6456 分不等。我们发现冠状动脉钙化评分与 CCC 之间无明显相关性(r = 0.203,p = 0.282)。中度/重度 CCC 患者的高磷血症发生率高于无/轻度 CCC 患者。我们的结论是,透析治疗的慢性肾脏病患者中经常出现 CCC,而且与冠状动脉钙化评分无关。高磷血症似乎是导致 CCC 的原因之一。© 2023 作者。JBMR Plus 由 Wiley Periodicals LLC 代表美国骨与矿物质研究学会出版。
{"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":"7 12","pages":""},"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}
引用次数: 0
The Dietary Fiber Inulin Slows Progression of Chronic Kidney Disease–Mineral Bone Disorder (CKD-MBD) in a Rat Model of CKD 膳食纤维菊粉可延缓慢性肾脏病大鼠模型中慢性肾脏病-矿物质骨病(CKD-MBD)的进展
IF 3.8 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2023-12-07 DOI: 10.1002/jbm4.10837
Annabel Biruete, Neal X. Chen, Corinne E. Metzger, Shruthi Srinivasan, Kalisha O'Neill, Paul B. Fallen, Austin Fonseca, Hannah E. Wilson, Henriette de Loor, Pieter Evenepoel, Kelly S. Swanson, Matthew R. Allen, Sharon M. Moe

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. JBMR Plus published by Wiley Periodicals LLC. on behalf of American Society for Bone and Mineral Research.

慢性肾脏疾病(CKD) -矿物质骨紊乱(CKD‐MBD)导致骨折和心血管疾病。观察性研究表明,膳食纤维对骨骼和心血管结果都有有益的影响,但纤维对CKD - MBD的影响尚不清楚。为了确定纤维对CKD - MBD的影响,我们在22周龄至30或32周龄期间(正常肾功能的~30%和~15%),给患有进行性CKD的Cy/+大鼠喂食含有0.7%磷酸盐和10%菊粉(可发酵纤维)或纤维素(不可发酵纤维)的酪蛋白饲粮。我们评估了CKD - MBD的生化终点、骨骼数量和质量、心血管健康、盲肠微生物群和血清肠道源性尿毒症毒素。结果通过双向方差分析(ANOVA)来评估CKD分期和菊粉的主要影响及其相互作用。结果显示,在CKD动物中,菊粉没有改变肾功能,但降低了从4期到5期血清磷酸盐和甲状旁腺激素水平的升高,但对成纤维细胞生长因子- 23 (FGF23)没有影响。骨转换和骨皮质参数同样得到改善,但力学性能没有改变。菊粉减缓了主动脉和心脏钙化、左心室质量指数和纤维化的进展。为了了解这一机制,我们评估了肠道微生物群,发现在菊粉的作用下,α和β多样性发生了变化,几个分类群发生了显著变化,同时循环肠道来源的尿毒症毒素(如硫酸吲哚酚和短链脂肪酸)减少。总之,在CKD大鼠的饮食中添加可发酵纤维菊粉可以减缓CKD - MBD的进展,而不影响肾功能,可能是通过改变肠道微生物群组成和降低肠道源性尿毒症毒素介导的。©2023作者。JBMR Plus由Wiley期刊有限责任公司代表美国骨与矿物研究协会出版。
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引用次数: 0
Correction to Osteoclast microRNA Profiling in Rheumatoid Arthritis to Capture the Erosive Factor 修正类风湿性关节炎破骨细胞 microRNA 图谱以捕捉侵蚀因子
IF 3.8 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2023-12-01 DOI: 10.1002/jbm4.10845

Nguyen HD, Lortie A, Mbous Nguimbus L, et al. Osteoclast microRNA profiling in rheumatoid arthritis to capture the erosive factor. JBMR Plus. 2023;7:e10776. https://doi.org/10.1002/jbm4.10776

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.

We apologize for this error.

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.

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.

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.

3Department of Medical Biology, CIUSS du Saguenay-Lac-Saint-Jean Hôpital Universitaire de Chicoutimi, Saguenay, Canada.

