The Role Of Simvastatin And PTHrP On Osteoclastogenesis In Vitro And Bone Resorption In Vivo.

Recently, many studies have found that statins can effectively improve the osteoporosis, lowering the morbidity of bone fracture. The underlying mechanism involved is that statins promote marrow stroma cell differentiation toward bone-forming cells. However, currently the effects of statins on the formation of osteoclast cells are still not clear, so the present study was designed to investigate the effect of simvastatins on osteoclasts formation and the induced bone resorption.Various bone resorptive diseases, such as osteoporosis, periodontal disease, inflammatory bone disease and bone metastasis, results from imbalance between bone resorption and bone formation, i.e. bone destruction exceeds bone formation. RANKL(Receptor activator of NF- k B Ligand, or OPGL/ODF, osteoprotegerin ligand/osteoclast differentiation factor), a membrane-bound cytokine of osteoblast/bone marrow stromal cell, plays a key role in differentiation and functional activity of osteoclast. RNAKL induce osteoclast differentiation and function by binding to its receptor RANK (receptor activator of NF- κ B) on the osteoclast precursor and mature osteoclast. OPG (Osteoprotegerin) is a 'decoy receptor' of RANKL and acts as antagonist of RANKL. In bone metastasis, PTHrP secreted by tumor cells upregulate the...