Database : MEDLINE
Search on : bone and resorption [Words]
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[PMID]: 29515110
[Au] Autor:Wang Q; Mo J; Zhao C; Huang K; Feng M; He W; Wang J; Chen S; Xie Z; Ma J; Fan S
[Ad] Address:Department of Orthopaedic Surgery, Sir Run Run Shaw Hospital, Medical College of Zhejiang University, Sir Run Run Shaw Institute of Clinical Medicine of Zhejiang University, 3# East Qingchun Road, Hangzhou, Zhejiang Province, 310016, China.
[Ti] Title:Raddeanin A suppresses breast cancer-associated osteolysis through inhibiting osteoclasts and breast cancer cells.
[So] Source:Cell Death Dis;9(3):376, 2018 Mar 07.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Bone metastasis is a severe complication of advanced breast cancer, resulting in osteolysis and increased mortality in patients. Raddeanin A (RA), isolated from traditional Chinese herbs, is an oleanane-type triterpenoid saponin with anticancer potential. In this study, we investigated the effects of RA in breast cancer-induced osteolysis and elucidated the possible mechanisms involved in this process. We first verified that RA could suppress osteoclast formation and bone resorption in vitro. Next, we confirmed that RA suppressed Ti-particle-induced osteolysis in a mouse calvarial model, possibly through inhibition of the SRC/AKT signaling pathway. A breast cancer-induced osteolysis mouse model further revealed the positive protective effects of RA by micro-computed tomography and histology. Finally, we demonstrated that RA inhibited invasion and AKT/mammalian target of rapamycin signaling and induced apoptosis in MDA-MB-231 cells. These results indicate that RA is an effective inhibitor of breast cancer-induced osteolysis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1038/s41419-018-0417-0

  2 / 60197 MEDLINE  
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[PMID]: 29511673
[Au] Autor:Chen HT; Wu CT; Huang TW; Shih HN; Wang JW; Lee MS
[Ad] Address:Department of Orthopaedic Surgery, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan.
[Ti] Title:Structural and Morselized Allografting Combined with a Cementless Cup for Acetabular Defects in Revision Total Hip Arthroplasty: A 4- to 14-Year Follow-Up.
[So] Source:Biomed Res Int;2018:2364269, 2018.
[Is] ISSN:2314-6141
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Using morselized and structural allograft to restore bone stock for massive acetabular bone defect in revision total hip arthroplasty (THA) is an appealing procedure. However, concerns about inability to achieve long-term stability following allograft resorption remained. From 2003 to 2012, 59 hips in 58 patients undergoing revision THA for Paprosky type II or III acetabular defects were retrospectively reviewed. The acetabular defects were managed with deep-frozen morselized and structural allografts, and a press-fit cementless cup along with supplementary screws. Clinical outcomes and radiographic results were analyzed with a mean follow-up of 8.7 years. The clinical successful rate was 100% for hips with Paprosky type II defect, 95.2% for IIIA defect, and 92.8% for IIIB defect. Three hips with type III defect failed at 4, 7, and 9 years, respectively. Harris Hip Score improved significantly from 60.1 preoperatively to 91.3 at the latest follow-up. All hips with good clinical results showed trabecular bridging in the allograft-host bone interface. Deep-frozen structural and morselized allograft in combination with a press-fit cementless cup represented a viable option to reconstruct acetabular defects in revision THA.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1155/2018/2364269

  3 / 60197 MEDLINE  
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[PMID]: 29511368
[Au] Autor:Fisher A; Fisher L; Srikusalanukul W; Smith PN
[Ad] Address:Department of Geriatric Medicine, The Canberra Hospital, Canberra, ACT Health, Canberra, Australia.
[Ti] Title:Bone Turnover Status: Classification Model and Clinical Implications.
[So] Source:Int J Med Sci;15(4):323-338, 2018.
