[Molecules which are involved in osteoclastic bone resorption: from the aspect of targets of treatment for osteoporosis].
Bone in vertebrates is continuously destroyed and reformed to maintain bone volume throughout their life. In normal bone remodeling, osteoblastic bone formation follows osteoclastic bone resorption in a precise and quantitative manner. In osteoporosis, the bone resorption surpasses the bone formation. Recent studies have shown that osteoclastic bone resorption is tightly regulated by bone-forming osteoblasts. Osteoblasts express RANKL (receptor activator of nuclear factor-KappaB ligand), which plays central roles in osteoclast differentiation and function. In this review article, we explain molecules which are involved in the RANKL-RANK interaction in the regulation of osteoclastic bone resorption.
Take
Ikuko
I
Matsumoto Dental University, Institute for Oral Science.
Takahash
Naoyuki
N
Kurihara
Saburo
S
D001862:Bone Resorption / Q000235:genetics*; D002352:Carrier Proteins / Q000502:physiology; D006801:Humans; D008562:Membrane Glycoproteins / Q000502:physiology; D010010:Osteoclasts / Q000502:physiology*; D010024:Osteoporosis; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B
D002352:Carrier Proteins; D008562:Membrane Glycoproteins; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; C505686:TNFRSF11A protein, human; C505688:TNFSF11 protein, human