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Pesquisa : A11.329.372.700 [Categoria DeCS]
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[PMID]:29302038
[Au] Autor:Lucas S; Omata Y; Hofmann J; Böttcher M; Iljazovic A; Sarter K; Albrecht O; Schulz O; Krishnacoumar B; Krönke G; Herrmann M; Mougiakakos D; Strowig T; Schett G; Zaiss MM
[Ad] Endereço:Department of Internal Medicine 3, Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, 91054, Erlangen, Germany.
[Ti] Título:Short-chain fatty acids regulate systemic bone mass and protect from pathological bone loss.
[So] Source:Nat Commun;9(1):55, 2018 01 04.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Microbial metabolites are known to modulate immune responses of the host. The main metabolites derived from microbial fermentation of dietary fibers in the intestine, short-chain fatty acids (SCFA), affect local and systemic immune functions. Here we show that SCFA are regulators of osteoclast metabolism and bone mass in vivo. Treatment of mice with SCFA as well as feeding with a high-fiber diet significantly increases bone mass and prevents postmenopausal and inflammation-induced bone loss. The protective effects of SCFA on bone mass are associated with inhibition of osteoclast differentiation and bone resorption in vitro and in vivo, while bone formation is not affected. Mechanistically, propionate (C3) and butyrate (C4) induce metabolic reprogramming of osteoclasts resulting in enhanced glycolysis at the expense of oxidative phosphorylation, thereby downregulating essential osteoclast genes such as TRAF6 and NFATc1. In summary, these data identify SCFA as potent regulators of osteoclast metabolism and bone homeostasis.
[Mh] Termos MeSH primário: Reabsorção Óssea/metabolismo
Osso e Ossos/metabolismo
Ácidos Graxos Voláteis/metabolismo
Osteoclastos/metabolismo
[Mh] Termos MeSH secundário: Animais
Densidade Óssea/efeitos dos fármacos
Reabsorção Óssea/prevenção & controle
Osso e Ossos/efeitos dos fármacos
Butiratos/metabolismo
Butiratos/farmacologia
Fibras na Dieta/administração & dosagem
Ácidos Graxos Voláteis/farmacologia
Feminino
Expressão Gênica/efeitos dos fármacos
Glicólise/efeitos dos fármacos
Seres Humanos
Camundongos Endogâmicos C57BL
Osteoclastos/efeitos dos fármacos
Propionatos/metabolismo
Propionatos/farmacologia
Substâncias Protetoras/metabolismo
Substâncias Protetoras/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Butyrates); 0 (Dietary Fiber); 0 (Fatty Acids, Volatile); 0 (Propionates); 0 (Protective Agents)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02490-4


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[PMID]:29370211
[Au] Autor:Hayes AR; Brungs D; Pavlakis N
[Ad] Endereço:Department of Medical Oncology, Royal North Shore Hospital, St Leonards, New South Wales, Australia.
[Ti] Título:Osteoclast inhibitors to prevent bone metastases in men with high-risk, non-metastatic prostate cancer: A systematic review and meta-analysis.
[So] Source:PLoS One;13(1):e0191455, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In advanced prostate cancer, osteoclast inhibitors prevent and palliate skeletal related events associated with bone metastases. However, it is uncertain whether they play a disease-modifying role earlier in the course of the disease. METHODS: Medline, EMBASE, Cochrane Central Register of Controlled Trials and Cochrane Database of Systematic Reviews and ASCO conference proceedings were searched for randomized controlled trials that compared osteoclast inhibitors with placebo and/or standard of care (SOC) in patients with high-risk, non-metastatic prostate cancer. The primary outcome measure was incidence of new bone metastases; secondary outcomes included overall survival (OS), prostate cancer specific survival, mortality unrelated to prostate cancer, toxicity and health related quality of life outcomes. Results are presented as relative risk (RR) with 95% confidence intervals (CI). RESULTS: Six randomized controlled trials (5947 participants) were included, five evaluating bisphosphonates and one denosumab. Overall, there was no difference in incidence of bone metastases between participants treated with osteoclast inhibitors versus placebo/SOC (RR 1.09, 95%CI 0.84-1.41, p = 0.51) however significant heterogeneity was observed between studies. The denosumab trial was the largest and only positive trial amongst the included studies (RR 0.83, 95%CI 0.73-0.95, p = 0.007). No significant difference was observed in OS (RR 0.99 95% CI 0.89-1.10, p = 0.84) nor prostate cancer specific survival (RR 1.12 95%CI 0.93-1.36, p = 0.24). Most studies reported increased rates of osteonecrosis of the jaw (5% or less) and hypocalcemia (2% or less) with osteoclast inhibitors. CONCLUSIONS: While there is limited evidence that bisphosphonates alter the natural history of high-risk, non-metastatic prostate cancer, denosumab delays onset of bone metastases in this patient population. Neither class of osteoclast inhibitor demonstrated an impact on survival outcomes. Future trials with better defined patient selection and a robust definition for high risk disease is critical.
