CTGF and Apoptosis in Mouse Osteocytes Induced by Tooth Movement

Sakai, Yuichi; Balam, Tarek A.; Kuroda, Shingo; Tamamura, Nagato; Fukunaga, Tomohiro; Takigawa, Masaharu; Takano‐Yamamoto, Teruko

doi:10.1177/0022034509334649

Cited by 45 publications

(44 citation statements)

References 24 publications

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“…In a preliminary study aimed at examining AMBN and Bril expression in actively-forming bone, the maxillary left fi rst molar of wild type mice was extracted with an excavator, and sacrificed 5 days after extraction. For ETM, nickeltitanium wire, 0.012 inches (304.8 μm) in diameter, was fi xed to the maxillary incisor by means of a composite resin for orthodontic bonding (Transbond ® ; 3M Unitek, St. Paul, MN, USA), and the left maxillary 1st molar was moved toward the palatal side with 10 g load as described previously, while the untreated contralateral teeth served as control (Sakai et al, 2009). For BDT, an incision was made over the left anterior-proximal tibia, and a hole was drilled mono-cortically with a high-speed dental engine (20,000 rpm) using a 1.0 mm carbide bar (Brasseler USA, Savannah, GA, USA).…”

Section: Animal Experimental Proceduresmentioning

confidence: 99%

Ameloblastin is not implicated in bone remodelling and repair

Kuroda

Wazen²,

Sellin³

et al. 2011

eCM

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Ameloblastin (AMBN) is an enamel matrix protein produced by ameloblasts. It has been suggested that AMBN might also be implicated in craniofacial bone formation. Our objective was to determine whether AMBN has an effect on osteogenic mineralisation and infl uences bone remodelling and repair. MC3T3-E1 cells were screened for endogenous expression of enamel proteins using real time PCR. Various osteogenic cells were infected with lentivirus encoding for AMBN and protein expression was verifi ed using immunochemistry. Cultures were stained with alizarin red and mineralisation was quantifi ed. Healing bone was probed for expression of AMBN by DNA microarray analysis. Tooth extraction, experimental tooth movement (ETM), and creation of a non-critical size bone defect in the tibia (BDT) were carried out in wild type and AMBN Δ5-6 mutant mice. Tissues were processed for immunolabelling of AMBN and Bril, an osteoblast specifi c protein associated with active bone formation. MC3T3-E1 cells and healing bone showed no significant expression of AMBN. Overexpression of AMBN in osteogenic cultures induced no noticeable changes in mineralisation. In wild type mice, AMBN was immunodetected in ameloblasts and enamel, but not in normal bone, and at sites where bone remodelling and repair were induced. Bone remodelling during ETM and BDT repair in AMBN Δ5-6 mice were not signifi cantly different from that in wild type animals. Our results suggest that AMBN does not infl uence osteogenic activity in vitro under the conditions used, and does not participate in craniofacial bone remodelling under mechanical stress and in repair of non-critical size bone defects.

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Section: Animal Experimental Proceduresmentioning

confidence: 99%

Ameloblastin is not implicated in bone remodelling and repair

Kuroda

Wazen²,

Sellin³

et al. 2011

eCM

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“…Although studies of orthodontic tooth movement have mainly examined the response of PDL cells, several studies have examined the role of osteocytes in alveolar bone remodeling. [8][9][10][11][12] For example, mRNA expression of cytokines and matrix molecules in osteocytes were elevated in response to orthodontic forces. [8][9][10] In addition, osteocytes adjacent to hyalinized PDL underwent cell death via apoptosis, which might have been associated with subsequent bone resorption.…”

Section: Introductionmentioning

confidence: 99%

“…[8][9][10][11][12] For example, mRNA expression of cytokines and matrix molecules in osteocytes were elevated in response to orthodontic forces. [8][9][10] In addition, osteocytes adjacent to hyalinized PDL underwent cell death via apoptosis, which might have been associated with subsequent bone resorption. 11,12 However, there is little information on the response of cementocytes during orthodontic tooth movement.…”

