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Bone. 2016 May;86:119-30. doi: 10.1016/j.bone.2016.02.020. Epub 2016 Mar 2.

Inflammation, fracture and bone repair.

Author information

1
300 Pasteur Drive, Edwards Building, Room R116, Department of Orthopaedic Surgery, Stanford University, Stanford, CA 94305, USA. Electronic address: floi@stanford.edu.
2
300 Pasteur Drive, Edwards Building, Room R116, Department of Orthopaedic Surgery, Stanford University, Stanford, CA 94305, USA; Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, University of Chile, Sergio Livingstone Polhammer 943, Independencia, 8380000 Santiago, Chile. Electronic address: lcordova@stanford.edu.
3
300 Pasteur Drive, Edwards Building, Room R116, Department of Orthopaedic Surgery, Stanford University, Stanford, CA 94305, USA. Electronic address: jpajari@stanford.edu.
4
300 Pasteur Drive, Edwards Building, Room R116, Department of Orthopaedic Surgery, Stanford University, Stanford, CA 94305, USA. Electronic address: tzuhua@stanford.edu.
5
300 Pasteur Drive, Edwards Building, Room R116, Department of Orthopaedic Surgery, Stanford University, Stanford, CA 94305, USA. Electronic address: zhenyuy@stanford.edu.
6
300 Pasteur Drive, Edwards Building, Room R116, Department of Orthopaedic Surgery, Stanford University, Stanford, CA 94305, USA; 300 Pasteur Drive, Edwards Building, Room R114, Department of Bioengineering, Stanford University, Stanford, CA 94305, USA. Electronic address: goodbone@stanford.edu.

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.

KEYWORDS:

Bone repair; Fracture healing; Inflammation; Tissue engineering

PMID:
26946132
PMCID:
PMC4833637
DOI:
10.1016/j.bone.2016.02.020
[Indexed for MEDLINE]
Free PMC Article

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