[Mh] Termos MeSH primário: Conservadores da Densidade Óssea/uso terapêutico
Neoplasias Ósseas/prevenção & controle
Neoplasias Ósseas/secundário
Osteoclastos/efeitos dos fármacos
Neoplasias da Próstata/tratamento farmacológico
[Mh] Termos MeSH secundário: Denosumab/uso terapêutico
Difosfonatos/uso terapêutico
Seres Humanos
Masculino
Osteoclastos/patologia
Avaliação de Resultados (Cuidados de Saúde)
Neoplasias da Próstata/patologia
Qualidade de Vida
Ensaios Clínicos Controlados Aleatórios como Assunto
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Bone Density Conservation Agents); 0 (Diphosphonates); 4EQZ6YO2HI (Denosumab)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191455


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[PMID]:29304080
[Au] Autor:Hong C; Quach A; Lin L; Olson J; Kwon T; Bezouglaia O; Tran J; Hoang M; Bui K; Kim RH; Tetradis S
[Ad] Endereço:Section of Orthodontics, Division of Growth and Development, UCLA School of Dentistry, Los Angeles, California, United States of America.
[Ti] Título:Local vs. systemic administration of bisphosphonates in rat cleft bone graft: A comparative study.
[So] Source:PLoS One;13(1):e0190901, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A majority of patients with orofacial cleft deformity requires cleft repair through a bone graft. However, elevated amount of bone resorption and subsequent bone graft failure remains a significant clinical challenge. Bisphosphonates (BPs), a class of anti-resorptive drugs, may offer great promise in enhancing the clinical success of bone grafting. In this study, we compared the effects of systemic and local delivery of BPs in an intraoral bone graft model in rats. We randomly divided 34 female 20-week-old Fischer F344 Inbred rats into four groups to repair an intraoral critical-sized defect (CSD): (1) Control: CSD without graft (n = 4); (2) Graft/Saline: bone graft with systemic administration of saline 1 week post-operatively (n = 10); (3) Graft/Systemic: bone graft with systemic administration of zoledronic acid 1 week post-operatively (n = 10); and (4) Graft/Local: bone graft pre-treated with zoledronic acid (n = 10). At 6-weeks post-operatively, microCT volumetric analysis showed a significant increase in bone fraction volume (BV/TV) in the Graft/Systemic (62.99 ±14.31%) and Graft/Local (69.35 ±13.18%) groups compared to the Graft/Saline (39.18±10.18%). Similarly, histological analysis demonstrated a significant increase in bone volume in the Graft/Systemic (78.76 ±18.00%) and Graft/Local (89.95 ±4.93%) groups compared to the Graft/Saline (19.74±18.89%). The local delivery approach resulted in the clinical success of bone grafts, with reduced graft resorption and enhanced osteogenesis and bony integration with defect margins while avoiding the effects of BPs on peripheral osteoclastic function. In addition, local delivery of BPs may be superior to systemic delivery with its ease of procedure as it involves simple soaking of bone graft materials in BP solution prior to graft placement into the defect. This new approach may provide convenient and promising clinical applications towards effectively managing cleft patients.