[Is] ISSN:1449-1907
[Cp] Country of publication:Australia
[La] Language:eng
[Ab] Abstract:To develop a practical model for classification bone turnover status and evaluate its clinical usefulness. Our classification of bone turnover status is based on internationally recommended biomarkers of both bone formation (N-terminal propeptide of type1 procollagen, P1NP) and bone resorption (beta C-terminal cross-linked telopeptide of type I collagen, bCTX), using the cutoffs proposed as therapeutic targets. The relationships between turnover subtypes and clinical characteristic were assessed in1223 hospitalised orthogeriatric patients (846 women, 377 men; mean age 78.1±9.50 years): 451(36.9%) subjects with hip fracture (HF), 396(32.4%) with other non-vertebral (non-HF) fractures (HF) and 376 (30.7%) patients without fractures. Six subtypes of bone turnover status were identified: 1 - normal turnover (P1NP>32 µg/L, bCTX≤0.250 µg/L and P1NP/bCTX>100.0[(median value]); 2- low bone formation (P1NP ≤32 µg/L), normal bone resorption (bCTX≤0.250 µg/L) and P1NP/bCTX>100.0 (subtype2A) or P1NP/bCTX<100.0 (subtype 2B); 3- low bone formation, high bone resorption (bCTX>0.250 µg/L) and P1NP/bCTX<100.0; 4- high bone turnover (both markers elevated ) and P1NP/bCTX>100.0 (subtype 4A) or P1NP/bCTX<100.0 (subtype 4B). Compared to subtypes 1 and 2A, subtype 2B was strongly associated with nonvertebral fractures (odds ratio [OR] 2.0), especially HF (OR 3.2), age>75 years and hyperparathyroidism. Hypoalbuminaemia and not using osteoporotic therapy were two independent indicators common for subtypes 3, 4A and 4B; these three subtypes were associated with in-hospital mortality. Subtype 3 was associated with fractures (OR 1.7, for HF OR 2.4), age>75 years, chronic heart failure (CHF), anaemia, and history of malignancy, and predicted post-operative myocardial injury, high inflammatory response and length of hospital stay (LOS) above10 days. Subtype 4A was associated with chronic kidney disease (CKD), anaemia, history of malignancy and walking aids use and predicted LOS>20 days, but was not discriminative for fractures. Subtype 4B was associated with fractures (OR 2.1, for HF OR 2.5), age>75 years, CKD and indicated risks of myocardial injury, high inflammatory response and LOS>10 days. We proposed a classification model of bone turnover status and demonstrated that in orthogeriatric patients altered subtypes are closely related to presence of nonvertebral fractures, comorbidities and poorer in-hospital outcomes. However, further research is needed to establish optimal cut points of various biomarkers and improve the classification model.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.7150/ijms.22747

  4 / 60197 MEDLINE  
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[PMID]: 29499415
[Au] Autor:Figeac F; Andersen DC; Nipper Nielsen CA; Ditzel N; Sheikh SP; Skjødt K; Kassem M; Jensen CH; Abdallah BM
[Ad] Address:Molecular Endocrinology Lab. (KMEB), Department of Endocrinology, Odense University Hospital & University of Southern Denmark, Odense, Denmark.
[Ti] Title:Antibody-based inhibition of circulating DLK1 protects from estrogen deficiency-induced bone loss in mice.
[So] Source:Bone;110:312-320, 2018 Feb 27.
[Is] ISSN:1873-2763
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Soluble delta-like 1 homolog (DLK1) is a circulating protein that belongs to the Notch/Serrate/delta family, which regulates many differentiation processes including osteogenesis and adipogenesis. We have previously demonstrated an inhibitory effect of DLK1 on bone mass via stimulation of bone resorption and inhibition of bone formation. Further, serum DLK1 levels are elevated and positively correlated to bone turnover markers in estrogen (E)-deficient rodents and women. In this report, we examined whether inhibition of serum DLK1 activity using a neutralizing monoclonal antibody protects from E deficiency-associated bone loss in mice. Thus, we generated mouse monoclonal anti-mouse DLK1 antibodies (MAb DLK1) that enabled us to reduce and also quantitate the levels of bioavailable serum DLK1 in vivo. Ovariectomized (ovx) mice were injected intraperitoneally twice weekly with MAb DLK1 over a period of one month. DEXA-, microCT scanning, and bone histomorphometric analyses were performed. Compared to controls, MAb DLK1 treated ovx mice were protected against ovx-induced bone loss, as revealed by significantly increased total bone mass (BMD) due to increased trabecular bone volume fraction (BV/TV) and inhibition of bone resorption. No significant changes were observed in total fat mass or in the number of bone marrow adipocytes. These results support the potential use of anti-DLK1 antibody therapy as a novel intervention to protect from E deficiency associated bone loss.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 60197 MEDLINE  
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[PMID]: 29467330
[Au] Autor:Christov M; Clark AR; Corbin B; Hakroush S; Rhee EP; Saito H; Brooks D; Hesse E; Bouxsein M; Galjart N; Jung JY; Mundel P; Jüppner H; Weins A; Greka A
[Ad] Address:Endocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.
