• 대한치과교정학회지
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• 제20권1호
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• pp.169-179
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• 1990

Utilizing the repelling force of permanent magnet of find out weather it shows the findings of molar intrusion histologically and compares the result with the resin bite plane. As for the experimental animals, 10 cats of completion of permanent dentition with mean weight of 2.2kg which have flat occlusal plane of molar areas were used. I raised the cats under the condition of their being attached with manufactured appliance by direct bonding system and of their wearing vertical chin strap anesthetized for 12-14 hours per day through 5 days. Then, observing the root apex areas with lightmicroscope. The results were as follows; 1. In the group with resin bite plane, osteoblasts and osteoclasts could not find out but could find out periodontal ligment fiber obliquely angulated in the apical and lingual direction. 2. In the group with the permanent magnet, not only the obliquely angulated periodontal ligament fiber but also the osteoclasts at the apical areas were observed.

• BMB Reports
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• 제43권8호
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• pp.524-529
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• 2010

Glucocorticoids (GCs) are useful drugs for the treatment of various diseases, but their use for prolonged periods can cause severe side effects such as osteoporosis. GCs have a direct effect on bone cells, where they can arrest bone formation, in part through the inhibition of osteoblast. On the other hand, GCs potently suppress osteoclast resorptive activity by disrupting its cytoskeleton based on the inhibition of RhoA, Rac and Vav3 in response to macrophage colony-stimulating factor. GCs also interfere with microtubule distribution and stability, which are critical for cytoskeletal organization in osteoclasts. Thus, GCs inhibit microtubule-dependent cytoskeletal organization in osteoclasts, which, in the context of bone remodeling, further dampens bone formation.

• Journal of Korean Neurosurgical Society
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• 제49권6호
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• pp.317-322
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• 2011

The prevalence of osteoporosis has been increasing globally. Recently surgical indications for elderly patients with osteoporosis have been increasing. However, only few strategies are available for osteoporotic patients who need spinal fusion. Osteoporosis is a result of negative bone remodeling from enhanced function of the osteoclasts. Because bone formation is the result of coupling between osteoblasts and osteoclasts, anti-resorptive agents that induce osteoclast apoptosis may not be effective in spinal fusion surgery, necessitating new bone formation. Therefore, anabolic agents may be more suitable for osteoporotic patients who undergo spinal fusion surgery. The instrumentations and techniques with increased pullout strength may increase fusion rate through rigid fixation. Studies on new osteoinductive materials, methods to increase osteogenic cells, strengthened and biocompatible osteoconductive scaffolds are necessary to enable osteoporotic patients to undergo spinal fusion. When osteoporotic patients undergo spinal fusion, surgeons should consider appropriate osteoporosis medication, instrumentation and technique.

• BMB Reports
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• 제51권6호
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• pp.263-264
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• 2018

We identified osteoclast-derived SLIT3 as a new coupling factor using fractionated secretomics. Coupling links bone resorption to bone formation. SLIT3 stimulated the recruitment and proliferation of osteoblasts into bone remodeling sites via activation of ${\beta}-catenin$. Autocrine signaling by SLIT3 also inhibited bone resorption by suppressing the fusion and differentiation of pre-osteoclasts. All mice lacking Slit3 or its receptor Robo1 showed an osteopenic phenotype with low bone formation and high bone resorption. A small truncated recombinant SLIT3 protein increased bone mass in an osteopenic mouse model. These results suggest that SLIT3 is a novel therapeutic target in metabolic bone diseases.

• International Journal of Oral Biology
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• 제44권1호
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• pp.1-7
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• 2019

Osteoporosis is a common disease characterized by bone mass reduction, leading to an increased risk of bone fracture, and it is caused by an imbalance of osteoblastic bone formation and osteoclastic bone resorption. Current osteoporosis drugs aim to reduce the risk of bone fracture, either by increasing osteoblastic bone formation or decreasing osteoclastic bone resorption. However, osteoblasts and osteoclasts are closely coupled, such that any reagent altering the differentiation or activity of one eventually affects the other. This tight coupling between osteoblasts and osteoclasts not only limits the therapeutic efficacy but also threatens the safety of osteoporosis drugs. This review will discuss the biological mechanisms of action of currently approved medications for osteoporosis treatment, focusing on the osteoblast-osteoclast coupling.

• The Korean Journal of Physiology and Pharmacology
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• 제3권6호
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• pp.539-546
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• 1999

Bone is a complex tissue in which resorption and formation continue throughout life. The bone tissue contains various types of cells, of which the bone forming osteoblasts and bone resorbing osteoclasts are mainly responsible for bone remodeling. Periodontal disease represents example of abnormal bone remodeling. Osteoclasts are multinucleated cells present only in bone. It is believed that osteoclast progenitors are hematopoietic origin, and they are recruited from hematopoietic tissues such as bone marrow and circulating blood to bone. Cells present in the osteoclast microenvironment include marrow stromal cells, osteoblasts, macrophages, T-lymphocytes, and marrow cells. These cells produce cytokines that can affect osteoclast formation. In vitro model systems using bone marrow cultures have demonstrated that $IL-l{\beta},\;IL-3,\;TNF-{\alpha},$ bFGF can stimulate the formation of osteoclasts. In contrast, IL-4 inhibits osteoclast formation. Knowledge of cytokines and bFGF that affect osteoclast formation and their capacity to modulate the bone-resorbing process should provide critical insights into normal calcium homeostasis and disorders of bone turnover such as periodontal disease, osteoporosis and Paget's disease.