[Mh] Termos MeSH primário: Transplante Ósseo
Fissura Palatina/cirurgia
Difosfonatos/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Fissura Palatina/tratamento farmacológico
Feminino
Osteoclastos/efeitos dos fármacos
Ratos
Ratos Endogâmicos F344
Microtomografia por Raio-X
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Diphosphonates)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190901


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[PMID]:29352112
[Au] Autor:Furuya M; Kikuta J; Fujimori S; Seno S; Maeda H; Shirazaki M; Uenaka M; Mizuno H; Iwamoto Y; Morimoto A; Hashimoto K; Ito T; Isogai Y; Kashii M; Kaito T; Ohba S; Chung UI; Lichtler AC; Kikuchi K; Matsuda H; Yoshikawa H; Ishii M
[Ad] Endereço:Department of Immunology and Cell Biology, Graduate School of Medicine & Frontier Biosciences, Osaka University, Osaka, 565-0871, Japan.
[Ti] Título:Direct cell-cell contact between mature osteoblasts and osteoclasts dynamically controls their functions in vivo.
[So] Source:Nat Commun;9(1):300, 2018 01 19.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Bone homeostasis is regulated by communication between bone-forming mature osteoblasts (mOBs) and bone-resorptive mature osteoclasts (mOCs). However, the spatial-temporal relationship and mode of interaction in vivo remain elusive. Here we show, by using an intravital imaging technique, that mOB and mOC functions are regulated via direct cell-cell contact between these cell types. The mOBs and mOCs mainly occupy discrete territories in the steady state, although direct cell-cell contact is detected in spatiotemporally limited areas. In addition, a pH-sensing fluorescence probe reveals that mOCs secrete protons for bone resorption when they are not in contact with mOBs, whereas mOCs contacting mOBs are non-resorptive, suggesting that mOBs can inhibit bone resorption by direct contact. Intermittent administration of parathyroid hormone causes bone anabolic effects, which lead to a mixed distribution of mOBs and mOCs, and increase cell-cell contact. This study reveals spatiotemporal intercellular interactions between mOBs and mOCs affecting bone homeostasis in vivo.
[Mh] Termos MeSH primário: Reabsorção Óssea/diagnóstico por imagem
Comunicação Celular/fisiologia
Osteoblastos/citologia
Osteoclastos/citologia
Osteogênese/fisiologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Feminino
Corantes Fluorescentes/química
Expressão Gênica
Genes Reporter
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Homeostase/fisiologia
Concentração de Íons de Hidrogênio
Microscopia Intravital/métodos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Osteoblastos/efeitos dos fármacos
Osteoblastos/fisiologia
Osteoclastos/efeitos dos fármacos
Osteoclastos/fisiologia
Hormônio Paratireóideo/farmacologia
Cultura Primária de Células
Crânio/citologia
Crânio/diagnóstico por imagem
Crânio/efeitos dos fármacos
Crânio/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fluorescent Dyes); 0 (Parathyroid Hormone); 0 (enhanced green fluorescent protein); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180121
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02541-w


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[PMID]:29342179
[Au] Autor:Ohyama Y; Ito J; Kitano VJ; Shimada J; Hakeda Y
[Ad] Endereço:Division of Oral Anatomy, Meikai University School of Dentistry, Sakado, Saitama, Japan.
[Ti] Título:The polymethoxy flavonoid sudachitin suppresses inflammatory bone destruction by directly inhibiting osteoclastogenesis due to reduced ROS production and MAPK activation in osteoclast precursors.
[So] Source:PLoS One;13(1):e0191192, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inflammatory bone diseases, including rheumatoid arthritis, periodontitis and peri-implantitis, are associated not only with the production of inflammatory cytokines but also with local oxidative status, which is defined by intracellular reactive oxygen species (ROS). Osteoclast differentiation has been reported to be related to increased intracellular ROS levels in osteoclast lineage cells. Sudachitin, which is a polymethoxyflavone derived from Citrus sudachi, possesses antioxidant properties and regulates various functions in mammalian cells. However, the effects of sudachitin on inflammatory bone destruction and osteoclastogenesis remain unknown. In calvaria inflamed by a local lipopolysaccharide (LPS) injection, inflammation-induced bone destruction and the accompanying elevated expression of osteoclastogenesis-related genes were reduced by the co-administration of sudachitin and LPS. Moreover, sudachitin inhibited osteoclast formation in cultures of isolated osteoblasts and osteoclast precursors. However, sudachitin rather increased the expression of receptor activator of NF-κB ligand (RANKL), which is an important molecule triggering osteoclast differentiation, and the mRNA ratio of RANKL/osteoprotegerin that is a decoy receptor for RANKL, in the isolated osteoblasts, suggesting the presence of additional target cells. When osteoclast formation was induced from osteoclast precursors derived from bone marrow cells in the presence of soluble RANKL and macrophage colony-stimulating factor, sudachitin inhibited osteoclastogenesis without influencing cell viability. Consistently, the expression of osteoclast differentiation-related molecules including c-fos, NFATc1, cathepsin K and osteoclast fusion proteins such as DC-STAMP and Atp6v0d2 was reduced by sudachitin. In addition, sudachitin decreased activation of MAPKs such as Erk and JNK and the ROS production evoked by RANKL in osteoclast lineage cells. Our findings suggest that sudachitin is a useful agent for the treatment of anti-inflammatory bone destruction.
