Osteoclasts are the sole bone resorbing cells. These cells are essential for skeletal development and remodeling throughout the life of animal and man. Deficiency of osteoclasts leads to osteopetrosis, a diseases manifested by increased non-remodeled bone mass, which ultimately leads to bone deformities and functional failure of other body systems. On the other hand, increased number and activity of osteoclasts under certain pathologic conditions causes accelerated bone resorption and may lead to osteoporosis and osteolytic diseases. To better understand the mechanisms underlying osteoclast-based diseases and design relevant therapies, one should unveil the molecular basis of osteoclast differentiation and function and regulatory mechanisms of osteoclast signaling. This review will outline up-to-date information regarding osteoclast differentiation and activation. Molecular mechanisms underlying osteoclast signaling pathways in inflammatory osteolysis and arthritis will be discussed. In addition, stimulators and inhibitors of osteoclasts, as well as current therapies for osteoclast activity will be addressed.
|Number of pages||9|
|Journal||Current Drug Targets: Immune, Endocrine and Metabolic Disorders|
|State||Published - Sep 1 2005|
- Bone resorption
- RANK ligand