[Pathophysiology of fracture healing].
This article briefly summarizes our present knowledge on regulation of proliferation, differentiation and function of bone cells (osteoblasts, osteoclasts) by hormones (1,25-dihydroxyvitamin D3, parathyroid hormone, thyroid hormone, sex steroids, glucocorticoids and calcitonin), cytokines (IL-1, IL-4, IL-6, IL-11 und IFN-gamma) and growth factors (IGF-I, TGF-beta). Interaction of these factors in "basic multicellular units" acting locally on bone surfaces is thought to result in tight coupling of bone formation and resorption in bone-remodelling processes. The significance of the latter in different phases of fracture healing, which proceeds from mesenchymal cell proliferation through callus formation to calcification and bone modelling, is emphasized.
Ludwig Boltzmann-Institut für Osteologie, Medizinische Abteilung, Universität Wien.
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Klaushofer
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Peterlik
D000818:Animals; D016723:Bone Remodeling / Q000502:physiology; D001842:Bone and Bones / Q000473:pathology / Q000503:physiopathology; D002146:Bony Callus / Q000503:physiopathology; D002455:Cell Division / Q000502:physiology; D016207:Cytokines / Q000502:physiology; D017102:Fracture Healing / Q000502:physiology*; D006133:Growth Substances / Q000502:physiology; D006728:Hormones / Q000502:physiology; D006801:Humans
D016207:Cytokines; D006133:Growth Substances; D006728:Hormones
Pathophysiologie der Knochenbruchheilung.