Osteoprotegerin (OPG) acts as a decoy receptor for the receptor activator of the nuclear factor κ B (RANK) ligand (RANKL) , preventing its association with RANK and inhibiting osteoclastogenesis. Therefore, mice homozygous for targeted disruption of the OPG gene reveal stimulated bone resorption and bone formation, resulting in enhanced bone remodeling. The OPG deficient (OPG( - / - )) mouse showed the diturbed distribution of collagen fibers and complex meshwork of cement lines, which implies weakened strength of OPG( - / - ) bone against mechanical stress. In addition, the abnormally promoted remodeling of the OPG( - / - ) bone caused the disorganized distribution of osteocyte lacunar canalicular system (OLCS) . Histochemical assessment revealed the markedly reduced synthesis of sclerostin in the OPG( - / - ) OLCS while the synthesis of dentin matrix protein-1 was not extremely affected by the OPG deficiency. Taken together, OPG deficient mouse appears to be a valid model for extremely-stimulated bone remodeling, and would provided important clues for better understanding for activities of bone cells in a pathological state in bone.