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Trauma-Induced Inflammation and Fracture Healing

Pape, Hans-Christophe MD*; Marcucio, Ralph PhD†; Humphrey, Catherine MD‡; Colnot, Celine PhD†; Knobe, Matthias MD*; Harvey, Edward J MDCM, MSc, FRCSC§

doi: 10.1097/BOT.0b013e3181ed1361
Review Article

Fracture healing is an extremely complex interaction of cells, biologic pathways, and molecules. Certainly, the inflammatory response is one of the initiating factors for bone healing. The inflammatory phase is a critical period characterized by low oxygen tension, impaired perfusion, and the migration of a wide array of cells and release of active molecules. Systemwide inflammatory conditions also modulate the primary processes of fracture management. Osteoprogenitor cells, mesenchymal cells, osteoblasts, and chondrocytes contribute to the healing and inflammatory response at the bone level. The inflammatory process is dependent on and propagates through proinflammatory cytokines, the transforming growth factor-β superfamily with other growth factors, and the metalloproteinases and angiogenic factors. Interference with any of these pathways or proteins either promotes or more likely decreases fracture healing. This article reviews the initial inflammatory response to trauma as it pertains to musculoskeletal healing.

From the *Aachen University, Aachen, Germany; †University of California at San Francisco, San Francisco, CA; ‡University of Rochester, Rochester, NY; and §McGill University, Montreal, Canada.

Accepted for publication June 15, 2010.

Financial support was received in the form of an NIH grant (NIH-RO1-AR053645), institutional support (UCSF) and funding from MTF and OTC.

Reprints: Edward J. Harvey, MDCM, MSc, FRCSC, McGill University Health Center, Division of Orthopaedic Surgery, MUHC-Montreal General Site, 1650 Cedar Avenue, Room B5.159.5, Montreal, Quebec, Canada H3G1A4 (e-mail:

© 2010 Lippincott Williams & Wilkins, Inc.