Journal of Bone and Mineral Research

Cover image for Vol. 32 Issue 2

Edited By: Juliet E Compston

Impact Factor: 5.622

ISI Journal Citation Reports © Ranking: 2015: 15/133 (Endocrinology & Metabolism)

Online ISSN: 1523-4681

Featured

  • DDR2–CYR61–MMP1 Signaling Pathway Promotes Bone Erosion in Rheumatoid Arthritis Through Regulating Migration and Invasion of Fibroblast-Like Synoviocytes

    DDR2–CYR61–MMP1 Signaling Pathway Promotes Bone Erosion in Rheumatoid Arthritis Through Regulating Migration and Invasion of Fibroblast‐Like Synoviocytes

    Radiographic changes in CIA rats upon CYR61 downregulation. (A) Representative X-ray images of the hind paws of CIA rats on day 37. (B) Hind paws of CIA rats were obtained on day 37 for radiological analysis. (C) Representative μCT images of the hind paws of CIA rats on day 37 are shown. Values are the mean ± SE of 3 independent experiments with 10 rats per group. **p < 0.01 compared with Ad-Scramble.

  • Suppression of Sclerostin Alleviates Radiation-Induced Bone Loss by Protecting Bone-Forming Cells and Their Progenitors Through Distinct Mechanisms

    Suppression of Sclerostin Alleviates Radiation‐Induced Bone Loss by Protecting Bone‐Forming Cells and Their Progenitors Through Distinct Mechanisms

    Focal radiation increases the amount of sclerostin in bone. (A) IHC of sclerostin (brown color) in trabecular bone from bilateral femurs of WT mice treated with either vehicle or Scl-Ab for 2 weeks. Bone marrow cells are shown as green and bone matrix are white. (B) Quantification of the relative intensity of sclerostin staining in trabecular osteocytes. n = 3 femurs/group. NR = non-radiated femur; R = radiated femur. a = p < 0.05 R versus NR.

  • Plasmin Prevents Dystrophic Calcification After Muscle Injury

    Plasmin Prevents Dystrophic Calcification After Muscle Injury

    Continuous muscle injury in the setting of plasminogen deficiency results in soft tissue calcification. Full body µCT reconstruction of Plg+/–, mdx, mdx/Plg+/– and mdx/Plg–/– mice with focused magnification of paraspinal and pelvic musculature. Plg+/– mice without muscle injury showed no apparent calcification within skeletal muscle. Similarly, plasminogen-competent, mdx mice suffering continuous, chronic muscle injury also showed no muscle calcification. In contrast, mdx mice with either a partial (mdx/Plg+/–) or complete plasminogen deficiency (mdx/Plg–/–) showed calcification within all major skeletal muscle groups. H&E staining of Plg+/– mice revealed unremarkable, uninjured sarcomeres with peripherally located nuclei, whereas mdx, mdx/Plg+/–, and mdx/Plg–/– mice demonstrated interspersed necrotic (glossy, hypereosinophilic with absent nuclei) and regenerating (centrally located nuclei) sarcomeres. Von Kossa stain demonstrates no calcifications in Plg+/– and mdx mice, but marked dystrophic calcifications within necrotic sarcomeres of mdx/Plg+/– and mdx/Plg–/– mice.

  • Prediction of Bone Mineral Density and Fragility Fracture by Genetic Profiling

    Prediction of Bone Mineral Density and Fragility Fracture by Genetic Profiling

    Relationship between GRS.FN and femoral neck BMD (left panel) and lumbar spine (right panel) for men and women.

  • A Novel ANO5 Mutation Causing Gnathodiaphyseal Dysplasia With High Bone Turnover Osteosclerosis

    A Novel ANO5 Mutation Causing Gnathodiaphyseal Dysplasia With High Bone Turnover Osteosclerosis

    Iliac crest bone morphometry. (A) Reconstruction of a μCT scan of the obtained iliac crest bone specimen. (B) Correspondent von Kossa section. (C–E) Undecalcified 5-μm sections stained by von Kossa and trichrome Masson-Goldner show the presence of osteoid produced by overactive osteoblasts (Ob., black arrows) as well as existent osteoclasts (Oc., white arrows). O. = osteoid.

  • Sex Differences and Growth-Related Adaptations in Bone Microarchitecture, Geometry, Density, and Strength From Childhood to Early Adulthood: A Mixed Longitudinal HR-pQCT Study

    Sex Differences and Growth‐Related Adaptations in Bone Microarchitecture, Geometry, Density, and Strength From Childhood to Early Adulthood: A Mixed Longitudinal HR‐pQCT Study

    Load to strength ratio at the distal radius. (A) Individual data and predicted growth curves for boys (thin black lines and thick black line) and girls (thin gray lines and thick dashed line). (B) Predicted sex differences (boys – girls) across maturity with 95% confidence intervals, correcting for multiple comparisons using a Bonferroni adjustment. Estimates above 0 indicate significantly greater values in boys, whereas estimates below zero indicate significantly greater values in girls. Confidence intervals that cross 0 indicate nonsignificant sex differences.

  • DDR2–CYR61–MMP1 Signaling Pathway Promotes Bone Erosion in Rheumatoid Arthritis Through Regulating Migration and Invasion of Fibroblast‐Like Synoviocytes
  • Suppression of Sclerostin Alleviates Radiation‐Induced Bone Loss by Protecting Bone‐Forming Cells and Their Progenitors Through Distinct Mechanisms
  • Plasmin Prevents Dystrophic Calcification After Muscle Injury
  • Prediction of Bone Mineral Density and Fragility Fracture by Genetic Profiling
  • A Novel ANO5 Mutation Causing Gnathodiaphyseal Dysplasia With High Bone Turnover Osteosclerosis
  • Sex Differences and Growth‐Related Adaptations in Bone Microarchitecture, Geometry, Density, and Strength From Childhood to Early Adulthood: A Mixed Longitudinal HR‐pQCT Study

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eCompendia

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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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Osteoporosis: The Treatment Gap


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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