Section: Introductionmentioning

confidence: 99%

Cementocyte cell death occurs in rat cellular cementum during orthodontic tooth movement

Matsuzawa

Toriya

Nakao

et al. 2016

The Angle Orthodontist

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Objective: To clarify the mechanism of root resorption during orthodontic treatment, we examined cementocyte cell death and root resorption in the cellular cementum on the pressure side during experimental tooth movement. Materials and Methods: Using 8-week-old male Wistar rats, the right first molar was pushed mesiobuccally with a force of 40 g by a Ni-Ti alloy wire while the contralateral first molar was used as a control. Localization and number of cleaved caspase-3-positive and single-stranded DNA (ssDNA) -positive cells were evaluated using dual-label immunohistochemistry with anticleaved caspase-3 and anti-ssDNA antibodies. In addition, tartrate-resistant acid phosphatase (TRAP)-positive cells in the cellular cementum were evaluated using TRAP histochemical staining. Results: Caspase-3-and ssDNA-positive cells appeared at 12 hours, but were restricted to the compressed periodontal ligament (PDL) and not the cellular cementum. Cleaved caspase-3-positive cementocytes were observed in the cellular cementum adjacent to the compressed PDL on day 1. From days 2 to 4, the number of caspase-3-and ssDNA-positive cementocytes increased. TRAP-positive cells appeared on the cellular cementum at the periphery of the hyalinized tissue on day 7, and resorption progressed into the broad surface of the cementum by day 14. Conclusion: Cementocytes adjacent to the hyalinized tissue underwent apoptotic cell death during orthodontic tooth movement, which might have been associated with subsequent root resorption. (Angle Orthod. 2017;87:416-422)

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“…These findings suggested that Ccn2 plays a role in the regulation of osteoblastic function during the mechanical stimulation of bone. Considering these findings together, we hypothesized that Ccn2 mRNA expression in osteocytes and osteoblasts is induced by continuous fluid shear stress (FSS) caused by orthodontic force, which might play a significant role in triggering bone remodeling (Sakai et al 2009). …”

Section: Introductionmentioning

confidence: 99%

Promotion of Ccn2 expression and osteoblastic differentiation by actin polymerization, which is induced by laminar fluid flow stress

Honjo

Kubota

Kamioka

et al. 2012

J. Cell Commun. Signal.

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Fluid flow stress (FSS) is a major mechanical stress that induces bone remodeling upon orthodontic tooth movement, whereas CCN family protein 2 (CCN2) is a potent regenerator of bone defects. In this study, we initially evaluated the effect of laminar FSS on Ccn2 expression and investigated its mechanism in osteoblastic MC3T3-E1 cells. The Ccn2 expression was drastically induced by uniform FSS in an intensity dependent manner. Of note, the observed effect was inhibited by a Rho kinase inhibitor Y27632. Moreover, the inhibition of actin polymerization blocked the FSS-induced activation of Ccn2, whereas inducing Factin formation using cytochalasin D and jasplakinolide enhanced Ccn2 expression in the same cells. Finally, Factin formation was found to induce osteoblastic differentiation. In addition, activation of cyclic AMP-dependent kinase, which inhibits Rho signaling, abolished the effect of FSS. Collectively, these findings indicate the critical role of actin polymerization and Rho signaling in CCN2 induction and bone remodeling provoked by FSS.

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CTGF and Apoptosis in Mouse Osteocytes Induced by Tooth Movement

Cited by 45 publications

References 24 publications

Ameloblastin is not implicated in bone remodelling and repair

Ameloblastin is not implicated in bone remodelling and repair

Cementocyte cell death occurs in rat cellular cementum during orthodontic tooth movement

Promotion of Ccn2 expression and osteoblastic differentiation by actin polymerization, which is induced by laminar fluid flow stress

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