Bone Journal Impact Factor & Information

Publisher: International Bone and Mineral Society, Elsevier

Current impact factor: 3.97

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 3.973
2013 Impact Factor 4.461
2012 Impact Factor 3.823
2011 Impact Factor 4.023
2010 Impact Factor 4.601
2009 Impact Factor 4.089
2008 Impact Factor 4.145
2007 Impact Factor 3.966
2006 Impact Factor 3.829
2005 Impact Factor 3.939
2004 Impact Factor 3.53
2003 Impact Factor 3.572
2002 Impact Factor 3.755
2001 Impact Factor 3.247
2000 Impact Factor 3.998
1999 Impact Factor 3.961
1998 Impact Factor 3.272
1997 Impact Factor 2.93
1996 Impact Factor 2.083
1995 Impact Factor 2.134
1994 Impact Factor 2.051
1993 Impact Factor 2.896
1992 Impact Factor 2.405

Impact factor over time

Impact factor

Additional details

5-year impact 4.31
Cited half-life 7.50
Immediacy index 0.77
Eigenfactor 0.04
Article influence 1.33
Other titles Bone (New York, N.Y.: Online), Bone
ISSN 1873-2763
OCLC 38871185
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Authors pre-print on any website, including arXiv and RePEC
    • Author's post-print on author's personal website immediately
    • Author's post-print on open access repository after an embargo period of between 12 months and 48 months
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months
    • Author's post-print may be used to update arXiv and RepEC
    • Publisher's version/PDF cannot be used
    • Must link to publisher version with DOI
    • Author's post-print must be released with a Creative Commons Attribution Non-Commercial No Derivatives License
    • Publisher last reviewed on 03/06/2015
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: While epidemiologic studies suggest that bone turnover biomarkers may predict hip fracture risk, findings are inconsistent and Asian data are lacking. We conducted a matched case-control (1:1) study nested in the Singapore Chinese Health Study, a population-based prospective cohort of Chinese men and women (45-74years) recruited from 1993 to 1998 in Singapore. One hundred cases with incident hip fracture and 100 individually matched controls were randomly selected from 63,257 participants. Serum bone turnover biomarkers, namely bone alkaline phosphatase (bone ALP), osteocalcin (OC), procollagen type I N propeptide (PINP), N-terminal and C-terminal crosslinking telopeptide of type I collagen (NTX-I and CTX-I) were measured using immunoassays. Hip fracture cases had significantly higher serum levels of OC, PINP, CTX-I and NTX-I than controls (p<0.05). There was a dose-dependent positive relationship between OC, PINP, CTX-I and NTX-I and risk of hip fracture (all Ps for trend≤0.006), where the risk was significantly increased by 4.32-8.23 folds for the respective BTM [Quartile (Q) 4 vs. Q1]. The odds ratio [OR (95% CI)] at the highest quartile (Q4) was 6.63 (2.02-21.18) for PINP and 4.92 (1.67-14.51) for CTX-I. The joint effect of PINP and CTX-I showed a 7-fold increase in risk (OR: 7.36; 95% CI: 2.53-21.41) comparing participants with higher levels of PINP (Q4) and CTX-I (Q3-Q4) to those with low levels of PINP (Q1-3) and CTX-I (Q1-Q2). Our data demonstrated that higher serum levels of bone turnover biomarkers were associated with increased risk of hip fracture in an Asian population.
    Bone 11/2015; DOI:10.1016/j.bone.2015.11.005
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    ABSTRACT: The CCN family of proteins plays important roles in development and homeostasis of bone and cartilage. To understand the role of CCN4 in chondrogenesis, human bone marrow stromal cells (hBMSCs) were transduced with CCN4 adenovirus (adCCN4) or siRNA to CCN4 (siCCN4) in the presence or absence of transforming growth factor-β3 (TGF-β3). Overexpression of CCN4 enhanced TGF-β3-induced SMAD2/3 phosphorylation and chondrogenesis of hBMSCs in an in vitro assay using a micromass culture model. On the other hand, knockdown of CCN4 inhibited the TGF-β3-induced SMAD2/3 phosphorylation and synthesis of cartilage matrix in micromass cultures of hBMSCs. Immunoprecipitation-Western blot analysis revealed that CCN4 bound to TGF-β3 and regulated the ability of TGF-β3 to bind to hBMSCs. In vivo analysis confirmed there was a significant decrease in the gene expression levels of chondrocyte markers in cartilage samples from Ccn4-knock out (KO) mice, compared to those from wild type (WT) control. In order to investigate the regenerative properties of the articular cartilage in Ccn4-KO mice, articular cartilage defects were surgically performed in the knee joints of young mice, and the results showed that the cartilage was partially repaired in WT mice, but not in Ccn4-KO mice. In conclusion, these results show, for the first time, that CCN4 has a positive influence on chondrogenic differentiation by modulating the effects of TGF-β3.
