Journal of Bone and Mineral Research

Cover image for Vol. 31 Issue 5

Edited By: Juliet E Compston

Impact Factor: 6.832

ISI Journal Citation Reports © Ranking: 2014: 12/128 (Endocrinology & Metabolism)

Online ISSN: 1523-4681

Featured

  • Examining the Relationships Between Bone Tissue Composition, Compositional Heterogeneity, and Fragility Fracture: A Matched Case-Controlled FTIRI Study

    Examining the Relationships Between Bone Tissue Composition, Compositional Heterogeneity, and Fragility Fracture: A Matched Case‐Controlled FTIRI Study

    Typical FTIRI images from two paired biopsies from women aged 56 and 58 years, respectively; BMD = 0.89 for both). Images from the no-fracture case (rows A, C, and E) and from the fracture case (rows B, D, and F) are shown with their respective pixel histograms to the right of each image. The mean and SD are superimposed on the pixel histogram. Rows A, B, E, and F show cancellous bone; rows C and D show cortical bone. The color scale for all images for an indicated variable (mineral-to-matrix [Min/Mat], carbonate-to-phosphate [CO3/PO4], collagen maturity [XLR], and crystallinity [XST]) are shown below the images for that group. All pixel histograms for the indicated variable are on the same scale, noted below the lowermost histogram. Scale bar = 100 µm.

  • Integrative Analysis of Genomics and Transcriptome Data to Identify Potential Functional Genes of BMDs in Females

    Integrative Analysis of Genomics and Transcriptome Data to Identify Potential Functional Genes of BMDs in Females

    WGCNA coexpression network composed of BMD GWAS genes. The hierarchical clustering dendogram for all 1574 genes used in the analysis. Each line is an individual gene. Genes were clustered based on a dissimilarity measure (1-TOM). The branches correspond to modules of highly interconnected groups of genes.

  • Coupling Effect of Water and Proteoglycans on the In Situ Toughness of Bone

    Coupling Effect of Water and Proteoglycans on the In Situ Toughness of Bone

    Removal of GAGs by PNGase F. The removal of GAGs by PNGase F was detected by (A) SDS-gel electrophoresis and (B) histochemical staining with DMMB and Alcian blue as compared to control bone samples. Arrows indicate the protein band shift after treatment.

  • Strontium Ranelate Reduces the Fracture Incidence in a Growing Mouse Model of Osteogenesis Imperfecta

    Strontium Ranelate Reduces the Fracture Incidence in a Growing Mouse Model of Osteogenesis Imperfecta

    (A) Tetracycline labels observed by fluorescence light microscopy in the frontal slices of the proximal tibia of wt/wt and oim/oim mice treated with Veh or SrR. (B) Tetracycline labels observed in the tibia mid-diaphysis cross-section of wt/wt and oim/oim mice treated with Veh or SrR.

  • Dihydroartemisinin, an Anti-Malaria Drug, Suppresses Estrogen Deficiency-Induced Osteoporosis, Osteoclast Formation, and RANKL-Induced Signaling Pathways

    Dihydroartemisinin, an Anti‐Malaria Drug, Suppresses Estrogen Deficiency‐Induced Osteoporosis, Osteoclast Formation, and RANKL‐Induced Signaling Pathways

    DHA protects against ovariectomy-induced bone loss via inhibiting osteoclast activity. (A) Representative images of decalcified bone stained with H&E and TRAcP from sham mice, OVX mice, and OVX mice treated with 1 mg/kg DHA. Mag = 4X, scale bar = 500 µm; Mag = 20X, scale bar = 100 µm. (B) Quantitative analyses of bone volume/total volume (BV/TV), osteoclast surface/bone surface (Oc.S/BS), osteoclast number/bone surface (N.Oc/BS), and osteoblast number/bone surface (N.Ob/BS). n = 3; *p < 0.05 and **p < 0.01 relative to OVX untreated controls.

  • 1,25-Dihydroxyvitamin D Alone Improves Skeletal Growth, Microarchitecture, and Strength in a Murine Model of XLH, Despite Enhanced FGF23 Expression

    1,25‐Dihydroxyvitamin D Alone Improves Skeletal Growth, Microarchitecture, and Strength in a Murine Model of XLH, Despite Enhanced FGF23 Expression

    1,25D and FGF23Ab effects on growth plate and metaphyseal morphology and growth in Hyp mice. (A) H&E, Col X in situ hybridization, pERK1/2 immunoreactivity, and TUNEL labeling of the growth plates of d75 mice. Yellow arrows indicate TUNEL-labeled hypertrophic chondrocytes. Data are representative of 3 mice per genotype/treatment group. (B) The number of TUNEL-labeled nuclei in the last two rows of the hypertrophic chondrocyte layer was quantitated. Data are representative of 3 mice per genotype/treatment group. (C) 1,25D increases basal and phosphate-induced mitochondrial pERK1/2. Subcellular fractionation of hypertrophic chondrocytes treated with 10−8 M 1,25D before addition of 7 mM sodium sulfate (-) or sodium phosphate (Pi). HSP90 is used as a cytosolic control and VDAC as a mitochondrial control. Data are representative of that obtained from 3 independent chondrocyte preparations. (D) Weight, lumbar vertebral height, tail length, and femur length of d75 mice. Data are representative of that obtained from 3 to 5 mice per genotype/treatment group. (E) Radiographs of representative femurs. *p < 0.05 versus WT, #p < 0 versus Hyp Con, ap < 0.05 versus Daily 1,25D, bp < 0.05 versus FGF23Ab.

