No abstract available.
Osteoblasts*

No abstract available.
Osteoblasts*

Within the past few years, information regarding osteocyte function as been emerging and expanding significantly. No longer is the osteocyte considered a passive cell acting simply as a 'placeholder' within mineralized bone. Osteocytes are derived from osteoblast progenitors and in the adult skeleton compose 90-95% of all bone cells. Therefore, the function of these cells in the adult and aging skeleton has become the focus of recent investigation. These cells are proving to be multifunctional, ranging from mechanotransduction, to regulation of mineral homeostasis, to control of bone remodeling. The osteocyte as a source and reservoir of signaling factors important in health and maintenance of the adult skeleton is addressed in this review.
Adult ; Aging ; Bone Remodeling ; Homeostasis ; Humans ; Osteoblasts ; Osteocytes ; Skeleton

The aim of this study was to investigate the role of osteal macrophages (osteomac) and osteocytes in bone remodeling using a mathematical model. We constructed the bone system with pre-osteoblasts, osteoclasts, osteocytes, and osteomac. Each link of the parameters and ordinary differential equations followed the Graham's model in 2013 except for the parameters of osteomac signaling and osteocytes signaling to link preosteoblasts and osteoblasts. We simulated the changes in each cell and bone volume according to the changes in the parameters of osteomac signaling and osteocytes signaling. The results showed bone volume was unstable and decreased gradually when the effectiveness of osteocytes and osteomac dropped below a certain level. When the parameters of osteomac signaling and osteocytes signaling to link preosteoblasts and osteoblasts had a value less than 1, bone volume increased with the increase in the parameter of osteomac signaling to link preosteoblasts and osteoblasts. Moreover, although the parameter of osteocytes signaling to link preosteoblasts and osteoblasts, increased in case of a small parameter of osteomac signaling, bone volulme decreased. If the parameters of osteomac signaling to link preosteoblasts and osteoblasts were over a certain level, bone volume was positively maintained, despite the parameter of osteocyte signaling to link preosteoblasts and osteoblasts. We suggested the osteomac may affect bone remodeling and may play an important role in bone cell network.
Bone and Bones* ; Bone Remodeling ; Macrophages* ; Models, Theoretical* ; Osteoblasts ; Osteoclasts ; Osteocytes*

No abstract available.
Fluorides* ; Osteoblasts*

Glucocorticoids* ; Osteoblasts*

Bone morphogenetic protein-2/4 are members of Transforming Growth Factor-beta(TGF-beta) superfamily and they may induce formation of cartilage and bone in vivo. This study was performed to investigate the cellular target and period of action of BMP-2/4 and understanding of actions of BMP-2/4 at cellular level. The appearance of BMP-2/4 during healing of mandibular and periodontal defect in rat was evaluated immunohistochemically. 40 Sprague-Dawley strain white male rats, each weighing about 300gm were used. Bony defect was performed in the mandible and they were sacrificed at the day of 3rd, 10th, 20th, 30th after operation. The specimens were harvested and examined histologically and immunohistochemically by localization of anti-BMP-2/4. The results were as follows: 1. Woven bone was observed at 10th day and perfect healing of defect with compact bone and periodontal ligment space at 30th day. 2. Osteoprogenitor cells, osteoblastic cells and periosteum were positive reaction to immunohistochemical stain at 10th day. 3. Cells of bone marrow space and surface cells of osteocytes and cementoblasts were positive reaction to immunohistochemical stain at 20th day. 4. Newly formed osteocytes and cementocytes were positive reaction to immunohistochemical stain at 30th day. From the above findings, we could conclude that BMP-2/4 acted significant roles as factors of induction, proliferation and differentiation during bone healing process.
Animals ; Bone Marrow ; Cartilage ; Dental Cementum ; Humans ; Male ; Mandible ; Osteoblasts ; Osteocytes ; Periosteum ; Rats* ; Rats, Sprague-Dawley

Nevus cell nevus in bone has been called osteo-nevus of Nanta since Nanta reported it in detail in 1911. We report a 46-year-old female patient with osteo-nevus of Nanta on her forehead. Histologic examination revealed nests of nevus cells, with numerous osteocytes and osteoblasts in the bony tissue. Inflammatory cell infiltrate and foreign body granuloma were not found.
Female ; Forehead ; Granuloma, Foreign-Body ; Humans ; Middle Aged ; Nevus ; Osteoblasts ; Osteocytes

The term "osteoma cutis" is limited only to primary cutaneous ossification in which there is no evidence of Albrights hereditary osteodystrophy in either the patient or his farnily. We herein present a case of osteorna cutis in a 2-year-old male. He had had multiple hard plaques on the extremities since birth and had not had the evidences of Albrights hereditary osteodystrophy and signs of secondary cutaneous ossification such as trauma, injection, previous skin lesions and abnormal laboratory findings. The histopathologic findings revealed bony spicules with numerous osteocytes, cement lines, Haversian canals, osteoblasts and osteoclasts.
Child, Preschool ; Extremities ; Haversian System ; Humans ; Infant* ; Male ; Osteoblasts ; Osteoclasts ; Osteocytes ; Osteoma* ; Parturition ; Skin

Osteocytes may function as mechanotransducers by regulating local osteoclastogenesis. Reduced availability of oxygen, i.e. hypoxia, could occur during disuse, bone development, and fracture. Receptor activator of nuclear factor-kappaB ligand (RANKL) is an osteoblast/stromal cell derived essential factor for osteoclastogenesis. The hypoxia induced osteoclastogenesis via increased RANKL expression in osteoblasts was demonstrated. Hypoxic regulation of gene expression generally involves activation of the hypoxia-inducible factor (HIF) transcription pathway. In the present study, we investigated whether hypoxia regulates RANKL expression in murine osteocytes and HIF-1alpha mediates hypoxia-induced RANKL expression by transactivating RANKL promoter, to elucidate the role of osteocyte in osteoclastogenesis in the context of hypoxic condition. The expression levels of RANKL mRNA and protein, as well as hypoxia inducible factor-1alpha (HIF-1alpha) protein, were significantly increased in hypoxic condition in MLO-Y4s. Constitutively active HIF-1alpha alone significantly increased the levels of RANKL expression in MLO-Y4s under normoxic conditions, whereas dominant negative HIF-1alpha blocked hypoxia-induced RANKL expression. To further explore to find if HIF-1alpha directly regulates RANKL transcription, a luciferase reporter assay was conducted. Hypoxia significantly increased RANKL promoter activity, whereas mutations of putative HIF-1alpha binding elements in RANKL promoter prevented this hypoxia-induced RANKL promoter activity in MLO-Y4s. These results suggest that HIF-1alpha mediates hypoxia-induced up-regulation of RANKL expression, and that in osteocytes of mechanically unloaded bone, hypoxia enhances osteoclastogenesis, at least in part, via an increased RANKL expression in osteocytes.
Anoxia* ; Bone Development ; Gene Expression Regulation ; Luciferases ; Osteoblasts ; Osteocytes* ; Oxygen ; RANK Ligand* ; RNA, Messenger ; Up-Regulation