[Ti] Title:Inducible podocyte-specific deletion of CTCF drives progressive kidney disease and bone abnormalities.
[So] Source:JCI Insight;3(4), 2018 Feb 22.
[Is] ISSN:2379-3708
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Progressive chronic kidney diseases (CKDs) are on the rise worldwide. However, the sequence of events resulting in CKD progression remain poorly understood. Animal models of CKD exploring these issues are confounded by systemic toxicities or surgical interventions to acutely induce kidney injury. Here we report the generation of a CKD mouse model through the inducible podocyte-specific ablation of an essential endogenous molecule, the chromatin structure regulator CCCTC-binding factor (CTCF), which leads to rapid podocyte loss (iCTCFpod-/-). As a consequence, iCTCFpod-/- mice develop severe progressive albuminuria, hyperlipidemia, hypoalbuminemia, and impairment of renal function, and die within 8-10 weeks. CKD progression in iCTCFpod-/- mice leads to high serum phosphate and elevations in fibroblast growth factor 23 (FGF23) and parathyroid hormone that rapidly cause bone mineralization defects, increased bone resorption, and bone loss. Dissection of the timeline leading to glomerular pathology in this CKD model led to the surprising observation that podocyte ablation and the resulting glomerular filter destruction is sufficient to drive progressive CKD and osteodystrophy in the absence of interstitial fibrosis. This work introduces an animal model with significant advantages for the study of CKD progression, and it highlights the need for podocyte-protective strategies for future kidney therapeutics.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher

  6 / 60197 MEDLINE  
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[PMID]: 29448032
[Au] Autor:Wang M; Wang L; Ye R
[Ad] Address:Department of Joint Surgery, The Affiliated Hospital of Medical School of Ningbo University, Ningbo, 315020, China.
[Ti] Title:Risedronate reduces postoperative bone resorption after cementless total hip arthroplasty: A systematic review and meta-analysis.
[So] Source:Int J Surg;52:189-200, 2018 Feb 12.
[Is] ISSN:1743-9159
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:OBJECTIVE: To examine the effects of risedronate for reducing periprosthetic bone loss after total hip arthroplasty (THA). METHODS: Two reviewers performed an electronic literature search for randomized controlled trial (RCTs) evaluating the risedronate in the management of periprosthetic bone loss after primary THA. The electronic databases include PubMed, Medline, Embase, Web of Science and the Cochrane Library from inception to January 2018. We assessed the risk of bias using the Cochrane risk-of-bias tool. STATA 14.0 was used to perform the meta-analysis. RESULTS: Four RCTs were included in our study. Current meta-analysis indicated that postoperative reduciton of periprosthetic BMD in the risedronate group was significantly lower than that in the placebo group in zones 1, 2, 3, 4, 6, and 7. There was no increased risk of adverse effects. CONCLUSION: The administration of risedronate was associates with a significantly improved periprosthetic BMD after primary THA. No increased risk of adverse events were observed. Higher quality RCTs are still required for further research.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  7 / 60197 MEDLINE  
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[PMID]: 29432919
[Au] Autor:Zhao L; Guan H; Song C; Wang Y; Liu C; Cai C; Zhu H; Liu H; Zhao L; Xiao J
[Ad] Address:Department of Orthopaedic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.
[Ti] Title:YAP1 is essential for osteoclastogenesis through a TEADs-dependent mechanism.
