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[PMID]: 29093341
[Au] Autor:Kanda J; Izumo N; Kobayashi Y; Onodera K; Shimakura T; Yamamoto N; Takahashi HE; Wakabayashi H
[Ad] Address:Department of Clinical Pharmacotherapy, Faculty of Pharmaceutical Sciences, Niigata University of Pharmacy and Applied Life Sciences.
[Ti] Title:Effects of the Antiepileptic Drugs Phenytoin, Gabapentin, and Levetiracetam on Bone Strength, Bone Mass, and Bone Turnover in Rats.
[So] Source:Biol Pharm Bull;40(11):1934-1940, 2017.
[Is] ISSN:1347-5215
[Cp] Country of publication:Japan
[La] Language:eng
[Ab] Abstract:Long-term treatment with antiepileptic drugs (AEDs) is accompanied by reduced bone mass that is associated with an increased risk of bone fractures. Although phenytoin has been reported to adversely influence bone metabolism, little is known pertaining to more recent AEDs. The aim of this study was to evaluate the effects of gabapentin or levetiracetam on bone strength, bone mass, and bone turnover in rats. Male Sprague-Dawley rats were orally administered phenytoin (20 mg/kg), gabapentin (30 or 150 mg/kg), or levetiracetam (50 or 200 mg/kg) daily for 12 weeks. Bone histomorphometric analysis of the tibia was performed and femoral bone strength was evaluated using a three-point bending method. Bone mineral density (BMD) of the femur and tibia was measured using quantitative computed tomography. Administration of phenytoin significantly decreased bone strength and BMD, which was associated with enhanced bone resorption. In contrast, treatment with gabapentin (150 mg/kg) significantly decreased bone volume and increased trabecular separation, as shown by bone histomorphometric analysis. Moreover, the bone formation parameters, osteoid volume and mineralizing surface, decreased after gabapentin treatment, whereas the bone resorption parameters, osteoclast surface and number, increased. Levetiracetam treatment did not affect bone strength, bone mass, and bone turnover. Our data suggested that gabapentin induced the rarefaction of cancellous bone, which was associated with decreased bone formation and enhanced bone resorption, and may affect bone strength and BMD after chronic exposure. To prevent the risk of bone fractures, patients prescribed a long-term administration of gabapentin should be regularly monitored for changes in bone mass.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171102
[Lr] Last revision date:171102
[St] Status:In-Process
[do] DOI:10.1248/bpb.b17-00482

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[PMID]: 29092978
[Au] Autor:Solan MC; Sakellariou A
[Ad] Address:Royal Surrey County Hospital, Egerton Road, Guildford, Surrey GU2 7XX, UK.
[Ti] Title:Posterior malleolus fractures: worth fixing.
[So] Source:Bone Joint J;99-B(11):1413-1419, 2017 Nov.
[Is] ISSN:2049-4408
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The posterior malleolus component of a fracture of the ankle is important, yet often overlooked. Pre-operative CT scans to identify and classify the pattern of the fracture are not used enough. Posterior malleolus fractures are not difficult to fix. After reduction and fixation of the posterior malleolus, the articular surface of the tibia is restored; the fibula is out to length; the syndesmosis is more stable and the patient can rehabilitate faster. There is therefore considerable merit in fixing most posterior malleolus fractures. An early post-operative CT scan to ensure that accurate reduction has been achieved should also be considered. Cite this article: 2017;99-B:1413-19.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171102
[Lr] Last revision date:171102
[St] Status:In-Process
[do] DOI:10.1302/0301-620X.99B11.BJJ-2017-1072

  3 / 54929 MEDLINE  
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[PMID]: 29055830
[Au] Autor:Fujita S; Mukai T; Mito T; Kodama S; Nagasu A; Kittaka M; Sone T; Ueki Y; Morita Y
[Ad] Address:Department of Rheumatology, Kawasaki Medical School, Kurashiki, Japan.
[Ti] Title:Pharmacological inhibition of tankyrase induces bone loss in mice by increasing osteoclastogenesis.
[So] Source:Bone;106:156-166, 2017 Oct 18.