[Mh] Termos MeSH primário: Flavonoides/farmacologia
Glicosídeos/farmacologia
Osteoclastos/efeitos dos fármacos
Osteoclastos/metabolismo
Osteogênese/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Conservadores da Densidade Óssea/farmacologia
Reabsorção Óssea/metabolismo
Reabsorção Óssea/patologia
Reabsorção Óssea/prevenção & controle
Diferenciação Celular/efeitos dos fármacos
Linhagem da Célula
Técnicas de Cocultura
Lipopolissacarídeos/toxicidade
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Osteíte/metabolismo
Osteíte/patologia
Osteíte/prevenção & controle
Osteoclastos/citologia
Osteogênese/fisiologia
Espécies Reativas de Oxigênio/metabolismo
Células-Tronco/citologia
Células-Tronco/efeitos dos fármacos
Células-Tronco/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bone Density Conservation Agents); 0 (Flavonoids); 0 (Glycosides); 0 (Lipopolysaccharides); 0 (Reactive Oxygen Species); 0 (sudachitin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191192


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[PMID]:29305867
[Au] Autor:Kamano Y; Watanabe J; Iida T; Kondo T; Okawa H; Yatani H; Saeki M; Egusa H
[Ad] Endereço:Division of Molecular and Regenerative Prosthodontics, Tohoku University Graduate School of Dentistry, 4-1 Seiryo-cho, Aoba-ku, Sendai, Miyagi 980-8575, Japan.
[Ti] Título:Binding of PICK1 PDZ domain with calcineurin B regulates osteoclast differentiation.
[So] Source:Biochem Biophys Res Commun;496(1):83-88, 2018 01 29.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The calcineurin/nuclear factor of activated T cell (NFAT) signaling pathway plays a major role in osteoclast differentiation; however, the proteins that react with the calcineurin-NFAT complex in osteoclasts to regulate osteoclastogenesis remain unclear. Here, we present evidence that PICK1 also positively regulates calcineurin B in osteoclasts to activate NFAT to promote osteoclastogenesis. mRNA and protein expression of PICK1 in murine primary bone marrow macrophages (BMMs) was significantly increased during RANKL-induced osteoclast differentiation. The interaction of PICK1 with calcineurin B in BMMs was confirmed by co-immunoprecipitation. An inhibitor of the PICK1 PDZ domain significantly decreased osteoclastogenesis marker gene expression and the number of TRAP-positive multinucleated cells among RAW264.7 osteoclast progenitor cells. Overexpression of PICK1 in RAW264.7 cells significantly increased the number of TRAP-positive mature osteoclasts. Increased NFAT activation with transcriptional activation of PICK1 during RAW264.7 osteoclastogenesis was also confirmed in a tetracycline-controlled PICK1 expression system. These results suggest that the PDZ domain of PICK1 directly interacts with calcineurin B in osteoclast progenitor cells and promotes osteoclast differentiation through activation of calcineurin-NFAT signaling.
