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.
Highlights
The bone is subject to constant remodeling
The remodeling process is controlled through the balanced interaction between osteoblasts and osteoclasts whereby the cellular balance of bone metabolism is safeguarded through molecular mechanisms
It could be shown that an adequate tumor necrosis factor (TNF)-α inhibition is able to neutralize the inflammation-mediated alterations in bone metabolism, i.e. increased bone formation and reduced bone resorption, it leads to a cessation or amelioration of radiographical erosive changes in patients with rheumatoid arthritis [44,45,46,47,48]
Summary
The bone is subject to constant remodeling. This enables bones to adapt to changing strain or stress situations and required reparative mechanisms in cases such as microcracks or fragility fractures which hazards the optimal bone structure. The remodeling process is controlled through the balanced interaction between osteoblasts and osteoclasts whereby the cellular balance of bone metabolism is safeguarded through molecular mechanisms (e.g. cytokines, hormones, and growth factors). Factors such as age, gender, post-menopausal estrogen loss, physical activity, and various drugs influence bone metabolism [2,3]. The immune system and bone metabolism are so closely intertwined that pro-inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, IL-6, and IL-17 could be identified as stimulators in the formation of osteoclasts They are essential mediators in bone resorption, primarily in chronic inflammatory diseases [4,5]. Further characteristics are successively decreased bone stability, increased fracture susceptibility and / or inflammatory destructive manifestations
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