[Is] ISSN:1873-2763
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Tankyrase is a poly (ADP-ribose) polymerase that leads to ubiquitination and degradation of target proteins. Since tankyrase inhibitors suppress the degradation of AXIN protein, a negative regulator of the canonical Wnt pathway, they effectively act as Wnt inhibitors. Small molecule tankyrase inhibitors are being investigated as drug candidates for cancer and fibrotic diseases, in which the Wnt pathways are aberrantly activated. Tankyrase is also reported to degrade the adaptor protein SH3BP2 (SH3 domain-binding protein 2). We have previously shown that SH3BP2 gain-of-function mutation enhances receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis in murine bone marrow-derived macrophages (BMMs). Although the interaction between tankyrase and SH3BP2 has been reported, it is not clear whether and how the inhibition of tankyrase affects bone cells and bone mass. Here, we have demonstrated that tankyrase inhibitors (IWR-1, XAV939, and G007-LK) enhanced RANKL-induced osteoclast formation and function in murine BMMs and human peripheral blood mononuclear cells through the accumulation of SH3BP2, subsequent phosphorylation of SYK, and nuclear translocation of NFATc1. Tankyrase inhibitors also enhanced osteoblast differentiation and maturation, represented by increased expression of osteoblast-associated genes accompanied by the accumulation of SH3BP2 protein and enhanced nuclear translocation of ABL, TAZ, and Runx2 in primary osteoblasts. Most importantly, pharmacological inhibition of tankyrase in mice significantly decreased tibia and lumbar vertebrae bone volumes in association with increased numbers of osteoclasts. Our findings uncover the role of tankyrase inhibition in bone cells and highlight the potential adverse effects of the inhibitor on bone.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1710
[Cu] Class update date: 171103
[Lr] Last revision date:171103
[St] Status:Publisher

  4 / 54929 MEDLINE  
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[PMID]: 29024060
[Au] Autor:Wang C; Abu-Amer Y; O'Keefe RJ; Shen J
[Ad] Address:Department of Orthopaedic Surgery, School of Medicine, Washington University, St. Louis, MO, USA.
[Ti] Title:Loss of Dnmt3b in Chondrocytes Leads to Delayed Endochondral Ossification and Fracture Repair.
[So] Source:J Bone Miner Res;, 2017 Oct 10.
[Is] ISSN:1523-4681
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Despite advanced understanding of signaling mediated by local and systemic factors, the role of epigenetic factors in the regulation of bone regeneration remains vague. The DNA methyltransferases (Dnmts) Dnmt3a and Dnmt3b have tissue specific expression patterns and create unique methylation signatures to regulate gene expression. Using a stabilized murine tibia fracture model we find that Dnmt3b is induced early in fracture healing, peaks at 10 days post fracture (dpf), and declines to nearly undetectable levels by 28 dpf. Dnmt3b expression was cell-specific and stage-specific. High levels were observed in chondrogenic lineage cells within the fracture callus. To determine the role of Dnmt3b in fracture healing, Agc1Cre ;Dnmt3b (Dnmt3b ) mice were generated to delete Dnmt3b in chondrogenic cells. Dnmt3b fracture displayed chondrogenesis and chondrocyte maturation defect, and a delay in the later events of angiogenesis, ossification, and bone remodeling. Biomechanical studies demonstrated markedly reduced strength in Dnmt3b fractures and confirmed the delay in repair. The angiogenic response was reduced in both vessel number and volume at 10 and 14 dpf in Dnmt3b mice. Immunohistochemistry showed decreased CD31 expression, consistent with the reduced angiogenesis. Finally, in vitro angiogenesis assays with human umbilical vein endothelial cells (HUVECs) revealed that loss of Dnmt3b in chondrocytes significantly reduced tube formation and endothelial migration. To identify specific angiogenic factors involved in the decreased callus vascularization, a protein array was performed using conditioned media isolated from control and Dnmt3b loss-of-function chondrocytes. Several angiogenic factors, including CXCL12 and osteopontin (OPN) were reduced in chondrocytes following loss of Dnmt3b. DNA methylation analysis further identified hypomethylation in Cxcl12 promoter region. Importantly, the defects in tube formation and cell migration could be rescued by administration of CXCL12 and/or OPN. Altogether, our findings establish that Dnmt3b positively regulates chondrocyte maturation process, and its genetic ablation leads to delayed angiogenesis and fracture repair. © 2017 American Society for Bone and Mineral Research.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1710
[Cu] Class update date: 171103
[Lr] Last revision date:171103
[St] Status:Publisher
[do] DOI:10.1002/jbmr.3305

  5 / 54929 MEDLINE  
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[PMID]: 29017892
[Au] Autor:Maratova K; Soucek O; Matyskova J; Hlavka Z; Petruzelkova L; Obermannova B; Pruhova S; Kolouskova S; Sumnik Z
[Ad] Address:Department of Pediatrics, Second Faculty of Medicine, Charles University in Prague and Motol University Hospital, V Uvalu 84, 150 06 Prague 5, Czech Republic. Electronic address: klara.maratova@fnmotol.cz.
