Experimental model of tooth movement in mice: A standardized protocol for studying bone remodeling under compression and tensile strains

Taddei, Silvana Rodrigues de Albuquerque; Moura, Adriana Pedrosa; Andrade, Ildeu; Garlet, Gustavo; Garlet, Thiago; Teixeira, Mauro Martins; Silva, Tarcı́lia Aparecida

doi:10.1016/j.jbiomech.2012.09.006

Cited by 80 publications

(65 citation statements)

References 29 publications

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“…This is consistent with reports from Yoshimatsu et al 15) and from In the agreement with these results, previous reports described elevated levels of TNF-α and RANKL in compression side following mechanical loading [18][19][20][21] . Given that the TNF-α and RANKL participate in osteoclastogenesis by upregulating osteoclast activity.…”

Section: Discussionsupporting

confidence: 93%

TNF-α Aggravates the Progression of Orthodontically-induced Inflammatory Root Resorption in the Presence of RANKL

Yoshino

Yamaguchi

Shimizu

et al. 2014

J. Hard Tissue Biology.

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Orthodontically-induced inflammatory root resorption (OIIRR) is one of the procedure-related adverse effects that occur during orthodontic treatment, and the incidence is related to the proinflammatory cytokine produced in response to the mechanical stress caused by the procedure. It is known that tumor necrosis factor (TNF)-is produced following environmental insults in vivo at an early stage, and that it deeply affects inflammatory bone resorption. However, the relationship between the TNF-level and root resorption is unclear. In this study, the relationship between TNF-and root resorption was evaluated using an experimental mouse tooth movement model and a pressure side model using human periodontal ligament (hPDL) cells, as well as an osteoclast culture system. Nine days after the tooth movement in the mouse model, an increase in TNFand receptor activator of nuclear factor-B ligand (RANKL) positive cells was observed. In vitro, their levels increased in the cultures of hPDL cells exposed to the 4 g/cm 2 pressure. In addition, the differentiation of osteo/ odontoclasts was promoted by TNF-weakly, but the ability to resorb the dentin was unchanged. However, the activation of osteo/odontoclastogenesis is more potent in the presence of RANKL and TNF-, which leads to synergistic activation. These results suggest that TNF-may be an aggravating factor for root resorption during orthodontic treatment.

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Section: Discussionsupporting

confidence: 93%

TNF-α Aggravates the Progression of Orthodontically-induced Inflammatory Root Resorption in the Presence of RANKL

Yoshino

Yamaguchi

Shimizu

et al. 2014

J. Hard Tissue Biology.

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“…This study used induced orthodontic tooth movement in rats as a model to evaluate the effect of LLLT on bone metabolism and bone turnover. A controlled force was applied to the first molar using a NiTi coin‐spring in order to create a compression area on adjacent bone in the force direction and a tension area at the opposite site . Also the control group was the contra‐lateral side, avoiding or at least reducing the differences among individual biologic response.…”

Section: Discussionmentioning

confidence: 99%

Low‐level laser therapy stimulates bone metabolism and inhibits root resorption during tooth movement in a rodent model

Suzuki

Garcez

Suzuki

et al. 2016

Journal of Biophotonics

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This study evaluated the biological effects of low-level laser therapy (LLLT) on bone remodeling, tooth displacement and root resorption, occurred during the orthodontic tooth movement. Upper first molars of a total of sixty-eight male rats were subjected to orthodontic tooth movement and euthanized on days 3, 6, 9, 14 and 21 days and divided as negative control, control and LLLT group. Tooth displacement and histomorphometric analysis were performed in all animals; scanning electron microscopy analysis was done on days 3, 6 and 9, as well as the immunohistochemistry analysis of RANKL/OPG and TRAP markers. Volumetric changes in alveolar bone were analyzed using MicroCT images on days 14 and 21. LLLT influenced bone resorption by increasing the number of TRAP-positive osteoclasts and the RANKL expression at the compression side. This resulted in less alveolar bone and hyalinization areas on days 6, 9 and 14. LLLT also induced less bone volume and density, facilitating significant acceleration of tooth movement and potential reduction in root resorption besides stimulating bone formation at the tension side by enhancing OPG expression, increasing trabecular thickness and bone volume on day 21. Taken together, our results indicate that LLLT can stimulate bone remodeling reducing root resorption in a rat model. LLLT improves tooth movement via bone formation and bone resorption in a rat model.

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“…Orthodontic forces were delivered by coiled springs (wire size, 0.2 mm; diameter, 1 mm; length, 1 mm; Smart Technology, Beijing, China) tied between the incisors and first molars with resin (3M ESPE, USA), as previously described (Cao et al 2014). Each coiled spring delivered approximately 30 g of force, measured by a dynamometer: the previous study showed that this force magnitude range was optimal for mice orthodontic treatment (Taddei, Moura, et al 2012). Both maxillary quadrants were used in this study to mimic clinical orthodontic treatment (Appendix Fig.).…”

Section: Orthodontic Force Applicationmentioning

confidence: 99%

Orthodontic Force Induces Systemic Inflammatory Monocyte Responses

et al. 2015

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Periodontal inflammation and alveolar bone remodeling during orthodontic tooth movement are considered regional reactions. However, how systemic immune responses are involved in this regional reaction remains unclear. In this study, we explored the systemic effects of orthodontic force by focusing on the mononuclear phagocyte system. Flow cytometric analysis showed that the percentage of inflammatory monocytes, in peripheral blood and in the monocyte reservoir spleen, decreased on days 1 and 3 and then recovered on day 7 after force application. Along with the systemic decrease of inflammatory monocyte percentage, the number of tartrate-resistant acid phosphatase-positive osteoclasts increased in the compression side of the periodontal tissue during orthodontic tooth movement. Systemic transfusion of enhanced green fluorescent protein-labeled inflammatory monocytes showed recruitment of these monocytes to the orthodontic force compression side of periodontal tissues. These monocytes were colocalized with tartrate-resistant acid phosphatase-positive osteoclasts. In vivo and in vitro experiments showed that orthodontic force could upregulate the expression of pivotal monocyte chemokine monocyte chemotactic protein 1 in periodontal tissues or cultured periodontal ligament cells, which may contribute to monocyte recruitment to regional sites. These data suggest that orthodontic force induces systemic immune responses related to inflammatory monocytes and that systemic inflammatory monocytes can be recruited to periodontal tissues by orthodontic force stimulus.

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Experimental model of tooth movement in mice: A standardized protocol for studying bone remodeling under compression and tensile strains

Cited by 80 publications

References 29 publications

TNF-α Aggravates the Progression of Orthodontically-induced Inflammatory Root Resorption in the Presence of RANKL

TNF-α Aggravates the Progression of Orthodontically-induced Inflammatory Root Resorption in the Presence of RANKL

Low‐level laser therapy stimulates bone metabolism and inhibits root resorption during tooth movement in a rodent model

Orthodontic Force Induces Systemic Inflammatory Monocyte Responses

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