Inflammation, Fracture and Bone Repair
Identifieur interne : 002734 ( Pmc/Corpus ); précédent : 002733; suivant : 002735Inflammation, Fracture and Bone Repair
Auteurs : Florence Loi ; Luis A. C Rdova ; Jukka Pajarinen ; Tzu-Hua Lin ; Zhenyu Yao ; Stuart B. GoodmanSource :
- Bone [ 8756-3282 ] ; 2016.
Abstract
The reconstitution of lost bone is a subject that is germane to many orthopaedic conditions including fractures and non-unions, infection, inflammatory arthritis, osteoporosis, osteonecrosis, metabolic bone disease, tumors, and periprosthetic particle-associated osteolysis. In this regard, the processes of acute and chronic inflammation play an integral role. Acute inflammation is initiated by endogenous or exogenous adverse stimuli, and can become chronic in nature if not resolved by normal homeostatic mechanisms. Dysregulated inflammation leads to increased bone resorption and suppressed bone formation. Crosstalk amongst inflammatory cells (polymorphonuclear leukocytes and cells of the monocyte-macrophage-osteoclast lineage) and cells related to bone healing (cells of the mesenchymal stem cell-osteoblast lineage and vascular lineage) is essential to the formation, repair and remodeling of bone. In this review, the authors provide a comprehensive summary of the literature related to inflammation and bone repair. Special emphasis is placed on the underlying cellular and molecular mechanisms, and potential interventions that can favorably modulate the outcome of clinical conditions that involve bone repair.
Url:
DOI: 10.1016/j.bone.2016.02.020
PubMed: 26946132
PubMed Central: 4833637
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PMC:4833637Le document en format XML
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</affiliation>
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<author><name sortKey="C Rdova, Luis A" sort="C Rdova, Luis A" uniqKey="C Rdova L" first="Luis A." last="C Rdova">Luis A. C Rdova</name>
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</affiliation>
<affiliation><nlm:aff id="A2">Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, University of Chile, Sergio Livingstone Polhammer 943, Independencia, 8380000, Santiago, Chile</nlm:aff>
</affiliation>
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<author><name sortKey="Pajarinen, Jukka" sort="Pajarinen, Jukka" uniqKey="Pajarinen J" first="Jukka" last="Pajarinen">Jukka Pajarinen</name>
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<author><name sortKey="Lin, Tzu Hua" sort="Lin, Tzu Hua" uniqKey="Lin T" first="Tzu-Hua" last="Lin">Tzu-Hua Lin</name>
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<author><name sortKey="Yao, Zhenyu" sort="Yao, Zhenyu" uniqKey="Yao Z" first="Zhenyu" last="Yao">Zhenyu Yao</name>
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<author><name sortKey="Goodman, Stuart B" sort="Goodman, Stuart B" uniqKey="Goodman S" first="Stuart B." last="Goodman">Stuart B. Goodman</name>
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<affiliation><nlm:aff id="A3">300 Pasteur Drive, Edwards Building, Room R114, Department of Bioengineering, Stanford University, Stanford, CA, 94305, USA</nlm:aff>
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<author><name sortKey="C Rdova, Luis A" sort="C Rdova, Luis A" uniqKey="C Rdova L" first="Luis A." last="C Rdova">Luis A. C Rdova</name>
<affiliation><nlm:aff id="A1">300 Pasteur Drive, Edwards Building, Room R116, Department of Orthopaedic Surgery, Stanford University, Stanford, CA, 94305, USA</nlm:aff>
</affiliation>
<affiliation><nlm:aff id="A2">Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, University of Chile, Sergio Livingstone Polhammer 943, Independencia, 8380000, Santiago, Chile</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Pajarinen, Jukka" sort="Pajarinen, Jukka" uniqKey="Pajarinen J" first="Jukka" last="Pajarinen">Jukka Pajarinen</name>
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<author><name sortKey="Lin, Tzu Hua" sort="Lin, Tzu Hua" uniqKey="Lin T" first="Tzu-Hua" last="Lin">Tzu-Hua Lin</name>
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<author><name sortKey="Yao, Zhenyu" sort="Yao, Zhenyu" uniqKey="Yao Z" first="Zhenyu" last="Yao">Zhenyu Yao</name>
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</affiliation>
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<author><name sortKey="Goodman, Stuart B" sort="Goodman, Stuart B" uniqKey="Goodman S" first="Stuart B." last="Goodman">Stuart B. Goodman</name>
<affiliation><nlm:aff id="A1">300 Pasteur Drive, Edwards Building, Room R116, Department of Orthopaedic Surgery, Stanford University, Stanford, CA, 94305, USA</nlm:aff>
</affiliation>
<affiliation><nlm:aff id="A3">300 Pasteur Drive, Edwards Building, Room R114, Department of Bioengineering, Stanford University, Stanford, CA, 94305, USA</nlm:aff>
</affiliation>
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<series><title level="j">Bone</title>
<idno type="ISSN">8756-3282</idno>
<idno type="eISSN">1873-2763</idno>
<imprint><date when="2016">2016</date>