[Ti] Title:Muscle functions and bone strength are impaired in adolescents with type 1 diabetes.
[So] Source:Bone;106:22-27, 2017 Oct 07.
[Is] ISSN:1873-2763
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Sarcopenia and osteoporosis are among the late complications of type 1 diabetes (T1D) in adults. Whether and to what extent musculoskeletal impairment is present in childhood and adolescence has yet to be determined. The aim of this study was to assess volumetric bone mineral density (BMD) and dynamic muscle function in adolescents with T1D and to assess the clinical and biochemical predictors of their musculoskeletal system. METHODS: Ninety-five children and adolescents (59 boys and 36 girls, mean age 16.2±1.2years) with T1D were included in this cross-sectional study. Study participants were divided into two groups according to the duration of the disease (<6years and >9years, respectively). Volumetric BMD of the non-dominant tibia was assessed using peripheral quantitative computed tomography (pQCT). Dynamic muscle function was evaluated using jumping mechanography. Gender- and height-specific Z-scores were calculated using published reference data. HbA1c was evaluated retrospectively as an average over the past 5years. RESULTS: Relative muscle power (P /mass) and force (F /body weight) were significantly decreased in T1D subjects (mean Z-scores -0.4±1.0; p<0.001, and -0.3±1.1; p<0.01, respectively). The duration of T1D negatively affected P /mass (p<0.01) but not F /body weight (p=0.54). Patients with T1D had also decreased trabecular BMD, the Strength-Strain Index and cortical thickness (mean Z-scores -0.8±1.3; -0.5±0.8 and -1.1±0.8, respectively, p<0.001 for all) whereas cortical BMD was increased when compared to controls (Z-score 1.2±0.90, p<0.001). No association was observed between the HbA1c and 25-hydroxyvitamin D levels and bone or muscle parameters. CONCLUSION: T1D influences the musculoskeletal system in adolescence. Decreased muscle function could contribute to the osteoporosis reported in adult diabetic patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1710
[Cu] Class update date: 171103
[Lr] Last revision date:171103
[St] Status:Publisher

  6 / 54929 MEDLINE  
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[PMID]: 28978416
[Au] Autor:Kitaguchi K; Kashii M; Ebina K; Kaito T; Okada R; Makino T; Noguchi T; Ishimoto T; Nakano T; Yoshikawa H
[Ad] Address:Department of Orthopedic Surgery, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan. Electronic address: kitaguchi-osk@umin.ac.jp.
[Ti] Title:Effects of single or combination therapy of teriparatide and anti-RANKL monoclonal antibody on bone defect regeneration in mice.
[So] Source:Bone;106:1-10, 2017 Oct 01.
