Abstract
Bone remodelling is characterized by a balance between bone resorption and bone formation. The osteoblasts are responsible for bone synthesis and the osteoclasts for bone resorption. A finely adjusted interaction between molecular mechanisms results, via cytokines, hormones and growth factors, in homeostasis of bone metabolism. Here, the RANK/RANKL/OPG-system is actively involved in the differentiation and function of osteoclasts and is known to play a central role in the majority of pathophysiological mechanisms. Also the Wnt and BMP signalling pathways play a major role in osteoblast differentiation and bone remodeling. An increased osteoclast activity contributes to inflammatory and destructive osteocatabolic manifestations and/or osteoporosis whereas an increased osteoblast activity can result in osteopetrosis. This overview describes the known relevant pathophysiological metabolic pathways in this remodelling process, especially the effect of inflammation on bone metabolism, and outlines the links from bench to bedside.
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