    Bone 11/2015; DOI:10.1016/j.bone.2015.11.007
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    ABSTRACT: Background: Diabetes mellitus is associated with an increased fracture risk, however the fracture risk is 7 fold increased in patients with type 1 diabetes (T1D) and 1.4 fold increased in patients with type 2 diabetes (T2D) with decreased and increased bone mineral density, respectively. Oral ingestion of glucose causes an acute decrease in bone turnover markers, and thus glucose levels may affect bone turnover in diabetes. Objective: The aim was to examine disparities in bone turnover markers between patients with T1D and T2D and evaluate the effect of glucose on bone turnover. Methods: A cross-sectional study was conducted. Patients diagnosed with T1D (n=98) or T2D (n=96) were included from the outpatient clinics at two University Hospitals. All individuals had normal renal function. Glucose and bone turnover markers were measured in non-fasting blood samples. Results: P-Procollagen type 1 amino terminal propeptide (P1NP), p-osteocalcin (OC), and s-Receptor Activator of Nuclear factor Kappa beta Ligand (RANKL) were lower in patients with T2D compared to T1D, and s-osteoprotegerin (OPG) was higher in T2D. P-C-terminal cross-linked telopeptide of type-I collagen (CTX), p-fibroblast growth factor-23 (FGF-23), p-sclerostin, and p-undercarboxylated osteocalcin (ucOC) were similar in between the two groups of patients. Increasing non-fasting glucose levels were inversely related to p-CTX, p-P1NP, p-OC, and p-ucOC and directly related to s-OPG in simple linear and multiple linear regressions adjusted for factors influencing bone turnover markers including HbA1c. Conclusion: Bone turnover markers were lower in patients with T2D compared to T1D. Acute blood glucose alterations may change bone turnover mediated by OPG and have detrimental effects on bone health in diabetes. Trial registration number: ClinicalTrials.govNCT01870557.
    Bone 11/2015; 83. DOI:10.1016/j.bone.2015.11.004
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    ABSTRACT: Since its discovery as a potent inhibitor for muscle development, myostatin has been actively pursued as a drug target for age- and disease-related muscle loss. However, potential adverse effects of long-term myostatin deficiency have not been thoroughly investigated. We report herein that male myostatin null mice (mstn(-/-)), in spite of their greater muscle mass compared to wild-type (wt) mice, displayed more significant functional decline from young (3-6months) to middle age (12-15months) than age-matched wt mice, measured as gripping strength and treadmill endurance. Mstn(-/-) mice displayed markedly restricted ankle mobility and degenerative changes of the ankle joints, including disorganization of bone, tendon and peri-articular connective tissue, as well as synovial thickening with inflammatory cell infiltration. Messenger RNA expression of several pro-osteogenic genes was higher in the Achilles tendon-bone insertion in mstn(-/-) mice than wt mice, even at the neonatal age. At middle age, higher plasma concentrations of growth factors characteristic of excessive bone remodeling were found in mstn(-/-) mice than wt controls. These data collectively indicate that myostatin may play an important role in maintaining ankle and wrist joint health, possibly through negative regulation of the pro-osteogenic WNT/BMP pathway.
    Bone 11/2015; 83. DOI:10.1016/j.bone.2015.11.003
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    ABSTRACT: Lycopene supplementation decreases oxidative stress and exhibits beneficial effects on bone health, but the mechanisms through which it alters bone metabolism in vivo remain unclear. The present study aims to evaluate the effects of lycopene treatment on postmenopausal osteoporosis. Six-month-old female Wistar rats (n=264) were sham-operated (SHAM) or ovariectomized (OVX). The SHAM group received oral vehicle only and the OVX rats were randomized into five groups receiving oral daily lycopene treatment (mg/kg body weight per day): 0 OVX (control), 15 OVX, 30 OVX, and 45 OVX, and one group receiving alendronate (ALN) (2μg/kg body weight per day), for 12weeks. Bone densitometry measurements, bone turnover markers, biomechanical testing, and histomorphometric analysis were conducted. Micro computed tomography was also used to evaluate changes in microarchitecture. Lycopene treatment suppressed the OVX-induced increase in bone turnover, as indicated by changes in biomarkers of bone metabolism: serum osteocalcin (s-OC), serum N-terminal propeptide of type 1 collagen (s-PINP), serum crosslinked carboxyterminal telopeptides (s-CTX-1), and urinary deoxypyridinoline (u-DPD). Significant improvement in OVX-induced loss of bone mass, bone strength, and microarchitectural deterioration was observed in lycopene-treated OVX animals. These effects were observed mainly at sites rich in trabecular bone, with less effect in cortical bone. Lycopene treatment down-regulated osteoclast differentiation concurrent with up-regulating osteoblast together with glutathione peroxidase (GPx) catalase (CAT) and superoxide dismutase (SOD) activities. These findings demonstrate that lycopene treatment in OVX rats primarily suppressed bone turnover to restore bone strength and microarchitecture.
