JBMR Plus最新文献

{"title":"Mer tyrosine kinase regulates bone metabolism, and its deficiency partially ameliorates periodontitis- and ovariectomy-induced bone loss in mice","authors":"Ka-Young Ryu, N. K. Pokhrel, Hye-Jin Jung, Hyo Jeong Kim, Jiwon Seok, Tae-Young Kim, Hyung Joon Kim, Ji Hye Lee, Jae-Young Kim, Yong-Gun Kim, Youngkyun Lee","doi":"10.1093/jbmrpl/ziad014","DOIUrl":"https://doi.org/10.1093/jbmrpl/ziad014","url":null,"abstract":"\u0000 Bone homeostasis is maintained by tightly coordinated activities of bone-forming osteoblasts and bone-resorbing osteoclasts. In the present report, the role of Mer tyrosine kinase (MerTK) in bone metabolism was investigated. The expression of MerTK decreased upon BMP2 stimulation of osteoblast precursors. The femurs of Mertk-deficient mice showed significantly increased bone volume with concomitant increase of bone formation and reduction in bone resorption. These bone phenotypes were attributed to the increased osteoblast differentiation and mineralization accounted by the enhanced β-Catenin and Smad signaling in the absence of MerTK in osteoblast precursors. Although the Mertk-deficient bone marrow macrophages were predisposed to enhanced osteoclast differentiation via augmented Ca2+-NFATc1 signaling, the dramatic increase of Tnfsf11b/Tnfsf11 (Opg/Rankl) ratio in Mertk knockout bones and osteoblast precursors corroborated the reduction of osteoclastogenesis in Mertk deficiency. In ligature-induced periodontitis and ovariectomy models, the bone resorption was significantly attenuated in Mertk-deficient mice compared with wild type control. Taken together, these data indicate novel role of MerTK in bone metabolism and suggest a potential strategy targeting MerTK in treating bone-lytic diseases including periodontitis and osteoporosis.","PeriodicalId":14611,"journal":{"name":"JBMR Plus","volume":"63 2","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139385613","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":"Individual trabecula segmentation validation in first- and second-generation high-resolution peripheral computed tomography compared to micro-computed tomography in the distal radius and tibia.","authors":"Andreea Teodora Dinescu, Bin Zhou, Yizhong Jenny Hu, Sanchita Agarwal, Elizabeth Shane, Xiang-Dong Edward Guo","doi":"10.1093/jbmrpl/ziae007","DOIUrl":"10.1093/jbmrpl/ziae007","url":null,"abstract":"<p><p>High-resolution peripheral quantitative computed tomography (HR-pQCT) has been used for in vivo 3D visualization of trabecular microstructure. Second-generation HR-pQCT (HR-pQCT II) has been shown to have good agreement with first generation HR-pQCT (HR-pQCT I). Advanced Individual Trabecula Segmentation (ITS) decomposes the trabecula network into individual plates and rods. ITS based on HR-pQCT I showed a strong correlation to ITS based on micro-computed tomography (μCT) and identified trabecular changes in metabolic bone diseases. ITS based on HR-pQCT II has new potential because of the enhanced resolution but has yet to be validated. The objective of this study was to assess the agreement between ITS based on HR-pQCT I, HR-pQCT II, and μCT to assess the capability of ITS on HR-pQCT images as a tool for studying bone structure. Freshly frozen tibia and radius bones were scanned in the distal region using HR-pQCT I at 82 μm, HR-pQCT II at 60.7 μm, and μCT at 37 μm. Images were registered, binarized, and ITS analysis was performed. Bone volume fraction (pBV/TV, rBV/TV), number density (pTb.N, rTb.N), thickness (pTb.Th, rTb.Th), and plate-to-rod (PR) ratio (pBV/rBV) of trabecular plates and rods were obtained. Paired Student's <i>t</i>-tests with post hoc Bonferroni analysis were used to examine the differences. Linear regression was used to determine the correlation coefficient. The HR-pQCT I parameters were different from the μCT measurements. The HR-pQCT II parameters were different from the μCT measurements except for rTb.N, and the HR-pQCT I parameters were different from the HR-pQCT II measurements except for pTb.Th. The strong correlation between HR-pQCT II and μCT microstructural analysis (R² = 0.55-0.94) suggests that HR-pQCT II can be used to assess changes in plate and rod microstructure and that values from HR-pQCT I can be corrected.</p>","PeriodicalId":14611,"journal":{"name":"JBMR Plus","volume":"8 3","pages":"ziae007"},"PeriodicalIF":3.4,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10945717/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140174720","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":"Chromatin accessibility and epigenetic DNA modifications in CKD osteoblasts: a study of bone and osteoblasts from pediatric patients with chronic kidney disease","authors":"Aline Martin, R. Kawaguchi, Qing Wang, I. Salusky, Renata C Pereira, K. Wesseling-Perry","doi":"10.1093/jbmrpl/ziad015","DOIUrl":"https://doi.org/10.1093/jbmrpl/ziad015","url":null,"abstract":"\u0000 Maturation defects are intrinsic features of osteoblast lineage cells in CKD patients. These defects persist ex vivo, suggesting that CKD induces epigenetic changes in bone cells. To gain insights into which signaling pathways contribute to