[So] Source:Bone;110:177-186, 2018 Feb 10.
[Is] ISSN:1873-2763
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Yes-associated protein 1 (YAP1), the core effector of the Hippo signaling pathway, has been identified as a key regulator of tissue homeostasis and organ development by controlling cell proliferation and differentiation. Previous studies have shown that YAP1 regulates multiple steps during skeletal development and bone remodeling, including the self-renewal and differentiation of mesenchymal stem cells (MSCs). However, its role in osteoclastogenesis remains largely unknown. Here, we report that YAP1 is an essential regulator for osteoclast differentiation and activity. Both mRNA and protein levels of YAP1 were downregulated during RANKL-induced osteoclastogenesis. Short hairpin RNA-mediated knockdown of YAP1 in bone marrow-derived macrophages (BMM) prevented the formation and function of multinucleated osteoclasts, and markedly abrogated the expression of osteoclast marker genes. Furthermore, the suppression of osteoclastogenesis and bone resorption activity were also observed in the BMM treated with verteporfin, a small molecule that inhibits the association of YAP1 with the transcriptional enhancer-associated domain (TEAD) family of transcription factors, the major partner of YAP1. Mechanistically, the interaction of YAP1/TEADs with AP-1 and cooperation on downstream gene transcription were confirmed, and RANKL-induced NF-κB signaling was also impaired in the YAP1-inhibited condition. Our results revealed the essential role of YAP1 and the YAP1-TEADs complex in regulating osteoclastogenesis and related gene expression.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  8 / 60197 MEDLINE  
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[PMID]: 29428552
[Au] Autor:De Luna G; Ranque B; Courbebaisse M; Ribeil JA; Khimoud D; Dupeux S; Silvera J; Offredo L; Pouchot J; Arlet JB
[Ad] Address:Internal Medicine Department, Sickle Cell Referral Center, Georges Pompidou European Hospital, AP-HP, Paris, France; Faculté de Médecine Paris Descartes, Sorbonne Paris-Cité, Paris, France. Electronic address: gonzalo.deluna@aphp.fr.
[Ti] Title:High bone mineral density in sickle cell disease: Prevalence and characteristics.
[So] Source:Bone;110:199-203, 2018 Feb 08.
[Is] ISSN:1873-2763
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Osteosclerosis (OSC) is a rarely studied complication of sickle cell disease (SCD). The objective of our study was to determine the prevalence and characteristics of high bone mineral density (BMD) and its radiological features in adult SCD patients. METHODS: This prospective observational study was conducted from May 2007 to May 2016 in consecutive patients with steady-state SCD at two university hospitals. The BMD of the lumbar spine (L1-L4) and right femoral neck was determined by dual energy X-ray absorptiometry. Clinical, laboratory and radiographic data were recorded. High BMD was defined as a BMD Z-score of at least +2.5 standard deviations at the lumbar spine or hip. The characteristics of the patients with high BMD were compared to those of individuals with low or middle BMD, using multivariate ordinal logistic regression. RESULTS: 135 patients (86 women and 49 men) with a median age of 27 (IQR 23-33) years were included. High BMD was diagnosed in 20 (15%) patients with a median age of 33.5 (IQR 28-45) years. The SCD genotypes of these patients were SS in 11, SC in 5, S/beta+ in 3, and S/beta0 in 1. High BMD patients more frequently harbored the S/beta SCD genotype (21% vs 5% in non-high BMD patients; p=0.047) and were older (p=0.0007). Compared to patients with low or middle BMD, after adjustment for age and SCD genotype, high BMD patients had a higher prevalence of avascular necrosis history (p=0.009), higher BMI (p=0.007), and lower serum resorption marker CTX (p=0.04), bilirubin (p=0.02) and parathyroid hormone levels (p=0.02). There were no differences between groups regarding fracture history, H-shaped vertebrae or other biological variables. CONCLUSION: High-BMD values is a common manifestation in SCD patients, especially in those with the S/beta-thalassemia genotypes. The prevalence of high-BMD in SCD is associated with older age, suggesting that it will be more common in the future because the life span of patients with SCD is increasing thanks to significant progress in SCD treatment.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  9 / 60197 MEDLINE  
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[PMID]: 29408511
[Au] Autor:Elsayed R; Abraham P; Awad ME; Kurago Z; Baladhandayutham B; Whitford GM; Pashley DH; McKenna CE; Elsalanty ME
[Ad] Address:Department of Oral Biology, Dental College of Georgia, Augusta University, Augusta, GA, USA.