  • Targeting VEGF and Its Receptors for the Treatment of Osteoarthritis and Associated Pain

    Targeting VEGF and Its Receptors for the Treatment of Osteoarthritis and Associated Pain

    Potential pathways of VEGF-mediated OA progression and pain. Suggested mediators of increased VEGF expression at the joint tissue include mechanical overload, hypoxia, inflammatory cytokines, NO, ROS, growth factors, chondrocyte hypertrophy, and aging. Cartilage degeneration. Chondrocyte-mediated pathways of cartilage degeneration include VEGF-mediated chondrocyte upregulation of MMP-1, MMP-3, MMP-9, MMP-13, and ADAMTS-5. VEGF can also decrease chondrocyte production of TIMP-1, TIMP-2, type II collagen, and aggrecan. VEGF can increase expression of NO in both chondrocytes and endothelial cells, leading to chondrocyte apoptosis. Increased levels of VEGF lead to a minor increase in expression of inflammatory cytokines from chondrocytes, including IL-1β, IL-6, TNF-α. Bone and neurovascular invasion of articular cartilage and osteophyte formation. VEGF stimulates vascular invasion of articular cartilage, and sensory nerve ingrowth can occur upon the tracks of vascular invasion. Increased sensory nerve ingrowth is a potential source of increased pain sensitivity in the joint. VEGF stimulates the recruitment and activity of osteo(chondro)clasts, which can resorb cartilage. Chondroclasts can express MMP-9, leading to matrix degradation of cartilage. Additionally, osteochondral angiogenesis is associated with increased fibrovascular tissue in the bone marrow expressing VEGF. Vascular invasion facilitates the migration of osteoblastic precursor cells toward the articular surface, which are further stimulated by VEGF to produce new bone. Synovitis. VEGF production is increased in synovial macrophages and fibroblasts. VEGF increases migration and/or activity of macrophages, fibroblasts, and neutrophils. Neutrophils may be an additional source of increased VEGF. VEGF stimulates macrophages to secrete MCP-1, TNF-α, and IL-6, and VEGF stimulates fibroblasts to express TNF-α and IL-6. VEGF stimulates endothelial cells to increase expression of IL-8 and MCP-1. IL-8 stimulates neutrophil recruitment, and MCP-1 stimulates macrophage recruitment. VEGF-mediated angiogenesis facilitates inflammatory cell infiltration at the synovium. Subchondral bone sclerosis and resorption. VEGF stimulates osteoclast and osteoblast differentiation, migration, and ultimately activity, leading to areas of increased bone resorption and bone formation. Additionally, VEGF can potentially stimulate RANKL expression at chondrocytes, synovial fibroblasts, and osteoblasts, further stimulating osteoclastogenesis. Direct pain sensitization: VEGF can directly stimulate nociceptive sensory neurons to increase pain sensitivity and potentially nerve ingrowth; this may occur in the synovium, osteochondral junction, and meniscus (not shown).

  • Examining the Relationships Between Bone Tissue Composition, Compositional Heterogeneity, and Fragility Fracture: A Matched Case‐Controlled FTIRI Study
  • Integrative Analysis of Genomics and Transcriptome Data to Identify Potential Functional Genes of BMDs in Females
  • Coupling Effect of Water and Proteoglycans on the In Situ Toughness of Bone
  • Strontium Ranelate Reduces the Fracture Incidence in a Growing Mouse Model of Osteogenesis Imperfecta
  • Dihydroartemisinin, an Anti‐Malaria Drug, Suppresses Estrogen Deficiency‐Induced Osteoporosis, Osteoclast Formation, and RANKL‐Induced Signaling Pathways
  • 1,25‐Dihydroxyvitamin D Alone Improves Skeletal Growth, Microarchitecture, and Strength in a Murine Model of XLH, Despite Enhanced FGF23 Expression
  • Targeting VEGF and Its Receptors for the Treatment of Osteoarthritis and Associated Pain

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eCompendia bring together recently published JBMR® articles on topical issues. Specific topics are selected for each eCompendium to provide the reader with an easy-to-access update that brings together original research articles in the chosen area.

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ASBMR 2015 Publications Workshop Presentation

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JBMR's 30th Anniversary: Cause for Celebration

30anniversary

Read the Editorial by Editor-in-Chief Juliet Compston right here

Announcing

JBMR® Announces Workflow Changes and Author Guidelines Updates

In response to rising concerns over the reproducibility of biomedical research, the author guidelines and submission procedures for the Journal of Bone and Mineral Research’s (JBMR®) have recently been updated. These updates affect the submission workflow of author forms required for peer review and publication, as detailed below:


ARRIVE: Authors submitting research on animal studies are now required to complete an adapted ARRIVE (Animals in Research: Reporting In Vivo Experiments) checklist at submission.


CONSORT: Authors of manuscripts reporting results of clinical trials are now required to upload the CONSORT checklist at submission.


Author Agreement: The conflict of interest (COI) and copyright transfer (CTA) portions of the current Author Agreement can now be completed electronically as a web form, eliminating the need for authors to print, scan and upload a PDF form upon submission.


• COI information will be collected during submission via an online questionnaire on ScholarOne.


• The CTA will be completed at manuscript acceptance: If a manuscript is accepted for publication, the corresponding author will receive an e-mail prompt to log in to Author Services. Author Services is a Wiley web application that provides production tracking, as well as other resources for authors. From this site, corresponding authors can complete the CTA on behalf of all authors on the paper.

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