[Mh] Termos MeSH primário: Calcineurina/metabolismo
Proteínas de Transporte/metabolismo
Fatores de Transcrição NFATC/metabolismo
Proteínas Nucleares/metabolismo
Osteoclastos/citologia
Osteoclastos/fisiologia
Osteogênese/fisiologia
Domínios PDZ/fisiologia
[Mh] Termos MeSH secundário: Animais
Sítios de Ligação
Diferenciação Celular/fisiologia
Camundongos
Ligação Proteica
Domínios Proteicos
Células RAW 264.7
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (NFATC Transcription Factors); 0 (Nuclear Proteins); 0 (Prkcabp protein, mouse); EC 3.1.3.16 (Calcineurin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180107
[St] Status:MEDLINE


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[PMID]:28458348
[Au] Autor:Lee DI; Jang SK; Park DW; Kim ST; Park JS; Jo BR; Park JY; Park HY; Joo SS
[Ad] Endereço:College of Pharmacy, Chung-Ang University.
[Ti] Título:Diarylheptanoid Hirsutenone Attenuates Osteoclastogenesis by Suppressing IFNγ and NF-κB Signaling in Th1 and Preosteoclastic Cells.
[So] Source:Biol Pharm Bull;40(5):630-637, 2017.
[Is] ISSN:1347-5215
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:The aim of the present study was to examine the inhibitory roles and mechanisms of hirsutenone (HTN) in the regulation of osteoclastogenesis. Gene levels were compared to assure the effects of HTN on osteoclastogenesis in mouse splenocytes/CD4 T cells, mouse macrophage-like cell line RAW264.7 (preosteoclast), MG63 (osteoblast), and RPMI1788 (B cell) cells. The mechanism by which HTN regulates the degradation of tumor necrosis factor receptor-associated factor 6 (TRAF6) and inhibits inhibitor of kappaB (IκB) and nuclear factor-kappaB (NF-κB) signaling was examined by Western blotting and luciferase reporter assays. Our results demonstrated that HTN effectively downregulated the expression of interferon γ (IFNγ), interleukin-22 (IL-22), IL-1ß, and tartrate-resistant acid phosphatase (TRAP) in splenocyte-/CD4 -RAW264.7 co-culture system. Moreover, receptor activator of nuclear factor-κB ligand (RANKL) and CD25 expression were also significantly inhibited in MG63 and CD4 single culture system, suggesting an additional independent effect of HTN on osteoclastogenesis. Notably, TRAF6 was markedly degraded along with a decrease in nuclear factor of activated T-cells (NFATc) and NF-κB activities in RAW264.7 cells. Finally, we concluded that HTN directly or indirectly inhibits osteoclastogenesis via the inhibition of NF-κB signaling by promoting TRAF6 degradation, and plays a crucial role in suppressing the expression of RANKL and cytokines expressed in IFNγ-producing T-helper 1 (Th1) cells. These findings suggest that HTN may be a promising therapeutic candidate for diseases resulting from bone loss.
[Mh] Termos MeSH primário: Catecóis/farmacologia
Diarileptanoides/farmacologia
Interferon gama/antagonistas & inibidores
NF-kappa B/antagonistas & inibidores
Osteoclastos/efeitos dos fármacos
Células Th1/efeitos dos fármacos
[Mh] Termos MeSH secundário: Alnus/química
Animais
Linfócitos T CD4-Positivos/metabolismo
Sobrevivência Celular/efeitos dos fármacos
Citocinas/antagonistas & inibidores
Citocinas/farmacologia
Camundongos
Camundongos Endogâmicos BALB C
Osteogênese/efeitos dos fármacos
Casca de Planta/química
Ligante RANK/genética
Células RAW 264.7
Transdução de Sinais/efeitos dos fármacos
Baço/química
Baço/citologia
Células-Tronco/efeitos dos fármacos
Fosfatase Ácida Resistente a Tartarato/biossíntese
Fosfatase Ácida Resistente a Tartarato/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Catechols); 0 (Cytokines); 0 (Diarylheptanoids); 0 (NF-kappa B); 0 (RANK Ligand); 0 (Tnfsf11 protein, mouse); 0 (hirsutenone); 82115-62-6 (Interferon-gamma); EC 3.1.3.2 (Acp5 protein, mouse); EC 3.1.3.2 (Tartrate-Resistant Acid Phosphatase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1248/bpb.b16-00876


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[PMID]:29275568
[Au] Autor:Wang ZX; Yang L; Tan JY; Chen LL
[Ad] Endereço:Department of Periodontology, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou 310009, China.
[Ti] Título:[Effects of T helper 1 cells and T helper 17 cells secreting cytokines on rat models of experimental periodontitis].