CKD-mediated, epigenetically-driven, impairments in osteoblast maturation, we characterized RNA expression and DNA methylation patterns by RNA-Seq and Methylation Epic in primary osteoblasts from 9 adolescent and young adult dialysis patients with end-stage kidney disease and 3 healthy references. ATAC-Seq was also performed on a subset of osteoblasts. Bone matrix protein expression was extracted from iliac crest and evaluated by proteomics. GSEA analysis was used to establish signaling pathways consistently altered in chromatin accessibility, DNA methylation, and RNA expression patterns. Single genes were suppressed in primary osteoblasts using shRNA and mineralization characterized in vitro. The effect of NFAT signaling suppression was also assessed using 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) incorporation. We found that signaling pathways critical for osteoblast differentiation were strongly downregulated in CKD osteoblasts. GSEA identified highly significant methylation changes, differential chromatin accessibility, and altered RNA expression in NFAT signaling targets. NFAT inhibition reduced osteoblast proliferation. Combined analysis of osteoblast RNA expression and whole bone matrix composition identified thirteen potential ligand-receptor pairs were identified. In summary, epigenetic changes in CKD osteoblasts associate with altered expression of multiple osteoblast genes and signaling pathways. An increase in NFAT signaling may play a role in impaired CKD osteoblast maturation. Epigenetic changes also associate with an altered bone matrix which may contribute to bone fragility. Further studies are necessary to elucidate the pathways affected by these genetic alterations since elucidating these pathways will be vital to correcting the underlying biology of bone disease in the CKD population.","PeriodicalId":14611,"journal":{"name":"JBMR Plus","volume":"5 10","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139385983","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":"Peripheral canalicular branching is decreased in streptozotocin-induced diabetes and correlates with decreased whole-bone ultimate load and perilacunar elastic work","authors":"Morgan W. Bolger, Tara Tekkey, David H. Kohn","doi":"10.1093/jbmrpl/ziad017","DOIUrl":"https://doi.org/10.1093/jbmrpl/ziad017","url":null,"abstract":"\u0000 Osteocytes are the most abundant cell type in bone, important for mechanosensation, signaling for bone formation, resorption and osteocytes reside in a complex lacuno-canalicular network (OLCN). Osteocyte signaling is reduced under diabetic conditions, and both type 1 and type 2 diabetes lead to reduced bone turnover, perturbed bone composition and increased fracture risk. We hypothesized this reduced bone turnover and altered bone composition with diabetes is associated with reduced OLCN architecture and connectivity. This study aimed to elucidate: 1) the sequence of OLCN changes with diabetes related to bone turnover, and 2) whether changes to the OLCN are associated with tissue composition and mechanical properties. 12–14 week old male C57BL/6 mice were administered streptozotocin at 50 mg/kg for 5 consecutive days to induce hyperglycemia, sacrificed at baseline (BL), or after being diabetic for 3 (D3), 7 (D7) weeks with age-matched (C3, C7) controls (n = 10–12 per group). Mineralized femoral sections were infiltrated with rhodamine, imaged with confocal microscopy, then the OLCN morphology and topology were characterized and correlated against bone histomorphometry, local and whole bone mechanics and composition. D7 mice exhibited a lower number of peripheral branches relative to C7. The total number of canalicular intersections (nodes) was lower in D3 and D7 relative to BL (p < 0.05 for all) and a reduced bone formation rate (BFR) was observed at D7 vs. C7. The number of nodes explained only 15% of BFR, but 45% of Ct.BV/TV, and 31% of ultimate load. The number of branches explained 30% and 22% of the elastic work at the perilacunar and intracortical region, respectively. Collectively, the reduction in OLCN architecture, and association of OLCN measures with bone turnover, mechanics and composition highlights the relevance of the osteocyte and the OLCN, and a potential therapeutic target for treating diabetic skeletal fragility.","PeriodicalId":14611,"journal":{"name":"JBMR Plus","volume":"26 3","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139385996","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":"17 11","pages":""},"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":"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":"45 11","pages":""},"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":"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":"52 15","pages":""},"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":"45 2","pages":""},"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":"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":"28 2","pages":""},"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":"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":"8 2","pages":"ziad012"},"PeriodicalIF":3.4,"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}