[Ti] Title:Removal of matrix-bound zoledronate prevents post-extraction osteonecrosis of the jaw by rescuing osteoclast function.
[So] Source:Bone;110:141-149, 2018 Feb 08.
[Is] ISSN:1873-2763
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Unlike other antiresorptive medications, bisphosphonate molecules accumulate in the bone matrix. Previous studies of side-effects of anti-resorptive treatment focused mainly on systemic effects. We hypothesize that matrix-bound bisphosphonate molecules contribute to the pathogenesis of bisphosphonate-related osteonecrosis of the jaw (BRONJ). In this study, we examined the effect of matrix-bound bisphosphonates on osteoclast differentiation in vitro using TRAP staining and resorption assay, with and without pretreatment with EDTA. We also tested the effect of zoledronate chelation on the healing of post-extraction defect in rats. Our results confirmed that bisphosphonates bind to, and can be chelated from, mineralized matrix in vitro in a dose-dependent manner. Matrix-bound bisphosphonates impaired the differentiation of osteoclasts, evidenced by TRAP activity and resorption assay. Zoledronate-treated rats that underwent bilateral dental extraction with unilateral EDTA treatment showed significant improvement in mucosal healing and micro-CT analysis on the chelated sides. The results suggest that matrix-bound bisphosphonates are accessible to osteoclasts and chelating agents and contribute to the pathogenesis of BRONJ. The use of topical chelating agents is a promising strategy for the prevention of BRONJ following dental procedures in bisphosphonate-treated patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  10 / 60197 MEDLINE  
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[PMID]: 29355746
[Au] Autor:Kohli N; Ho S; Brown SJ; Sawadkar P; Sharma V; Snow M; García-Gareta E
[Ad] Address:Regenerative Biomaterials Group, RAFT Institute, Leopold Muller Building, Mount Vernon Hospital, Northwood HA6 2RN, UK. Electronic address: kohliN@raft.ac.uk.
[Ti] Title:Bone remodelling in vitro: Where are we headed?: -A review on the current understanding of physiological bone remodelling and inflammation and the strategies for testing biomaterials in vitro.
[So] Source:Bone;110:38-46, 2018 Feb 02.
[Is] ISSN:1873-2763
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Bone remodelling is a dynamic process required for the maintenance of bone architecture in response to the changing mechanical needs. It is also a vital process during the repair of bone tissue following injury. Clinical intervention in terms of autografting or allografting is often required to heal bone injuries where physiological healing fails. The use of biomaterials as alternatives to autografts and allografts has spurred a significant research interest into further development of biomaterials for better clinical outcomes. Unfortunately, many biomaterials fail to make it to the clinic or fail after implantation due to the inconsistencies observed between in vitro and in vivo studies. It is therefore important to mimic the in vivo situation as closely as possible in an in vitro setting for testing biomaterials. The current in vitro models focus mostly on investigating the behaviour of osteoblast progenitors with the biomaterial under development as well as assessing the behaviour of osteoclasts, endothelial cells etc. However, the sequence of events that take place during bone healing or remodelling are not incorporated into the current in vitro models. This review highlights our current understanding of the physiological bone remodelling and the bone healing process followed by strategies to incorporate both the physiological and pathophysiological events into an in vitro environment. Here, we propose three strategies for the assessment of biomaterials for bone, which includes; (1) testing biomaterials in the presence of immune cells, (2) testing biomaterials for osteogenesis, and (3) testing biomaterials in the presence of osteoclasts followed by osteoblasts to recapitulate the physiological events of bone resorption prior to bone formation. The focus of this review is to discuss the third strategy in details as the first two strategies are currently incorporated into a majority of in vitro experiments.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1801
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher


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