An Anti-c-Fms Antibody Inhibits Orthodontic Tooth Movement

Fujimura

Yoshimatsu

et al. 2009

The Angle Orthodontist

Objective:To examine the effect of anti-c-Fms antibody on odontoclastogenesis and root resorption in an orthodontic tooth movement mouse model. Materials and Methods: We used orthodontic tooth movement in which an Ni-Ti coil spring was inserted between the upper incisors and the upper first molar. Root resorption occurred in this model. Anti-c-Fms antibody was injected daily into a local site for 12 days during mechanical loading. Odontoclastogenesis and root resorption were assessed by histology and scanning electron microscopy. Results:The anti-c-Fms antibody significantly inhibited odontoclastogenesis and root resorption during orthodontic tooth movement. Conclusion: M-CSF and/or its receptor is a potential therapeutic target in mechanical stressinduced odontoclastogenesis, and injection of an anti-c-Fms antibody might be useful for inhibition of mechanical stress-induced root resorption during orthodontic tooth movement. (Angle Orthod. 2009;79:835-841.)

Section: Introductionmentioning

confidence: 77%

Section: Introductionmentioning

confidence: 99%

An M-CSF Receptor c-Fms Antibody Inhibits Mechanical Stress–Induced Root Resorption during Orthodontic Tooth Movement in Mice

Fujimura

Yoshimatsu

et al. 2009

The Angle Orthodontist

“…To further investigate the role of TNFRs, tooth movement experiments using double-mutated mice for both TNFR1 and TNFR2 were performed. The experiment showed significant decreases in the amount of tooth movement in the double-mutated mice [45]. These results suggested that TNF-α is associated with orthodontic tooth movement.…”

Section: Mechanical Force Loading-induced Osteoclast Formation and Bomentioning

confidence: 75%

“…Therefore, the mice tooth movement models can provide an understanding of the molecular mechanisms involved not only in tooth movement but also in mechanical loadinginduced bone remodeling. A nickel-titanium (Ni-Ti) coil spring to obtain a continuous force for tooth movement is suitable for exerting continuous orthodontic force in mice models [44,45]. The process of orthodontic tooth movement occurs by repeated alveolar bone resorption on the pressure side and bone formation on the tension side of teeth [46].…”

Section: Mechanical Force Loading-induced Osteoclast Formation and Bomentioning

confidence: 99%

The Role of Th1 Cytokines on Mechanical Loading-Induced Osteoclastogenesis and Bone Resorption

Interface Oral Health Science 2014

Kimura

Ishida

et al. 2015

Mechanical loading exerts important effects on the skeleton by controlling bone mass and strength. Osteoclasts are required for bone resorption and remodeling. Two cytokines are required for osteoclast formation: macrophage colony-stimulating factor and receptor activator of nuclear factor kappa-B ligand (RANKL). Tumor necrosis factor-α (TNF-α) has also been recognized as an important factor for osteoclastogenesis. It has previously been reported that interleukin (IL)-12 and IL-18, and interferon gamma (IFN-γ), which are type 1T helper cell (Th1) cytokines, inhibited RANKL-and TNF-α-mediated osteoclastogenesis. It also been reported that TNF-α plays an important role in mechanical loadinginduced osteoclastogenesis and bone resorption. Orthodontic tooth movement is a good model for exploring the mechanism underlying mechanical loading-induced bone changes. Orthodontic tooth movement in a mouse model was established, and we investigated whether Th1 cytokines such as IL-12 and IFN-γ inhibit osteoclastogenesis and bone resorption upon mechanical loading. The number of tartrateresistant acid phosphatase (TRAP)-positive cells increased at the pressure side of the first molar. Conversely, the amount of tooth movement and the number of TRAP-positive cells at the pressure side in IL-12-and IFN-γ-injected mice was less than that of non-injected mice. The results suggested that IL-12 and IFN-γ might have an inhibitory effect on mechanical loading-induced osteoclastogenesis. In this review, we describe and discuss the effect of Th1 cytokines on mechanical loadinginduced osteoclastogenesis and bone resorption.

“…Bacterial infection and lipopolysaccharide (LPS) are reported to induce osteoclast formation and inflammatory bone loss, as seen in periodontal diseases [40,41]. LPS is major component of bacteria and is reported to be an inducer of inflammation and pathological bone resorption.…”

Section: The Inhibitory Effect Of the Anti-c-fms Antibody In Pathologmentioning

confidence: 99%

Effect of Macrophage Colony-Stimulating Factor Receptor c-Fms Antibody on Lipopolysaccharide-Induced Pathological Osteoclastogenesis and Bone Resorption

Kimura

Interface Oral Health Science 2014

Ishida

et al. 2015

Lipopolysaccharide (LPS) is a major component of Gram-negative bacteria cell walls and is a well-known potent inducer of inflammation and pathogens of inflammatory bone loss. Formation of osteoclasts is highly dependent on the presence of macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor kappa-B ligand (RANKL). Recent reports indicate that biological preparations, including anti-RANKL antibody and anti-tumor necrosis factor-α antibody, positively influence rheumatoid arthritis and osteoporosis. In this study, we aimed to investigate whether the M-CSF receptor c-Fms antibody would inhibit the formation of osteoclasts. C57BL6/J mice were injected with either LPS, LPS and anti-c-Fms antibody, anti-c-Fms antibody, or PBS into the supracalvariae. Animals were sacrificed and calvariae fixation and demineralization were performed. Histological sections of calvariae were stained for tartrate-resistant acid phosphatase (TRAP). In mice administered with both LPS and the anti-cFms antibody, osteoclast numbers were lower than those in mice administered with LPS alone. Moreover, levels of TRACP-5b, a bone resorption marker in mice serum, were lower in mice administered with both LPS and the anti-c-Fms antibody than in mice administered with LPS alone. These results suggest that M-CSF and its receptor are potential therapeutic targets in LPS-induced osteoclastogenesis, and that the anti-c-Fms antibody might be useful for inhibition of inflammation-induced bone erosion. In this study, we describe and discuss the effect the anti-c-Fms antibody has on pathological osteoclastogenesis and bone resorption.