    Bone 11/2015; 83. DOI:10.1016/j.bone.2015.10.017
  • [Show abstract] [Hide abstract]
    ABSTRACT: Obesity and osteoporosis have become major public health challenges worldwide. The brain is well established as a pivotal regulator of energy homeostasis, appetite and fuel metabolism. However, there is now clear evidence for regulation between the brain and bone. Similarly, evidence also indicates that the involvement of brain in bone and adipose regulation is both related and interdependent.The hypothalamus, with its semi-permeable blood brain barrier, is one of the most powerful regulatory regions within the body, integrating and relaying signals not only from peripheral tissues but also from within the brain itself. Two main neuronal populations within the arcuate nucleus of the hypothalamus regulate energy homeostasis: The orexigenic, appetite-stimulating neurons that co-express neuropeptide Y and agouti-related peptide and the anorexigenic, appetite-suppressing neurons that co-express proopiomelanocortin and cocaine- and amphetamine related transcript. From within the arcuate, these four neuropeptides encompass some of the most powerful control of energy homeostasis in the entire body. Moreover, they also regulate skeletal homeostasis, identifying a co-ordination network linking the processes of bone and energy homeostasis. Excitingly, the number of central neuropeptides and neural factors known to regulate bone and energy homeostasis continues to grow, with cannabinoid receptors and semaphorins also involved in bone homeostasis. These neuronal pathways represent a growing area of research that is identifying novel regulatory axes between the brain and the bone, and links with other homeostatic networks; thereby revealing a far more complex, and interdependent bone biology than previously envisioned. This review examines the current understanding of the central regulation of bone and energy metabolism.
    Bone 11/2015; DOI:10.1016/j.bone.2015.10.020
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    ABSTRACT: Atypical femur fractures (AFF) arise in the subtrochanteric and diaphyseal regions. Because of this unique distribution, we hypothesized that patients with AFF demonstrate specific geometrical variations of their lower limb whereby baseline tensile forces applied to the lateral cortex are higher and might favor the appearance of these rare stress fractures, when exposed to bisphosphonates. Using the low irradiation 2D-3D X-Ray scanner EOS™ imaging technology we aimed to characterize and compare femur geometric parameters between women who sustained bisphosphonate- associated AFF and those who had experienced similar duration of exposure to bisphosphonates but did not sustain fractures. Conditional logistic regression models were constructed to estimate the association between selected geometric parameters and the occurrence of AFF. We identified 16 Caucasian women with AFF and recruited 16 ethnicity-, sex-, age-, height- and cumulative bisphosphonate exposure-matched controls from local osteoporosis clinics. Compared to controls, those with AFF had more lateral femur bowing (-3.2° SD [3.4] versus -0.8° SD [1.9] p=0.02). In regression analysis, lateral femur bowing was associated with the risk of AFF (aOR 1.54; 95% CI 1.04-2.28, p=0.03). Women who sustained a subtrochanteric AFF demonstrated a lesser femoral neck shaft angle (varus geometry) than those with a fracture at a diaphyseal site (121.9 [3.6]° versus 127.6 [7.2]°, p=0.07), whereas femur bowing was more prominent in those with a diaphyseal fracture compared to those with a subtrochanteric fracture (-4.3 [3.2]° versus -0.9 [2.7]°, p=0.07). Our analyses support that subjects with AFF exhibit femoral geometry parameters that result in higher tensile mechanical load on the lateral femur. This may play a critical role in the pathogenesis of AFF and requires further evaluation in a larger size population.
