Molecular Markers of Early Orthodontic Tooth Movement

Brooks, Patricia J.; Nilforoushan, Dorrin; Manolson, Morris F.; Simmons, Craig A.; Gong, Siew‐Ging

doi:10.2319/121508-638r.1

Cited by 49 publications

(29 citation statements)

References 30 publications

(38 reference statements)

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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: 83%

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: 83%

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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“…These abrupt alterations lead to the generation and propagation of signaling cascades and associated tissue remodeling by delineating biochemical and cellular reactions occurring in mineralized (alveolar bone) and nonmineralized (periodontium) paradental tissues ( Figure 2). Several possible biomarkers representing these biological modifications are expressed during specific phenomena, that is, simileinflammatory process, bone resorption and formation, periodontal ligament changes, and vascular and neural responses [1].…”

Section: Introductionmentioning

confidence: 99%

Biomarkers of Periodontal Tissue Remodeling during Orthodontic Tooth Movement in Mice and Men: Overview and Clinical Relevance

d’Apuzzo¹,

Nucci²,

Jamilian³

et al. 2017

Periodontitis - A Useful Reference

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Biologically active substances are expressed by cells within the periodontium in response to mechanical stimuli from orthodontic appliances. Several possible biomarkers representing biological modifications during specific phenomena as simile-inflammatory process, bone resorption and formation, periodontal ligament changes, and vascular and neural responses are proposed. Citations to potentially published trials were conducted by searching PubMed, Cochrane databases, and scientific textbooks. Additionally, hand searching and contact with experts in the area were undertaken to identify potentially relevant published and unpublished studies. Selection criteria were as follows: animal models involving only mice and rats undergoing orthodontic treatment; collection of gingival crevicular fluid (GCF) as a noninvasively procedure for humans; no other simultaneous treatment that could affect experimental orthodontic movement. The data suggest that knowledge of the remodeling process occurring in periodontal tissues during orthodontic and orthopedic therapies may be a clinical usefulness procedure leading to proper choice of mechanical stress to improve and to shorten the period of treatment, avoiding adverse consequences. The relevance for clinicians of evaluating the rate of some substances as valid biomarkers of periodontal effects during orthodontic movement, by means of two models of study, mice and men, is underlined.

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“…For the second part of the study, the PDL of the experimental and control first maxillary molars was extracted and frozen at 280uC until RNA extraction. No distinction was made between the mesial and distal surfaces of each tooth because it was technically unfeasible due to the small size of murine molars and also, as previously shown by us, 10 areas of compression occur in both mesial and distal regions of the PDL during force application.…”

Section: Animal Modelsmentioning

confidence: 97%

M-CSF accelerates orthodontic tooth movement by targeting preosteoclasts in mice

Brooks¹,

Heckler²,

Wei³

et al. 2011

The Angle Orthodontist

Self Cite

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Objective: To test the use of macrophage colony-stimulating factor (M-CSF), an early osteoclast recruitment/differentiation factor, in increasing the rate of osteoclastic recruitment and differentiation as a means of accelerating tooth movement. Materials and Methods: The distribution of osteoclasts and their precursors in the periodontal ligament (PDL) of teeth was initially characterized in a mouse model by immunohistochemical expression analyses of markers of osteoclast differentiation. We next administered two different dosages of M-CSF in the PDL of molars subject to force. Tooth movement was measured and correlated with changes in expression of M-CSF downstream genes in the PDL. Results: We found that monocytes may have differentiated into preosteoclasts before being recruited to the PDL during the lag phase of tooth movement, and an influx of multinucleated osteoclasts occurred after 6 days. The lower dose of M-CSF was found to be most effective in increasing the amount of tooth movement and expression of M-CSF downstream genes and TRAP, an osteoclast marker. In contrast, administration of a higher dose of M-CSF resulted in a decrease in the expression of one gene downstream of M-CSF and possible inhibition of osteoclast formation. Conclusions: Exogenous administration of optimal dosages of M-CSF to orthodontically moved teeth provides potential for clinical studies in accelerating tooth movement. (Angle Orthod. 2011;81:277-283.)

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Molecular Markers of Early Orthodontic Tooth Movement

Cited by 49 publications

References 30 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

Biomarkers of Periodontal Tissue Remodeling during Orthodontic Tooth Movement in Mice and Men: Overview and Clinical Relevance

M-CSF accelerates orthodontic tooth movement by targeting preosteoclasts in mice

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