• Journal of Periodontal and Implant Science
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• 제26권4호
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• pp.823-840
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• 1996

The purpose of this study was to evaluate the effect of dexamethasone on the healing aspect of gingiva and alveolar bone after extraction. Extracted socket of 24 Sprague-Dawley rat was used. To extract easily and minimize injury, ${\beta}-APN$ 0.2g/kg/day soluted in mineral water was administrated for 5 days before extraction in both group. Ampicillin 1.5ml/kg i.m.,q.d, was administered for preventing infection after teeth extraction in both group, and dexamethasone 0.2mg/kg/day was injected for 3 days in experimental group.3 rats on each day was sacrificed on 1, 3, 7, 15 days after extraction. Histologic examination and the activity of osteoclasts by tartrate resistant acid phosphatase was observed. The results were as follows : 1. The Overall healing pattern was similar with both the experimental and control group, but in experimental group osseous healing was delayed. 2. The activity of osteoclasts was increased to day 3 and then decreased after day 3 in the experimental group. In comparison to the control group, the experimental group showed increased appearance to day 7 and then decreased appearance following day. 3. Regarding to the change of osseous tissue, the activity of osteoblasts was shown at day 7,but osteoclastic activity of the experimental group was less than that of the control group. The osteoclastic activity was statistically significant between two groups except day 7(p<0.05, p<0.01). In conclusion, the effects of dexamethasone for healing of extraction socket were considered as limiting the activity of osteoclasts, and the healing of extraction socket was delayed.

• 동의생리병리학회지
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• 제23권4호
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• pp.860-865
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• 2009

Osteoclasts are bone-resorbing multinucleated cells derived from the monocyte/macrophage lineage. The differentiation of osteoclasts are regulated by osteoblastic cells expressed RANKL, which is the most critical molecule for osteoclast differentiation. In this study, we found that water extracts of cuscuta inhibited RANKL-mediated osteoclast differentiation by direct action on bone marrow macrophages (BMMs) without cytotoxicity. In BMMs, water extracts of cuscuta inhibited the mRNA expression of c-Fos, NFATc1, TRAP, and OSCAR. Also, the protein expression of c-Fos and NFATc1 was inhibited by water extracts of cuscuta treatement. Water extracts of cuscuta inhibited the phosphorylation of p38, ERK, and JNK in BMMs treated with RANKL. However, water extracts of cuscuta did not inhibit RANKL-induced I-${\kappa}B$ activation. Water extract of cuscuta failed to inhibit bone resorption by osteoclasts cultured on hydroxyapatite plates. These results suggest that cuscuta may be a promising drug for use against bone disorders such as osteoporosis and rheumatoid arthritis.

• Molecules and Cells
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• 제37권8호
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• pp.628-635
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• 2014

2-(Trimethylammonium) ethyl (R)-3-methoxy-3-oxo-2-stearamidopropyl phosphate [(R)-TEMOSPho], a derivative of an organic chemical identified from a natural product library, promotes highly efficient megakaryopoiesis. Here, we show that (R)-TEMOSPho blocks osteoclast maturation from progenitor cells of hematopoietic origin, as well as blocking the resorptive function of mature osteoclasts. The inhibitory effect of (R)-TEMOSPho on osteoclasts was due to a disruption of the actin cytoskeleton, resulting from impaired downstream signaling of c-Fms, a receptor for macrophage-colony stimulating factor linked to c-Cbl, phosphoinositol-3-kinase (PI3K), Vav3, and Rac1. In addition, (R)-TEMOSPho blocked inflammation-induced bone destruction by reducing the numbers of osteoclasts produced in mice. Thus, (R)-TEMOSPho may represent a promising new class of antiresorptive drugs for the treatment of bone loss associated with increased osteoclast maturation and activity.

• Molecules and Cells
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• 제40권10호
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• pp.706-713
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• 2017

Osteoclasts are bone-resorbing cells that are derived from hematopoietic precursor cells and require macrophage-colony stimulating factor and receptor activator of nuclear factor-${\kappa}B$ ligand (RANKL) for their survival, proliferation, differentiation, and activation. The binding of RANKL to its receptor RANK triggers osteoclast precursors to differentiate into osteoclasts. This process depends on RANKL-RANK signaling, which is temporally regulated by various adaptor proteins and kinases. Here we summarize the current understanding of the mechanisms that regulate RANK signaling during osteoclastogenesis. In the early stage, RANK signaling is mediated by recruiting adaptor molecules such as tumor necrosis factor receptorassociated factor 6 (TRAF6), which leads to the activation of mitogen-activated protein kinases (MAPKs), and the transcription factors nuclear factor-${\kappa}B$ (NF-${\kappa}B$) and activator protein-1 (AP-1). Activated NF-${\kappa}B$ induces the nuclear factor of activated T-cells cytoplasmic 1 (NFATc1), which is the key osteoclastogenesis regulator. In the intermediate stage of signaling, the co-stimulatory signal induces $Ca^{2+}$ oscillation via activated phospholipase $C{\gamma}2$ ($PLC{\gamma}2$) together with c-Fos/AP-1, wherein $Ca^{2+}$ signaling facilitates the robust production of NFATc1. In the late stage of osteoclastogenesis, NFATc1 translocates into the nucleus where it induces numerous osteoclast-specific target genes that are responsible for cell fusion and function.