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 leads, via cytokines, hormones and growth factors, to a homeostasis of the bone metabolism. Here, the RANK/RANKL/OPG-system is actively involved in the differentiation and function of osteoclasts and seems to play a central role in most pathophysiological mechanisms. An increased osteoclast activity results in inflammatory destructive manifestations and/or osteoporosis whereas an increased osteoblast activity can result in osteopetrosis. The present overview describes the known pathophysiological relevant metabolic pathways in this remodelling process especially the effect of inflammation on bone metabolism, and presents the links from bench to bedside.

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