[Is] ISSN:1873-2763
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: The purpose of this study is to investigate the effects of a single or combination therapy of teriparatide (TPTD) and anti-RANKL Ab (anti-murine receptor activator of nuclear factor κB ligand monoclonal antibody) on the regeneration of both cancellous and cortical bone. METHODS: Nine-week-old mice underwent bone defect surgery on the left femoral metaphysis (cancellous-bone healing model) and right femoral mid-diaphysis (cortical-bone healing model). After surgery, the mice were assigned to 1 of 4 groups to receive 1) saline (5 times a week; CNT group), 2) TPTD (40µg/kg 5 times a week; TPTD group), 3) anti-RANKL Ab (5mg/kg once; Ab group), or 4) a combination of TPTD and anti-RANKL Ab (COMB group). The following analyses were performed: Time-course microstructural analysis of healing in both cancellous and cortical bone in the bone defect, the volumetric bone mineral density of the tibia with micro-computed tomography, histological, histomorphometrical, and biomechanical analysis of regenerated bone. RESULTS: Regeneration of cancellous bone volume in the COMB group was the highest among the 4 groups, and this combined administration prompted medullary callus formation in the early phase of bone regeneration. On the other hand, regeneration of cortical bone volume in the COMB group was significantly higher than in the Ab group and was almost same as in the TPTD group. Histological analysis showed remaining woven bones, cartilage matrix, and immature lamellar bone in the COMB and Ab groups. However, biomechanical analysis showed that hardness and Young's modulus of regenerated cortical bone in the COMB group was not lower than in both the CNT and TPTD groups. Volumetric bone mineral density in the tibia was significantly increased in the COMB group compared with the other 3 groups. CONCLUSION: In the early phase of bone regeneration, the combination of TPTD and anti-RANKL Ab accelerates regeneration of cancellous bone in bone defects and increases cancellous bone mass in the tibia more effectively than either agent does individually, but these additive effects are not observed in the regeneration of cortical bone.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1710
[Cu] Class update date: 171103
[Lr] Last revision date:171103
[St] Status:Publisher

  7 / 54929 MEDLINE  
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[PMID]: 28974461
[Au] Autor:Campbell TM; Reilly K; Laneuville O; Uhthoff H; Trudel G
[Ad] Address:Elizabeth Bruyère Hospital, Ottawa, Ontario, Canada. Electronic address: tcampbell@bruyere.org.
[Ti] Title:Bone replaces articular cartilage in the rat knee joint after prolonged immobilization.
[So] Source:Bone;106:42-51, 2017 Sep 30.
[Is] ISSN:1873-2763
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Lost joint range of motion (ROM) is common in chronic osteoarthritis, alters regional weight-bearing across the articular surfaces, and contributes to loss of cartilage and bone alterations. Limited data exist on the regional effects on joints subjected to chronic losses of ROM. OBJECTIVE: To characterize the regional replacement by bone as part of articular cartilage degeneration after prolonged immobilization. METHODS: Eleven rat knees were rigidly-immobilized in flexion for 32weeks with contralateral and sham-operated (n=6) knees as controls. Sagittal medial tibial epiphysis histological sections assessed the anterior (non-weight-bearing), middle and posterior (both weight-bearing) regions. We quantified the distribution of collagen I, collagen II, cartilage thickness, glycosaminoglycan (GAG) staining, Mankin scoring, and subchondral bone plate cross-sectional area. Using immunohistochemistry (IHC), we visualized blood vessels, osteoblasts, and mesenchymal stem cells (MSCs). RESULTS: Immobilized cartilage had increased collagen I content in the anterior tibial region with picrosirius red staining (immobilized=61±20%; contralateral=43±12%, p=0.033; sham=20±10%, p=0.028) and collagen I IHC (immobilized=40±10%; contralateral=11±4%, p=0.003; sham=5±3%, p=0.043). Articular cartilage was thinner anteriorly (18±30µm) in immobilized knees versus contralateral (124±40µm, p<0.001) and sham (125±43µm, p=0.043). GAG staining covered 2±4% of the anterior articular area in immobilized knees versus 28±12% contralaterally (p=0.003) and 26±7% in sham (p=0.043). Mankin scores in immobilized knees were 4.7±1.7 versus 0.2±0.4 and 0±0 for contralateral and sham (p=0.003, p=0.042), respectively. The trabecular bone plate area of anterior and posterior regions showed relative loss of cross-sectional area in immobilized knees compared to controls (immobilized/contralateral area ratios of 0.67 and 0.46 respectively, both p=0.003), while the area in the middle region was preserved. Movat's pentachrome stain and CD31 staining showed chondral vascular ingrowth from subchondral bone. Osteocalcin and CD90 MSC staining were decreased in immobilized knees versus contralateral (p=0.003, p=0.036 respectively). CONCLUSIONS: Bony replacement characterizes articular cartilage degeneration of knees immobilized for 32weeks in the anterior, non-weight bearing region of the tibia. Replacement of cartilage by bone may have been mediated by chondral vascularization, suggesting irreversible changes. These findings stress the importance of weight-bearing and joint motion to maintain cartilage structure.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1710
[Cu] Class update date: 171103
[Lr] Last revision date:171103
[St] Status:Publisher

  8 / 54929 MEDLINE  
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[PMID]: 28914985
[Au] Autor:Kittaka M; Mayahara K; Mukai T; Yoshimoto T; Yoshitaka T; Gorski JP; Ueki Y
[Ad] Address:Department of Oral and Craniofacial Sciences, School of Dentistry, University of Missouri-Kansas City, Kansas City, MO, USA.
