Physiopathology of osteoclast in bone.

摘要

Bone is constantly remodeled by osteoclastic bone resorption and osteoblastic bone formation. Abnormal remodeling can result in bone mass change; bone loss is implicated in a number of bone diseases, representing an increase in bone resorption relative to formation. Therefore, an understanding of osteoclast biology is important to demystify the pathogenesis of bone diseases and to develop treatment strategies. Osteoclasts are formed by fusion of hematopoietic monocyte/macrophage lineage cells, in which osteoblasts/stromal cells play a central role by producing macrophage-colony stimulating factor and receptor activator of nuclear factor kappa B ligand. Characterization of osteoclastogenesis has provided new insight into our understanding of bone diseases with excessive bone resorption. Moreover, anti-resorptive drugs, bisphosphonates, have been developed to target osteoclasts and their function. Additionally, a better understanding of the interactions of fluoride between osteoclasts may help harness the desirable effects of fluoride on bone while limiting its undesirable effects.