Journal of Bone and Mineral Research

Cover image for Vol. 31 Issue 9

Edited By: Juliet E Compston

Impact Factor: 5.622

ISI Journal Citation Reports © Ranking: 2015: 15/131 (Endocrinology & Metabolism)

Online ISSN: 1523-4681

Featured

  • Idiopathic Acquired Osteosclerosis in a Middle-Aged Woman With Systemic Lupus Erythematosus

    Idiopathic Acquired Osteosclerosis in a Middle‐Aged Woman With Systemic Lupus Erythematosus

    (A, B) Anteroposterior radiographs of the thoracic and lumbar spine show severe diffuse osteosclerosis of the vertebral bodies with loss of normal cortical-medullary differentiation. Imaged portions of the ribs and pelvis display similar findings. (C) Anteroposterior radiograph of the right proximal humerus shows patchy intramedullary sclerosis of the proximal shaft (ellipse), different in character from the diffuse marrow replacement of the axial skeleton.

  • Skeletal Characteristics of WNT1 Osteoporosis in Children and Young Adults

    Skeletal Characteristics of WNT1 Osteoporosis in Children and Young Adults

    Lower extremity radiographs for 4 subjects with a heterozygous p.C218G WNT1 mutation. The images show abnormally thin diaphyses of the fibulas and tibias.

  • Sclerostin Expression in Bile Ducts of Patients With Chronic Cholestasis May Influence the Bone Disease in Primary Biliary Cirrhosis

    Sclerostin Expression in Bile Ducts of Patients With Chronic Cholestasis May Influence the Bone Disease in Primary Biliary Cirrhosis

    Sclerostin was detected in the epithelial cells of the bile ducts (arrows) surrounded by lymphocyte inflammation.

  • The Actin-Binding Protein Cofilin and Its Interaction With Cortactin Are Required for Podosome Patterning in Osteoclasts and Bone Resorption In Vivo and In Vitro

    The Actin‐Binding Protein Cofilin and Its Interaction With Cortactin Are Required for Podosome Patterning in Osteoclasts and Bone Resorption In Vivo and In Vitro

    Depletion of cofilin in OCs disrupts microtubule network and dynamics. (A) Confocal images of tubulin and actin immunolocalization in OCs generated from control and COFOC-/- BMMs treated with RANKL/M-CSF for 3 days. Scale bar = 10 µm for whole-cell and 6 µm for zoomed images. (B) Mature OCs were fixed at day 3 of differentiation, permeabilized, and stained with cofilin, EB1, and phalloidin (actin) antibodies and examined by IF microscopy. Scale bar = 4 µm. (C) Control and COFOC-/-were stained for tubulin, EB1, and phalloidin (actin). Scale bar = 10 µm. (D) 293-VnR cells were transfected with Flag, Flag-CTTN alone, and Flag-CTTN with either RFP-COF-WT, RFP-COF-S3A (mimicking dephosphorylated-active cofilin), or RFP-COF-S3E (mimicking phosphorylated-inactive cofilin). Cell lysates were immunoprecipitated using Flag-M2-resin, and the immunoprecipitates immunoblotted with Flag and RFP antibodies, respectively. (E) Mature OCs at day 3 of differentiation generated from control BMMs with RANKL/M-CSF were treated with DMSO or nocodazole (Noc) (200 nM, 1 hour), and immunoprecipitated with IgG (control), cofilin (COF), or phosphoSer3-cofilin (P-COF) antibodies. The immunoprecipitates were immunoblotted with cortactin (CTTN), phosphotyr421-CTTN (P-CTTN), COF, and P-COF antibodies.

  • Deletion of FGFR3 in Osteoclast Lineage Cells Results in Increased Bone Mass in Mice by Inhibiting Osteoclastic Bone Resorption

    Deletion of FGFR3 in Osteoclast Lineage Cells Results in Increased Bone Mass in Mice by Inhibiting Osteoclastic Bone Resorption

    Increased osteoclastic bone resorption by FGF2 is impaired after Fgfr3 ablated in osteoclasts. (A, B) Toluidine blue staining and quantification of resorption pits on bone slices after osteoclast treated with or without FGF2 for 10 days. The bone resorption area of WT and MUT osteoclasts treated with FGF2 were both significantly increased compared with untreated groups. However, the bone resorption area of MUT osteoclasts treated with FGF2 was reduced compared with WT osteoclasts treated with or without FGF2 (n = 6). (C–E) qRT-PCR analysis of Trap, Ctsk, and Mmp 9 of osteoclasts treated with or without FGF2 treatment for 8 days. MUT osteoclasts treated with FGF2 showed lower expressions of these three genes compared with WT osteoclasts treated with or without FGF2. The graphs show mean value ± SD (two-way ANOVA test, *p < 0.05, **p < 0.01, ***p < 0.001).