[Ti] Title:Cherubism Mice Also Deficient in c-Fos Exhibit Inflammatory Bone Destruction Executed by Macrophages That Express MMP14 Despite the Absence of TRAP+ Osteoclasts.
[So] Source:J Bone Miner Res;, 2017 Sep 15.
[Is] ISSN:1523-4681
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Currently, it is believed that osteoclasts positive for tartrate-resistant acid phosphatase (TRAP+) are the exclusive bone-resorbing cells responsible for focal bone destruction in inflammatory arthritis. Recently, a mouse model of cherubism (Sh3bp2 ) with a homozygous gain-of-function mutation in the SH3-domain binding protein 2 (SH3BP2) was shown to develop auto-inflammatory joint destruction. Here, we demonstrate that Sh3bp2 mice also deficient in the FBJ osteosarcoma oncogene (c-Fos) still exhibit noticeable bone erosion at the distal tibia even in the absence of osteoclasts at 12 weeks old. Levels of serum collagen I C-terminal telopeptide (ICTP), a marker of bone resorption generated by matrix metalloproteinases (MMPs), were elevated, whereas levels of serum cross-linked C-telopeptide (CTX), another resorption marker produced by cathepsin K, were not increased. Collagenolytic MMP levels were increased in the inflamed joints of the Sh3bp2 mice deficient in c-Fos. Resorption pits contained a large number of F4/80+ macrophages and genetic depletion of macrophages rescued these erosive changes. Importantly, administration of NSC405020, an MMP14 inhibitor targeted to the hemopexin (PEX) domain, suppressed bone erosion in c-Fos-deficient Sh3bp2 mice. After activation of the NF-κB pathway, macrophage colony-stimulating factor (M-CSF)-dependent macrophages from c-Fos-deficient Sh3bp2 mice expressed increased amounts of MMP14 compared with wild-type macrophages. Interestingly, receptor activator of NF-κB ligand (RANKL)-deficient Sh3bp2 mice failed to show notable bone erosion, whereas c-Fos deletion did restore bone erosion to the RANKL-deficient Sh3bp2 mice, suggesting that osteolytic transformation of macrophages requires both loss-of-function of c-Fos and gain-of-function of SH3BP2 in this model. These data provide the first genetic evidence that cells other than osteoclasts can cause focal bone destruction in inflammatory bone disease and suggest that MMP14 is a key mediator conferring pathological bone-resorbing capacity on c-Fos-deficient Sh3bp2 macrophages. In summary, the paradigm that osteoclasts are the exclusive cells executing inflammatory bone destruction may need to be reevaluated based on our findings with c-Fos-deficient cherubism mice lacking osteoclasts. © 2017 American Society for Bone and Mineral Research.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1709
[Cu] Class update date: 171103
[Lr] Last revision date:171103
[St] Status:Publisher
[do] DOI:10.1002/jbmr.3295

  9 / 54929 MEDLINE  
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[PMID]: 28880998
[Au] Autor:Simm PJ; Seah S; Gorelik A; Gilbert L; Nuguid J; Werther GA; Mackay MT; Freeman JL; Petty SJ; Wark JD
[Ad] Address:Department of Endocrinology and Diabetes, Royal Children's Hospital, Melbourne, Victoria, Australia.
[Ti] Title:Impaired bone and muscle development in young people treated with antiepileptic drugs.
[So] Source:Epilepsia;58(11):1931-1938, 2017 Nov.
