Inflammation, fracture and bone repair
The reconstitution of lost bone is a subject that is germane to many orthopedic conditions including fractures and non-unions, infection, inflammatory arthritis, osteoporosis, osteonecrosis, metabolic bone disease, tumors, and periprosthetic particle-associated osteolysis. In this regard, the proces...
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Published in | Bone (New York, N.Y.) Vol. 86; pp. 119 - 130 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
01.05.2016
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Subjects | |
Online Access | Get full text |
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Abstract | The reconstitution of lost bone is a subject that is germane to many orthopedic 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 among 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.
•Fundamental principles of bone healing and repair are summarized.•Crosstalk among inflammatory cells and bone cells is important for bone repair.•Opportunities for enhancing bone repair by modulating inflammation are discussed. |
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AbstractList | The reconstitution of lost bone is a subject that is germane to many orthopedic 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 among 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. 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. The reconstitution of lost bone is a subject that is germane to many orthopedic 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 among 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. •Fundamental principles of bone healing and repair are summarized.•Crosstalk among inflammatory cells and bone cells is important for bone repair.•Opportunities for enhancing bone repair by modulating inflammation are discussed. Abstract The reconstitution of lost bone is a subject that is germane to many orthopedic 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 among 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. |
Author | Córdova, Luis A. Pajarinen, Jukka Lin, Tzu-hua Loi, Florence Yao, Zhenyu Goodman, Stuart B. |
AuthorAffiliation | a 300 Pasteur Drive, Edwards Building, Room R116, Department of Orthopaedic Surgery, Stanford University, Stanford, CA, 94305, USA c 300 Pasteur Drive, Edwards Building, Room R114, Department of Bioengineering, Stanford University, Stanford, CA, 94305, USA b Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, University of Chile, Sergio Livingstone Polhammer 943, Independencia, 8380000, Santiago, Chile |
AuthorAffiliation_xml | – name: a 300 Pasteur Drive, Edwards Building, Room R116, Department of Orthopaedic Surgery, Stanford University, Stanford, CA, 94305, USA – name: b Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, University of Chile, Sergio Livingstone Polhammer 943, Independencia, 8380000, Santiago, Chile – name: c 300 Pasteur Drive, Edwards Building, Room R114, Department of Bioengineering, Stanford University, Stanford, CA, 94305, USA |
Author_xml | – sequence: 1 givenname: Florence surname: Loi fullname: Loi, Florence email: floi@stanford.edu organization: 300 Pasteur Drive, Edwards Building, Room R116, Department of Orthopaedic Surgery, Stanford University, Stanford, CA 94305, USA – sequence: 2 givenname: Luis A. surname: Córdova fullname: Córdova, Luis A. email: lcordova@stanford.edu organization: 300 Pasteur Drive, Edwards Building, Room R116, Department of Orthopaedic Surgery, Stanford University, Stanford, CA 94305, USA – sequence: 3 givenname: Jukka surname: Pajarinen fullname: Pajarinen, Jukka email: jpajari@stanford.edu organization: 300 Pasteur Drive, Edwards Building, Room R116, Department of Orthopaedic Surgery, Stanford University, Stanford, CA 94305, USA – sequence: 4 givenname: Tzu-hua surname: Lin fullname: Lin, Tzu-hua email: tzuhua@stanford.edu organization: 300 Pasteur Drive, Edwards Building, Room R116, Department of Orthopaedic Surgery, Stanford University, Stanford, CA 94305, USA – sequence: 5 givenname: Zhenyu surname: Yao fullname: Yao, Zhenyu email: zhenyuy@stanford.edu organization: 300 Pasteur Drive, Edwards Building, Room R116, Department of Orthopaedic Surgery, Stanford University, Stanford, CA 94305, USA – sequence: 6 givenname: Stuart B. surname: Goodman fullname: Goodman, Stuart B. email: goodbone@stanford.edu organization: 300 Pasteur Drive, Edwards Building, Room R116, Department of Orthopaedic Surgery, Stanford University, Stanford, CA 94305, USA |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26946132$$D View this record in MEDLINE/PubMed |
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Snippet | The reconstitution of lost bone is a subject that is germane to many orthopedic conditions including fractures and non-unions, infection, inflammatory... Abstract The reconstitution of lost bone is a subject that is germane to many orthopedic conditions including fractures and non-unions, infection, inflammatory... The reconstitution of lost bone is a subject that is germane to many orthopaedic conditions including fractures and non-unions, infection, inflammatory... |
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SubjectTerms | Animals Bone repair Cell Communication Fracture Healing Fractures, Bone - pathology Humans Inflammation Inflammation - pathology Orthopedics Osteocytes - pathology Tissue engineering |
Title | Inflammation, fracture and bone repair |
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