  • Palovarotene Inhibits Heterotopic Ossification and Maintains Limb Mobility and Growth in Mice With the Human ACVR1R206H Fibrodysplasia Ossificans Progressiva (FOP) Mutation

    Palovarotene Inhibits Heterotopic Ossification and Maintains Limb Mobility and Growth in Mice With the Human ACVR1R206H Fibrodysplasia Ossificans Progressiva (FOP) Mutation

    Palovarotene preserves long bone growth and growth plate organization in Prrx1-R206H mice. (A) Control and mutant mice were treated with palovarotene (drug) or vehicle from birth (P1) to age 30 days and then examined by µCT analysis to visualize skeletons and heterotopic bone (arrows) (n = 6 mice per group). The observed spinal curvatures are an artifact of sample position in µCT tubes, not the result of defects in the spine. (B) Quantification of femur and tibia lengths by µCT imaging (n = 6 mice per group). (C) Proximal tibial growth plates were stained with Alcian blue, Orange G, and eosin. Note that Alcian blue staining cartilage matrix is markedly reduced in drug-treated controls (second panel from left) but is preserved in drug-treated mutants (rightmost panel) (n = 4 mice per group). Scale bar = 100 μm. (D) Quantification of upper zones and hypertrophic zones from histological analysis. In B and D, red bars indicate data from control and blue bars from mutant mice; hatched bars represent data from palovarotene-treated mice. Data shown are mean ± SEM; statistics compared control versus control+drug or mutant versus mutant+drug using a two-way ANOVA; **p < 0.01, *p < 0.05. Note that (in panel D), lengths of hypertrophic zones in mutants treated with drug (blue hatched bar) are protected and not significantly (NS) different from untreated controls (red bar).

  • Cellular Hypoxia Promotes Heterotopic Ossification by Amplifying BMP Signaling

    Cellular Hypoxia Promotes Heterotopic Ossification by Amplifying BMP Signaling

    mACVR1 enhances chondrogenesis of SHED cells under hypoxia. (A) Representative chondrocyte pellets and quantification of chondrocyte pellet size under the indicated conditions (n = 6). Scale bar = 1 mm. (B) Histological appearance and quantification of extracellular matrix showing enhanced chondrocyte differentiation (n = 3). Scale bar = 100 μm. (C) Upregulation of chondrocyte markers COL2A1, Sox9, and aggrecan (ACAN) in SHED cells under hypoxic conditions (n = 3). Genotype and hypoxia are significantly related to pellet size and chondrocyte extracellular matrix by 2-way ANOVA (p < 0.01; interaction, p < 0.01). Post hoc analysis: ****p < 0.0001; ***p < 0.001; **p < 0.01; *p < 0.05.

  • Idiopathic Acquired Osteosclerosis in a Middle‐Aged Woman With Systemic Lupus Erythematosus
  • Skeletal Characteristics of WNT1 Osteoporosis in Children and Young Adults
  • Sclerostin Expression in Bile Ducts of Patients With Chronic Cholestasis May Influence the Bone Disease in Primary Biliary Cirrhosis
  • The Actin‐Binding Protein Cofilin and Its Interaction With Cortactin Are Required for Podosome Patterning in Osteoclasts and Bone Resorption In Vivo and In Vitro
  • Deletion of FGFR3 in Osteoclast Lineage Cells Results in Increased Bone Mass in Mice by Inhibiting Osteoclastic Bone Resorption
  • Palovarotene Inhibits Heterotopic Ossification and Maintains Limb Mobility and Growth in Mice With the Human ACVR1R206H Fibrodysplasia Ossificans Progressiva (FOP) Mutation
  • Cellular Hypoxia Promotes Heterotopic Ossification by Amplifying BMP Signaling

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eCompendia – special issues of recent JBMR® articles on hot topics

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.

Examples of topics addressed in recent eCompendia include Kidney Disease and Bone, Sclerostin: Preclinical and Clinical Studies and Genetics of Osteogenesis Imperfecta.

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ASBMR 2016 Publications Workshop Presentation

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JBMR's 30th Anniversary: Cause for Celebration

eCompendia Series

Celebrate the Journal of Bone and Mineral Research 30th Anniversary! Browse our new timeline and see key milestones over the years!

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.


STROBE: Authors of manuscripts reporting results of human observational case-control, cohort, or cross-sectional studies are now required to upload the STROBE 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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