    Bone 11/2015; DOI:10.1016/j.bone.2015.10.016
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    ABSTRACT: The high resolution peripheral computed tomography (HR-pQCT) technique has seen recent developments with regard to the assessment of cortical porosity. In this study, we investigated the role of cortical porosity on bone strength in a large cohort of women. The distal radius and distal tibia were scanned by HR-pQCT. We assessed bone strength by estimating the failure load by microfinite element analysis (μFEA), with isotropic and homogeneous material properties. We built a multivariate model to predict it, using a few microarchitecture variables including cortical porosity. Among 857 Caucasian women analyzed with μFEA, we found that cortical and trabecular properties, along with the failure load, impaired slightly with advancing age in premenopausal women, the correlations with age being modest, with |rage| ranging from 0.14 to 0.38. After the onset of the menopause, those relationships with age were stronger for most parameters at both sites, with |rage| ranging from 0.10 to 0.64, notably for cortical porosity and failure load, which were markedly deteriorated with increasing age. Our multivariate model using microarchitecture parameters revealed that cortical porosity played a significant role in bone strength prediction, with semipartial r(2)=0.22 only at the tibia in postmenopausal women. In conclusion, in our large cohort of women, we observed a small decline of bone strength at the tibia before the onset of menopause. We also found an age-related increase of cortical porosity at both scanned sites in premenopausal women. In postmenopausal women, the relatively high increase of cortical porosity accounted for the decline in bone strength only at the tibia.
    Bone 11/2015; DOI:10.1016/j.bone.2015.10.012
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    ABSTRACT: Subclinical hyperthyroidism has been reported to increase the fracture risk. However, the effect of thyroid stimulating hormone (TSH) suppressive therapy on bone geometry in the hip area of patients with differentiated thyroid carcinoma (DTC) is still unclear. The aim of this study was to investigate the effect of TSH suppression on bone geometry in the hip area of pre- and postmenopausal women with DTC. We conducted a retrospective cohort study including 99 women with DTC (25 pre- and 74 postmenopausal) who had received TSH suppressive therapy for at least 3years and 297 control subjects (75 and 222, respectively) matched for sex and age. Bone mineral density (BMD) in the spine and hip area and bone geometry at the femoral neck measured by dual energy X-ray absorptiometry (DXA) were compared between patients and controls. The association between thyroid hormone and bone parameters was investigated. All analyses of bone parameters were adjusted for age, body mass index, and serum calcium levels. In premenopausal subjects, TSH suppressive therapy was not associated with poor bone parameters. In postmenopausal subjects, patients with DTC undergoing TSH suppression showed lower cross-sectional moment of inertia (CSMI), cross-sectional area, and section modulus and thinner cortical thickness at the femoral neck than those of control subjects, whereas their femoral neck BMD was comparable with controls. Total hip BMD was lower in postmenopausal patients than in controls. CSMI and section modulus at the femoral neck were independently associated with serum free T4 levels in postmenopausal patients. The difference in femoral neck bone geometry between patients and controls was only apparent in postmenopausal DTC patients with free T4 >1.79ng/dL, and not in those with free T4 levels ≤1.79ng/dL. TSH suppression in postmenopausal DTC patients was associated with decreased bone strength by altering bone geometry rather than BMD in the hip area, especially the femoral neck. This alteration in bone quality was observed only in patients with free T4 levels above the upper normal limit.
    Bone 11/2015; 83. DOI:10.1016/j.bone.2015.10.015
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    ABSTRACT: Areal bone mineral density (BMD) by DXA, although an important index, does not accurately assess risk of fragility fracture. Another bone structural parameter, the orientation of type I collagen, is known to add to risk determination, independently of BMD. Accordingly, we investigated the Haversian systems of transiliac crest biopsies from non-osteoporotic women with low-trauma fractures, matched to healthy women without fracture by age and BMD. We employed circularly polarized light (CPL) microscopy because 1) each of the extinct and bright birefringent signals of CPL corresponds to a specific collagen arrangement; and 2) CPL can employ magnification suitable to provide data, of manageable size, from the whole cortical component of a section of biopsy. Under CPL, the coaxial layers of osteons, called lamellae, appear either birefringent extinct or bright. On a section transverse to the Haversian system, the extinct lamella comprises mainly collagen forming small angles, and the bright lamella comprises mainly collagen forming large angles, relative to the general orientation of the Haversian system. We performed semi-automatic morphometry for birefringent and structural parameters for which we computed intra- and inter- observer errors. The statistical analysis used a linear mixed model to compare fracturing and non-fracturing groups while addressing pairing of fracturing and non-fracturing subjects, and linear regression to assess differences between matched subjects. We found significant reduction in 1) lamellar width and area for extinct lamella and bright lamella; 2) percentage of extinct birefringence in osteons, and 3) single osteon area; in the fracturing group; and in lamellar width in the fracturing subject of all pairs. Our results evidence the need to investigate, in a larger sample of subjects, the distribution of collagen orientation as a parameter diagnostic of increased fracture risk.
