Protein and mRNA expressions of IL-6 and its key signaling factors under orthodontic forces in mice: An in-vivo study

Long, Yi; Song, Fang; Wu, Shu; He, Shushu; Meng, Mingmei; Lv, Chunxiao; Yang, Qingqing; Song, Chen

doi:10.1016/j.ajodo.2017.03.026

Cited by 8 publications

(5 citation statements)

References 42 publications

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“…Janus kinase (JAK) activation by gp130 results in activation of the signal transducers and activators of transcription STAT1 and STAT3 and the SHP2/Ras/MAPK signaling pathway. Liu et al observed enhanced expression of IL-6 and its key signaling factors gp130, STAT3, and SHP2 protein and mRNA at the tension and compression sides of the teeth in a mice OTM model, indicating the special role of IL-6 in the bone remodeling process 112 . IL-8 is secreted by monocytes and its expression induced by the initial orthodontic force on the first day significantly increased in the tension side, stimulating RANKL expression to regulate bone resorption 113 .…”

Section: Fig 3 Hypothetical Mechanisms Of Mechanical Signal Transduct...mentioning

confidence: 99%

Biomechanical and biological responses of periodontium in orthodontic tooth movement: up-date in a new decade

et al. 2021

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Nowadays, orthodontic treatment has become increasingly popular. However, the biological mechanisms of orthodontic tooth movement (OTM) have not been fully elucidated. We were aiming to summarize the evidences regarding the mechanisms of OTM. Firstly, we introduced the research models as a basis for further discussion of mechanisms. Secondly, we proposed a new hypothesis regarding the primary roles of periodontal ligament cells (PDLCs) and osteocytes involved in OTM mechanisms and summarized the biomechanical and biological responses of the periodontium in OTM through four steps, basically in OTM temporal sequences, as follows: (1) Extracellular mechanobiology of periodontium: biological, mechanical, and material changes of acellular components in periodontium under orthodontic forces were introduced. (2) Cell strain: the sensing, transduction, and regulation of mechanical stimuli in PDLCs and osteocytes. (3) Cell activation and differentiation: the activation and differentiation mechanisms of osteoblast and osteoclast, the force-induced sterile inflammation, and the communication networks consisting of sensors and effectors. (4) Tissue remodeling: the remodeling of bone and periodontal ligament (PDL) in the compression side and tension side responding to mechanical stimuli and root resorption. Lastly, we talked about the clinical implications of the updated OTM mechanisms, regarding optimal orthodontic force (OOF), acceleration of OTM, and prevention of root resorption.

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Section: Fig 3 Hypothetical Mechanisms Of Mechanical Signal Transduct...mentioning

confidence: 99%

Biomechanical and biological responses of periodontium in orthodontic tooth movement: up-date in a new decade

et al. 2021

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“…The expression of the inflammatory gene IL6 was increased in the periodontal ligament after orthodontic treatment [20][21][22]. Here, IL6 was significantly higher in the absence of RUNX2 or after tensile strain in the control osteoblasts.…”

Section: Discussionmentioning

confidence: 81%

Impact of Mechanical Strain and Nicotinamide on RUNX2-Deficient Osteoblast Mimicking Cleidocranial Dysplasia

Schröder,

Örs,

Byeon

et al. 2023

IJMS

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Cleidocranial dysplasia (CCD) is a rare genetic defect caused by a heterozygous mutation of runt-related transcription factor 2 (RUNX2), which is important for osteoblast and skeletal development. RUNX2-deficiency causes extra- and intra-oral malformations that often require orthodontic treatment. Nicotinamide (NAM) affects bone remodelling processes. As these are crucial for orthodontic therapy, NAM could improve orthodontic treatment in CCD patients. This study investigates the effect of NAM in control and RUNX2-deficient osteoblasts under mechanical strain mimicking orthodontic treatment. First, the optimal NAM concentration and the differences in the expression profile of control and RUNX2-deficient osteoblasts were determined. Subsequently, osteoblasts were exposed to tensile and compressive strain with and without NAM, and the expression of genes critically involved in bone remodelling was investigated. NAM increased the expression of bone remodelling genes. RUNX2-deficient osteoblasts expressed more receptor activator of NFkB ligand (RANKL) and interleukin-6 (IL6), but less colony-stimulating factor-1 (CSF1). Most of the positive effects of NAM on bone remodelling genes were impaired by mechanical loading. In conclusion, NAM stimulated osteoblast differentiation by increasing the expression of RUNX2 and regulated the expression of osteoclastogenic factors. However, the positive effects of NAM on bone metabolism were impaired by mechanical loading and RUNX2 deficiency.

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“… 6 However, evidence about how mechanical loading activates JAK2/STAT3 is scarce. In cardiomyocytes, loading-induced JAK2/STAT3 activation is correlated with the interleukin-6 (IL-6) family, autocrine/paracrine-secreted angiotensin II, intracellular Ca 2 level, and protein kinase C. 6 Liu, et al 36 (2017) highlighted the critical role of IL-6 in STAT3 phosphorylation in orthodontic tooth movement. Thus, information on the precise mechanism by which mechanical loading induces phosphorylation of JAK2/STAT3 is scarce.…”

Section: Discussionmentioning

confidence: 99%

Suppressing STAT3 activation impairs bone formation during maxillary expansion and relapse

et al. 2023

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Objectives The mid-palatal expansion technique is commonly used to correct maxillary constriction in dental clinics. However, there is a tendency for it to relapse, and the key molecules responsible for modulating bone formation remain elusive. Thus, this study aimed to investigate whether signal transducer and activator of transcription 3 (STAT3) activation contributes to osteoblast-mediated bone formation during palatal expansion and relapse. Methodology In total, 30 male Wistar rats were randomly allocated into Ctrl (control), E (expansion only), and E+Stattic (expansion plus STAT3-inhibitor, Stattic) groups. Micro-computed tomography, micromorphology staining, and immunohistochemistry of the mid-palatal suture were performed on days 7 and 14. In vitro cyclic tensile stress (10% magnitude, 0.5 Hz frequency, and 24 h duration) was applied to rat primary osteoblasts and Stattic was administered for STAT3 inhibition. The role of STAT3 in mechanical loading-induced osteoblasts was confirmed by alkaline phosphatase (ALP), alizarin red staining, and western blots. Results The E group showed greater arch width than the E+Stattic group after expansion. The differences between the two groups remained significant after relapse. We found active bone formation in the E group with increased expression of ALP, COL-I, and Runx2, although the expression of osteogenesis-related factors was downregulated in the E+stattic group. After STAT3 inhibition, expansive force-induced bone resorption was attenuated, as TRAP staining demonstrated. Furthermore, the administration of Stattic in vitro partially suppressed tensile stress-enhanced osteogenic markers in osteoblasts. Conclusions STAT3 inactivation reduced osteoblast-mediated bone formation during palatal expansion and post-expansion relapse, thus it may be a potential therapeutic target to treat force-induced bone formation.

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Protein and mRNA expressions of IL-6 and its key signaling factors under orthodontic forces in mice: An in-vivo study

Cited by 8 publications

References 42 publications

Biomechanical and biological responses of periodontium in orthodontic tooth movement: up-date in a new decade

Biomechanical and biological responses of periodontium in orthodontic tooth movement: up-date in a new decade

Impact of Mechanical Strain and Nicotinamide on RUNX2-Deficient Osteoblast Mimicking Cleidocranial Dysplasia

Suppressing STAT3 activation impairs bone formation during maxillary expansion and relapse

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