[So] Source:Zhonghua Kou Qiang Yi Xue Za Zhi;52(12):740-747, 2017 Dec 09.
[Is] ISSN:1002-0098
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the effects of secreting cytokines interferon-gamma (IFN-γ) and interleukin-17 (IL-17) of T helper 1 cells (Th1) and T helper 17 cells (Th17) on the peripheral blood and alveolar bone destruction, so as to provide a new explanation for cellular immunity-mediated alveolar bone destruction. Eighteen eight-week-old male Sprague-Dawley rats were divided, randomly and equally, into 3 groups: lipopolysaccharide (LPS) group, ligation group and normal control group. In the LPS group, LPS was injected into the alveolar mucosa on the buccalmedian site of the left upper first molar, while the right upper first molar was injected with equal volume of physiological saline as self-controls. The injections were performed every other day for four times totally. In the ligation group, the left upper first molars were ligatured with 0.2 mm orthodontic cords, while the right upper first molars were left untreated as self-controls, and supplemented with high-sugar diet to promote the periodontitis status. The rats in normal control group were fed normally. The concentrations of IFN-γ and IL-17 in peripheral blood were measured using enzyme linked immunosorbent assay (ELISA) method at the fourth week after the start of injection and at the eighth week after ligation. The histological of periodontal tissues were observed after hematoxylin-eosin (HE) staining and osteoclast count was performed under light microscope. The histological of osteoclasts were observed after tartrate-resistant acid phosphatase (TRAP) staining. Expression of IFN-γ and IL-17 were detected by immunohistochemical assay. The concentrations of IFN-γ in peripheral blood of LPS group [(185.0±50.7) ng/L] and ligation group [(202.9±60.4) ng/L] were significantly higher than that of normal control group [(106.3±17.2) ng/L]( 0.05). Meanwhile, histological examination showed inflammatory cells infiltration in the gingival epithelium, the height reduction of alveolar bone accompanied with absorption lacuna. There were significantly higher HE and TRAP stained osteoclasts in LPS group (9.50±1.05) and ligation group (10.83±1.17) than that in controlgroup (0.33±0.52)( 0.05). Moreover, the expressions of IL-17 in alveolar bone absorption area of LPS group and ligation group were significantly stronger than that in control group ( 0.05). The rat models of experimental periodontitis and alveolar bone resorption could be successfully established by means of ligationand LPS injection, respectively. The periodontal inflammatory responses were related to secreting cytokines IFN-γ and IL-17 of Th1 and Th17 cells, while Th17 cells might exert a positive effect on alveolar bone destruction.
[Mh] Termos MeSH primário: Perda do Osso Alveolar/imunologia
Interferon gama/secreção
Interleucina-17/secreção
Periodontite/metabolismo
Células Th1/secreção
Células Th17/secreção
[Mh] Termos MeSH secundário: Perda do Osso Alveolar/metabolismo
Animais
Modelos Animais de Doenças
Escherichia coli
Interferon gama/sangue
Interleucina-17/sangue
Ligadura
Lipopolissacarídeos
Masculino
Osteoclastos/citologia
Periodontite/etiologia
Periodontite/patologia
Distribuição Aleatória
Ratos
Ratos Sprague-Dawley
Fosfatase Ácida Resistente a Tartarato
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IL17 protein, rat); 0 (Interleukin-17); 0 (Lipopolysaccharides); 82115-62-6 (Interferon-gamma); EC 3.1.3.2 (Tartrate-Resistant Acid Phosphatase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:171226
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1002-0098.2017.12.006


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[PMID]:29238019
[Au] Autor:Yokota K
[Ad] Endereço:Department of Rheumatology and Applied Immunology, Faculty of Medicine, Saitama Medical University.
[Ti] Título:[Inflammation and osteoclasts].
[So] Source:Nihon Rinsho Meneki Gakkai Kaishi;40(5):367-376, 2017.
