Academic Thesis

Basic information

Name Ono Takehito
Belonging department
Occupation name
researchmap researcher code 7000026328
researchmap agency Okayama University of Science

Title

The interleukin-6 signal regulates orthodontic tooth movement and pain

Bibliography Type

Joint Author

Author

Toyama N, Ono T, Ono T, Nakashima T

Summary

Orthodontic tooth movement (OTM) is accomplished by controlling the mechanical loading onto the bone around the roots of target teeth. The precise orthodontic force induces osteoclastic bone resorption on the compression side and osteoblastic bone formation on the tension side of the alveolar bone. Orthodontic intervention causes inflammation in the periodontal ligament (PDL), which manifests as acute pain. Because inflammation is deeply connected to bone remodeling, it has been indicated that the inflammation after orthodontic intervention affects both the movement of teeth and generation of pain. However, the precise mechanisms underlying the immune regulation of OTM and the related pain are not well elucidated. Here, we found from the search of a public database that the interleukin (IL)-6 family of cytokines are highly expressed in the PDL by mechanical loading. The IL-6 signal was activated in the PDL after orthodontic intervention. The signal promoted OTM by inducing osteoclastic bone resorption. IL-6 was found to increase the number of osteoclasts by suppressing apoptosis and increasing their responsiveness to macrophage colony–stimulating factor (M-CSF) and receptor activator of NF-κB ligand (RANKL). Furthermore, IL-6 signal was shown to elicit orthodontic pain by inducing neuroinflammation in the trigeminal ganglion (TG). Taken together, it was demonstrated that the IL-6 signal regulates tooth movement and pain during orthodontic treatment. It was also indicated that local blockade of the IL-6 signal is a promising therapeutic option in orthodontic treatment, targeting both tooth movement and pain.

Magazine(name)

Biochemical and Biophysical Research Communications 

Publisher

Volume

684

Number Of Pages

StartingPage

149068

EndingPage

Date of Issue

2023/12

Referee

Exist

Invited

Not exist

Language

English

Thesis Type

Research papers (academic journals)

ISSN

DOI

https://doi.org/10.1016/j.bbrc.2023.09.096

NAID

PMID

URL

J-GLOBAL ID

arXiv ID

ORCID Put Code

DBLP ID