[Is] ISSN:1528-1167
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Antiepileptic drugs (AEDs) are associated with reduced bone density, balance impairment, and increased fracture risk in adults. However, pediatric data are limited. Therefore, we aimed to examine bone, muscle, and balance outcomes in young patients taking AEDs. METHODS: We undertook a case-control study utilizing an AED exposure-discordant matched-pair approach. Subjects were aged 5-18 years with at least 12 months of AED exposure. Pairs were twins, nontwin siblings and first cousins, sex- and age-matched (to within 2 years), allowing for greater power than with unrelated control subjects. Dual energy x-ray absorptiometry (DXA), peripheral quantitative computed tomography (pQCT), and muscle force/balance were tested, with questionnaires were administered for bone health and epilepsy details. RESULTS: Twenty-three pairs were recruited, (median age 12.9 years [subjects] and 13.5 years [controls])-7 twin, 14 sibling, and 2 cousin pairs. Those taking AEDs had an increased prevalence of fractures (15 fractures in 8 subjects, compared with 4 fractures in 3 controls, p < 0.01). Trabecular volumetric bone mineral density (vBMD) measured by pQCT at the 4% site (tibia) was reduced by 14% (p = 0.03) in subjects. Subjects exerted a decreased maximum force compared to body weight (F total/g) at the tibia. There were no differences seen in either bone mineral parameters measured by DXA or balance measures. SIGNIFICANCE: Young people taking AEDs reported more fractures and had reductions in tibial vBMD and lower limb muscle force compared to their matched controls. These findings suggest that further exploration of bone health issues of young patients on AED therapy is required. Longitudinal studies are required to confirm these changes in the muscle-bone unit and to further explore the clinical outcomes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1709
[Cu] Class update date: 171103
[Lr] Last revision date:171103
[St] Status:In-Process
[do] DOI:10.1111/epi.13893

  10 / 54929 MEDLINE  
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[PMID]: 28694162
[Au] Autor:Singhal V; Tulsiani S; Campoverde KJ; Mitchell DM; Slattery M; Schorr M; Miller KK; Bredella MA; Misra M; Klibanski A
[Ad] Address:Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, United States; Pediatric Endocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, United States. Electronic address: vsinghal1@partners.org.
[Ti] Title:Impaired bone strength estimates at the distal tibia and its determinants in adolescents with anorexia nervosa.
[So] Source:Bone;106:61-68, 2017 Jul 08.
[Is] ISSN:1873-2763
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Altered bone microarchitecture and higher marrow adipose tissue (MAT) may reduce bone strength. High resolution pQCT (HRpQCT) allows assessment of volumetric BMD (vBMD), and size and microarchitecture parameters of bone, while 1H-magnetic resonance spectroscopy (1H-MRS) allows MAT evaluation. We have reported impaired microarchitecture at the non-weight bearing radius in adolescents with anorexia nervosa (AN) and that these changes may precede aBMD deficits. Data are lacking regarding effects of AN on microarchitecture and strength at the weight-bearing tibia in adolescents and young adults, and the impact of changes in microarchitecture and MAT on strength estimates. OBJECTIVE: To compare strength estimates at the distal tibia in adolescents/young adults with AN and controls in relation to vBMD, bone size and microarchitecture, and spine MAT. DESIGN AND METHODS: This was a cross-sectional study of 47 adolescents/young adults with AN and 55 controls 14-24years old that assessed aBMD and body composition using DXA, and distal tibia vBMD, size, microarchitecture and strength estimates using HRpQCT, extended cortical analysis, individual trabecular segmentation, and finite element analysis. Lumbar spine MAT (1H-MRS) was assessed in a subset of 19 AN and 22 controls. RESULTS: Areal BMD Z-scores were lower in AN than controls. At the tibia, AN had greater cortical porosity, lower total and cortical vBMD, cortical area and thickness, trabecular number, and strength estimates than controls. Within AN, strength estimates were positively associated with lean mass, aBMD, vBMD, bone size and microarchitectural parameters. MAT was higher in AN, and associated inversely with strength estimates. CONCLUSIONS: Adolescents/young adults with AN have impaired microarchitecture at the weight-bearing tibia and higher spine MAT, associated with reduced bone strength.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1707
[Cu] Class update date: 171103
[Lr] Last revision date:171103
[St] Status:Publisher


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