[Is] ISSN:1349-7413
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:  Osteoclasts are differentiated from precursors of the monocyte/macrophage lineage originated from bone marrow hematopoietic stem cells and are the sole bone-resorbing cells in the body. Osteoclast differentiation is thought to require M-CSF (macrophage colony-stimulating factor) and RANKL (receptor activator of nuclear factor kappa-B ligand) signaling. However, it has recently been proposed that under chronic inflammatory conditions, such as systemic autoimmune diseases (e.g., rheumatoid arthritis), an increase in inflammatory cytokine levels within joints induces pathological osteoclast differentiation, causing excessive bone resorption. In addition, the authors have reported that stimulating mouse bone marrow monocytes and human CD14 monocytes with combination of TNFα and IL-6 can induce differentiation of osteoclast-like cells, which are cells with bone resorption activity. In the present article, we discuss the mechanism of osteoclast differentiation of RANKL-independent bone-resorbing cells, using both data from the aforementioned report as well as the latest findings. Understanding the mechanisms underlying RANKL-independent, cytokine-mediated osteoclast differentiation could facilitate the development of novel therapies for inflammatory joint diseases.
[Mh] Termos MeSH primário: Diferenciação Celular/genética
Inflamação/etiologia
Inflamação/patologia
Osteoclastos/citologia
Osteoclastos/fisiologia
[Mh] Termos MeSH secundário: Animais
Artrite Reumatoide/etiologia
Artrite Reumatoide/patologia
Reabsorção Óssea/etiologia
Citocinas/fisiologia
Descoberta de Drogas
Seres Humanos
Mediadores da Inflamação/fisiologia
Interleucina-6/fisiologia
Fator Estimulador de Colônias de Macrófagos
Camundongos
Terapia de Alvo Molecular
Osteoclastos/patologia
Ligante RANK/fisiologia
Transdução de Sinais/fisiologia
Fator de Necrose Tumoral alfa/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cytokines); 0 (Inflammation Mediators); 0 (Interleukin-6); 0 (RANK Ligand); 0 (Tumor Necrosis Factor-alpha); 81627-83-0 (Macrophage Colony-Stimulating Factor)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.2177/jsci.40.367


  10 / 14386 MEDLINE  
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[PMID]:29238018
[Au] Autor:Okamoto K
[Ad] Endereço:Department of Osteoimmunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo.
[Ti] Título:[Regulation of bone by IL-17-producing T cells].
[So] Source:Nihon Rinsho Meneki Gakkai Kaishi;40(5):361-366, 2017.
[Is] ISSN:1349-7413
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:  Bone is a component of the skeletal-locomotor system but also functions as an immunological organ that harbors hematopoietic stem and progenitor cells. Since the immune and skeletal systems are closely related through a number of shared regulatory molecules including cytokines and receptors, bone can be affected in various immune disorders. Rheumatoid arthritis is a typical disease in which the immune system affects the bone metabolism. The enhanced activity of osteoclasts by the activation of Th17 cells causes the joint destruction in rheumatoid arthritis. Studies on bone destruction associated rheumatoid arthritis have highlighted the importance of the interplay between the immune and bone systems, and promoted the new interdisciplinary field of "osteoimmunology". Furthermore, recent studies have suggested that regulation of bone tissues by IL-17 is more complicated than we had expected. IL-17-prodcuing cells contribute to new bone formation at the enthesis in ankylosing spondylitis, and IL-17-producing γδ T cells promote bone regeneration by acting on the mesenchymal stem cells in bone fracture healing. It would be necessary to comprehensively understand the interplay between the immune and bone systems for elucidation of the molecular mechanisms underlying the pathogenesis of various diseases that involves the two systems.
[Mh] Termos MeSH primário: Regeneração Óssea/genética
Osso e Ossos/imunologia
Interleucina-17/fisiologia
Linfócitos Intraepiteliais/imunologia
Linfócitos Intraepiteliais/fisiologia
Osteogênese/genética
[Mh] Termos MeSH secundário: Animais
Artrite Reumatoide/imunologia
Artrite Reumatoide/patologia
Osso e Ossos/citologia
Osso e Ossos/metabolismo
Osso e Ossos/patologia
Células-Tronco Hematopoéticas
Seres Humanos
Interleucina-17/metabolismo
Células Mesenquimais Estromais/imunologia
Células Mesenquimais Estromais/fisiologia
Camundongos
Osteoblastos/imunologia
Osteoblastos/fisiologia
Osteoclastos/imunologia
Osteoclastos/fisiologia
Células-Tronco
Células Th17/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Interleukin-17)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.2177/jsci.40.361



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