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<front><div type="abstract" xml:lang="en"><p id="P2">The reconstitution of lost bone is a subject that is germane to many orthopaedic conditions including fractures and non-unions, infection, inflammatory arthritis, osteoporosis, osteonecrosis, metabolic bone disease, tumors, and periprosthetic particle-associated osteolysis. In this regard, the processes of acute and chronic inflammation play an integral role. Acute inflammation is initiated by endogenous or exogenous adverse stimuli, and can become chronic in nature if not resolved by normal homeostatic mechanisms. Dysregulated inflammation leads to increased bone resorption and suppressed bone formation. Crosstalk amongst inflammatory cells (polymorphonuclear leukocytes and cells of the monocyte-macrophage-osteoclast lineage) and cells related to bone healing (cells of the mesenchymal stem cell-osteoblast lineage and vascular lineage) is essential to the formation, repair and remodeling of bone. In this review, the authors provide a comprehensive summary of the literature related to inflammation and bone repair. Special emphasis is placed on the underlying cellular and molecular mechanisms, and potential interventions that can favorably modulate the outcome of clinical conditions that involve bone repair.</p>
</div>
</front>
</TEI>
<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">8504048</journal-id>
<journal-id journal-id-type="pubmed-jr-id">1710</journal-id>
<journal-id journal-id-type="nlm-ta">Bone</journal-id>
<journal-id journal-id-type="iso-abbrev">Bone</journal-id>
<journal-title-group><journal-title>Bone</journal-title>
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<issn pub-type="ppub">8756-3282</issn>
<issn pub-type="epub">1873-2763</issn>
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<article-meta><article-id pub-id-type="pmid">26946132</article-id>
<article-id pub-id-type="pmc">4833637</article-id>
<article-id pub-id-type="doi">10.1016/j.bone.2016.02.020</article-id>
<article-id pub-id-type="manuscript">NIHMS770705</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Inflammation, Fracture and Bone Repair</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Loi</surname>
<given-names>Florence</given-names>
</name>
<xref ref-type="aff" rid="A1">a</xref>
<email>floi@stanford.edu</email>
</contrib>
<contrib contrib-type="author"><name><surname>Córdova</surname>
<given-names>Luis A.</given-names>
</name>
<xref ref-type="aff" rid="A1">a</xref>
<xref ref-type="aff" rid="A2">b</xref>
<email>lcordova@stanford.edu</email>
</contrib>
<contrib contrib-type="author"><name><surname>Pajarinen</surname>
<given-names>Jukka</given-names>
</name>
<xref ref-type="aff" rid="A1">a</xref>
<email>jpajari@stanford.edu</email>
</contrib>
<contrib contrib-type="author"><name><surname>Lin</surname>
<given-names>Tzu-hua</given-names>
</name>
<xref ref-type="aff" rid="A1">a</xref>
<email>tzuhua@stanford.edu</email>
</contrib>
<contrib contrib-type="author"><name><surname>Yao</surname>
<given-names>Zhenyu</given-names>
</name>
<xref ref-type="aff" rid="A1">a</xref>
<email>zhenyuy@stanford.edu</email>
</contrib>
<contrib contrib-type="author"><name><surname>Goodman</surname>
<given-names>Stuart B.</given-names>
</name>
<xref ref-type="aff" rid="A1">a</xref>
<xref ref-type="aff" rid="A3">c</xref>
<email>goodbone@stanford.edu</email>
</contrib>
</contrib-group>
<aff id="A1"><label>a</label>
300 Pasteur Drive, Edwards Building, Room R116, Department of Orthopaedic Surgery, Stanford University, Stanford, CA, 94305, USA</aff>
<aff id="A2"><label>b</label>
Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, University of Chile, Sergio Livingstone Polhammer 943, Independencia, 8380000, Santiago, Chile</aff>
<aff id="A3"><label>c</label>
300 Pasteur Drive, Edwards Building, Room R114, Department of Bioengineering, Stanford University, Stanford, CA, 94305, USA</aff>
<author-notes><corresp id="FN1">Please address correspondence to: Stuart B. Goodman MD PhD, Department of Orthopaedic Surgery, Stanford University School of Medicine, 450 Broadway Street, Redwood City, CA, USA, 94063, Phone: 01-650-721-7662, Fax: 01-650-721-3470, <email>goodbone@stanford.edu</email>
</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>22</day>
<month>3</month>
<year>2016</year>
</pub-date>
<pub-date pub-type="epub"><day>02</day>
<month>3</month>
<year>2016</year>
</pub-date>
<pub-date pub-type="ppub"><month>5</month>
<year>2016</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>01</day>
<month>5</month>
<year>2017</year>
</pub-date>
<volume>86</volume>
<fpage>119</fpage>
<lpage>130</lpage>
<pmc-comment>elocation-id from pubmed: 10.1016/j.bone.2016.02.020</pmc-comment>
<abstract><p id="P2">The reconstitution of lost bone is a subject that is germane to many orthopaedic conditions including fractures and non-unions, infection, inflammatory arthritis, osteoporosis, osteonecrosis, metabolic bone disease, tumors, and periprosthetic particle-associated osteolysis. In this regard, the processes of acute and chronic inflammation play an integral role. Acute inflammation is initiated by endogenous or exogenous adverse stimuli, and can become chronic in nature if not resolved by normal homeostatic mechanisms. Dysregulated inflammation leads to increased bone resorption and suppressed bone formation. Crosstalk amongst inflammatory cells (polymorphonuclear leukocytes and cells of the monocyte-macrophage-osteoclast lineage) and cells related to bone healing (cells of the mesenchymal stem cell-osteoblast lineage and vascular lineage) is essential to the formation, repair and remodeling of bone. In this review, the authors provide a comprehensive summary of the literature related to inflammation and bone repair. Special emphasis is placed on the underlying cellular and molecular mechanisms, and potential interventions that can favorably modulate the outcome of clinical conditions that involve bone repair.</p>
</abstract>
<kwd-group><kwd>Inflammation</kwd>
<kwd>Bone Repair</kwd>
<kwd>Fracture Healing</kwd>
<kwd>Tissue Engineering</kwd>
</kwd-group>
</article-meta>
</front>
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