[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.
Klaushofer
K
K
Ludwig Boltzmann-Institut für Osteologie, Medizinische Abteilung, Universität Wien.
Peterlik
M
M
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.