    Bone 10/2015; DOI:10.1016/j.bone.2015.10.010
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    ABSTRACT: It is known that osteogenic differentiation of mesenchymal stem cells (MSCs) can be promoted by suppression of adipogenesis of MSCs. We have recently found that the chemical chaperone tauroursodeoxycholic acid (TUDCA) significantly reduces adipogenesis of MSCs. In the present study, we examined whether TUDCA can promote osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMMSCs) by regulating Integrin 5 (ITGA5) associated with activation of ERK1/2 signal pathway and thereby enhance bone tissue regeneration by reducing apoptosis and the inflammatory response. TUDCA treatment promoted in vitro osteogenic differentiation of BMMSCs and in vivo bone tissue regeneration in a calvarial defect model, as confirmed by micro-computed tomography, histological staining, and immunohistochemistry for osteocalcin. In addition, TUDCA treatment significantly decreased apoptosis and the inflammatory response in vivo and in vitro, which is important to enhance bone tissue regeneration. These results indicate that TUDCA plays a critical role in enhancing osteogenesis of BMMSCs, and is therefore a potential alternative drug for bone tissue regeneration.
    Bone 10/2015; 83. DOI:10.1016/j.bone.2015.10.011
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    ABSTRACT: Introduction: AHSG, a serum glycoprotein with recognized anti-calcification activity, has also been suggested to modulate both bone formation and resorption. Though the bulk of AHSG is mostly synthesized in the liver, it has been claimed that also bone cells might produce it. However, it remains to be definitively proven the extent of the bone AHSG production and the potential controlling factors. A relevant number of studies support the notion that FGF23, a bone-derived hormone, not only regulates the most important mineral metabolism (MM) related factors (phosphate, parathyroid hormone, vitamin D, etc), but might be also involved in cardiovascular (CV) outcome, both in chronic kidney disease (CKD) patients and in the general population. Furthermore, in addition to some direct autocrine and paracrine effects in bone, FGF23 has been suggested to interact with AHSG. In this study we investigated if AHSG is really produced by bone cells, and if its bone production is related and/or controlled by FGF23, using cultured bone cells, according to a new method recently published by our group. Results: Our data show that AHSG is consistently produced in osteocytes and to a far lesser extent in osteoblasts. Both FGF23 addition to the culture medium and its over-expression in osteocytes were associated with a consistent increase of both AHSG mRNA and protein, while FGF23 silencing was followed by opposite effects. Though most of these results were largely affected by the blockage of FGF23 receptors, the role of these receptors in the different experimental sets is still not completely clarified. In addition, we found that FGF23 and AHSG proteins co-localized both in cytoplasm and nucleus, which suggests a possible reciprocal interactivity. Conclusions: Our data not only confirm that AHSG is produced in bone, mainly in osteocytes, but show for the first time that its production is modulated by FGF23. Since both proteins play important roles in the bone and cardiovascular pathology, these results add new pieces to the puzzling relationship between bone and vascular pathology, in particular in CKD patients, prompting future investigations in this field.
    Bone 10/2015; 83. DOI:10.1016/j.bone.2015.10.008
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    ABSTRACT: We investigated age-related changes in bone strength and cross-sectional structure of the femoral neck (FN) in mainland Chinese men and women (according to age and sex) using dual-energy X-ray absorptiometry (DXA). A total of 3855 healthy adults (2713 women, 1142 men; ages 25-91years) were analyzed by FN bone mineral density (BMD) assessment and hip structural/strength analysis (HSA), including cross-sectional moment of inertia (CSMI), cross-sectional area (CSA), section modulus (Z), periosteal diameter (PD), endocortical diameter (ED), and cortical thickness (CT) using DXA. HSA differences between age and sex groups were adjusted for body weight, height and FN BMD. Trends according to age were estimated by linear regression analysis. There was no inverse correlation between HSA parameters and age in young adults. Some HSA parameters (CSMI, CSA, Z, CT) decreased significantly with age, whereas PD and ED increased significantly. Older adults had less bone strength and CT and higher PD and ED (p<0.05) than young adults. Men had greater increases in PD and ED than women across all ages. FN strength decreases with age in both sexes, caused by FN cross-sectional structural deterioration. Indirect comparison of our data with those from other populations showed less age-related FN periosteal apposition in Chinese than Caucasian men, but similar amounts in women. This may partly explain different male/female hip fracture rates among ethnic groups. Chinese men have more structural disadvantages regarding FN geometry during aging than Caucasian men, possibly conferring added susceptibility to hip fracture.
    Bone 10/2015; 83. DOI:10.1016/j.bone.2015.09.017