Nguyen HD、Lortie A、Mbous Nguimbus L 等:类风湿性关节炎破骨细胞微RNA图谱分析捕捉侵蚀因子。JBMR Plus.2023;7:e10776。https://doi.org/10.1002/jbm4.10776In,在文章最初发表的版本中,作者姓名不慎调换。正确的作者名单如下。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 2.1 加拿大舍布鲁克大学生物化学和功能基因组学系及埃斯特里大学保健和社会服务综合中心-舍布鲁克大学医院中心(CIUSSSE-CHUS)研究中心。加拿大舍布鲁克,舍布鲁克大学医学与健康科学学院医学系风湿病学部,以及爱斯特里省大学健康与社会服务综合中心--舍布鲁克大学医院中心(CIUSSSE-CHUS)研究中心.3 加拿大萨格奈-拉克-圣让大学医学生物学系,加拿大萨格奈,奇库蒂米大学医院.4 加拿大萨格奈-拉克-圣让大学医学生物学系,加拿大萨格奈,奇库蒂米大学医院.5 加拿大萨格奈-拉克-圣让大学医学生物学系,加拿大萨格奈,奇库蒂米大学医院.6 加拿大萨格奈-拉克-圣让大学医学生物学系,加拿大萨格奈,奇库蒂米大学医院.7 加拿大萨格奈-拉克-圣让大学医学生物学系,加拿大萨格奈,奇库蒂米大学医院.
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引用次数: 0
When Cortical Bone Matrix Properties Are Indiscernible between Elderly Men with and without Type 2 Diabetes, Fracture Resistance Follows Suit 当患有和未患有 2 型糖尿病的老年男性之间的骨皮质基质特性无法区分时,骨折抵抗力也会随之发生变化
IF 3.8 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2023-12-01 DOI: 10.1002/jbm4.10839
Eva M. Wölfel, Benjamin Bartsch, Jasmin Koldehoff, Imke A. K. Fiedler, Sofie Dragoun-Kolibova, Felix N. Schmidt, Johannes Krug, Mei-Chun Lin, Klaus Püschel, Benjamin Ondruschka, Elizabeth A. Zimmermann, Hans Jelitto, Gerold Schneider, Bernd Gludovatz, Björn Busse

Type 2 diabetes mellitus (T2DM) is a metabolic disease affecting bone tissue and leading to increased fracture risk in men and women, independent of bone mineral density (BMD). Thus, bone material quality (i.e., properties that contribute to bone toughness but are not attributed to bone mass or quantity) is suggested to contribute to higher fracture risk in diabetic patients and has been shown to be altered. Fracture toughness properties are assumed to decline with aging and age-related disease, while toughness of human T2DM bone is mostly determined from compression testing of trabecular bone. In this case-control study, we determined fracture resistance in T2DM cortical bone tissue from male individuals in combination with a multiscale approach to assess bone material quality indices. All cortical bone samples stem from male nonosteoporotic individuals and show no significant differences in microstructure in both groups, control and T2DM. Bone material quality analyses reveal that both control and T2DM groups exhibit no significant differences in bone matrix composition assessed with Raman spectroscopy, in BMD distribution determined with quantitative back-scattered electron imaging, and in nanoscale local biomechanical properties assessed via nanoindentation. Finally, notched three-point bending tests revealed that the fracture resistance (measured from the total, elastic, and plastic J-integral) does not significantly differ in T2DM and control group, when both groups exhibit no significant differences in bone microstructure and material quality. This supports recent studies suggesting that not all T2DM patients are affected by a higher fracture risk but that individual risk profiles contribute to fracture susceptibility, which should spur further research on improving bone material quality assessment in vivo and identifying risk factors that increase bone fragility in T2DM. © 2023 The Authors. JBMR Plus published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research.

2型糖尿病(T2DM)是一种影响骨组织并导致男性和女性骨折风险增加的代谢性疾病,与骨矿物质密度(BMD)无关。因此,骨材料质量(即有助于骨韧性但不归因于骨量或数量的特性)被认为是糖尿病患者骨折风险较高的因素,并且已被证明是可以改变的。断裂韧性特性被认为随着年龄和年龄相关疾病而下降,而人类T2DM骨的韧性主要通过小梁骨的压缩试验来确定。在这项病例对照研究中,我们测定了男性T2DM皮质骨组织的骨折抵抗性,并结合多尺度方法评估骨材料质量指标。所有皮质骨样本均来自男性非骨质疏松症患者,两组、对照组和T2DM患者的微结构无显著差异。骨材料质量分析显示,对照组和T2DM组在拉曼光谱评估的骨基质组成、定量背散射电子成像确定的骨密度分布以及纳米压痕评估的纳米尺度局部生物力学性能方面均无显著差异。最后,缺口三点弯曲试验显示,当两组在骨微观结构和材料质量上没有显着差异时,T2DM组和对照组的断裂抗力(从总、弹性和塑性J积分测量)没有显着差异。这支持了最近的研究表明,并非所有T2DM患者都有较高的骨折风险,但个体风险概况有助于骨折易感性,这应该促进进一步研究,以改善体内骨材料质量评估,并确定增加T2DM患者骨易碎性的危险因素。©2023作者。JBMR Plus由Wiley期刊有限责任公司代表美国骨骼和矿物研究协会出版。
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