Lithium chloride promotes osteogenesis and suppresses apoptosis during orthodontic tooth movement in osteoporotic model via regulating autophagy.
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ABSTRACT:
SUBMITTER: Huang L
PROVIDER: S-EPMC7960682 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:As the number of elderly orthodontic patients increases, the impact of postmenopausal osteoporosis on orthodontic tooth movement (OTM) has attracted a great deal of attention because OTM relies on alveolar bone remodeling. The question of whether OTM causes subsequent alveolar bone loss and is harmful to alveolar bone health under osteoporotic conditions remains to be answered. The present study aimed to clarify the influences of OTM on alveolar bone in osteoporotic rats. OTM was accelerated in ovariectomized (OVX) rats as a result of increased bone resorption in the pressure area. At the same time, anabolic bone formation was promoted in the tension area during OTM in OVX rats. Micro-CT analysis of alveolar bone revealed a decrease in BMD, BV/TV and Tb.Th. in the OTM group compared with that in non-OTM rats on day 21 of OTM, suggesting that OTM caused alveolar bone loss in OVX rats during OTM. However, the OTM-induced bone loss could be recovered 3 months after OTM in OVX rats. Thus, our findings suggest that increased osteogenesis may compensate for the increased bone resorption during and after OTM and enable effective accelerated OTM in OVX rats.
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Project description:Clinical evidence has suggested that surgical corticotomy of the alveolar bone can accelerate local orthodontic tooth movement (OTM), but the underlying cell and molecular mechanisms remain largely unclear. The present study examined the role of macrophages played in corticotomy-assisted OTM. Orthodontic nickel-titanium springs were applied to the left maxillary first molars of rats or mice to induce OTM with or without corticotomy. Corticotomy enhanced OTM distance by accelerating movement through induction of local osteoclastogenesis and macrophage infiltration during OTM. Further analysis showed that macrophages were polarized toward an M1-like phenotype immediately after corticotomy and then switched to an M2-like phenotype during OTM. The microenvironment of corticotomy induced macrophage infiltration and polarization through the production of TNF-α. More importantly, the amount of OTM induced by corticotomy was significantly decreased after mice were depleted of monocyte/macrophages by injection of liposome-encapsulated clodronate. Further experiments by incubating cultured macrophages with fresh tissue suspension obtained from post-corticotomy gingiva switched the cells to an M1 phenotype through activation of the nuclear factor-κB (NF-κB) signaling pathway, and to an M2 phenotype through activation of the JAK/STAT3 signaling pathway. Our results suggest that corticotomy induces macrophage polarization first by activating the NF-κB signaling pathway and later by activating the JAK/STAT3 signaling pathway, and that these processes contribute to OTM by triggering production of inflammatory cytokines and osteoclastogenesis.
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Project description:The stromal cell-derived factor 1 (SDF-1)/chemokine receptor type 4 (CXCR4) axis plays a key role in alveolar bone metabolism during orthodontic tooth movement (OTM). Herein, the effects of the SDF-1/CXCR4 axis on the regional acceleratory phenomenon (RAP) in OTM velocity and on changes in the surrounding periodontium after adjacent tooth extraction in rats were investigated. Six-week-old male Wistar/ST rats underwent left maxillary first molar (M1) extraction and mesial OTM of the left maxillary second molar (M2) with a 10-g force closed-coil spring. Phosphate-buffered saline, immunoglobulin G (IgG) isotype control antibody, or anti-SDF-1 neutralizing monoclonal antibody were injected at the M1 and M2 interproximal areas (10 μg/0.1 mL) for the first three days. Analyses were performed after 1, 3, and 7 days (n = 7). The results demonstrated a significant increase in SDF-1 expression from day 1, which was effectively blocked via anti-SDF-1 neutralizing monoclonal antibody injection. On day 3, the M2 OTM distance and the number of positively stained osteoclasts significantly reduced alongside a reduction in inflammatory markers in the experimental group. Our results demonstrated that serial local injection of the anti-SDF-1 neutralizing monoclonal antibody reduces M2 OTM, osteoclast accumulation, and localized inflammatory responses in an OTM model with tooth extraction-induced RAP.
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Project description:Tooth movement induced by orthodontic treatment can cause sequential reactions involving the periodontal tissue and alveolar bone, resulting in the release of numerous substances from the dental tissues and surrounding structures. To better understand the biological processes involved in orthodontic treatment, improve treatment, and reduce adverse side effects, several of these substances have been proposed as biomarkers. Potential biological markers can be collected from different tissue samples, and suitable sampling is important to accurately reflect biological processes. This paper covers the tissue changes that are involved during orthodontic tooth movement such as at compression region (involving osteoblasts), tension region (involving osteoclasts), dental root, and pulp tissues. Besides, the involvement of stem cells and their development towards osteoblasts and osteoclasts during orthodontic treatment have also been explained. Several possible biomarkers representing these biological changes during specific phenomenon, that is, bone remodelling (formation and resorption), inflammation, and root resorption have also been proposed. The knowledge of these biomarkers could be used in accelerating orthodontic treatment.
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Project description:Orthodontic tooth movement (OTM) is a "sterile" inflammatory process. The present study aimed to reveal the underlying biological mechanisms, by studying the force associated-gene expression changes, in a time-dependent manner. Ni-Ti springs were set to move the upper 1st-molar in C57BL/6 mice. OTM was measured by ?CT. Total-RNA was extracted from tissue blocks at 1,3,7 and 14-days post force application, and from two control groups: naïve and inactivated spring. Gene-expression profiles were generated by next-generation-RNA-sequencing. Gene Set Enrichment Analysis, K-means algorithm and Ingenuity pathway analysis were used for data interpretation. Genes of interest were validated with qRT-PCR. A total of 3075 differentially expressed genes (DEGs) were identified, with the greatest number at day 3. Two distinct clusters patterns were recognized: those in which DEGs peaked in the first days and declined thereafter (tissue degradation, phagocytosis, leukocyte extravasation, innate and adaptive immune system responses), and those in which DEGs were initially down-regulated and increased at day 14 (cell proliferation and migration, cytoskeletal rearrangement, tissue homeostasis, angiogenesis). The uncovering of novel innate and adaptive immune processes in OTM led us to propose a new term "Immunorthodontics". This genomic data can serve as a platform for OTM modulation future approaches.
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Project description:UnlabelledEnoxacin inhibits binding between the B-subunit of vacuolar H(+)-ATPase (V-ATPase) and microfilaments, and also between osteoclast formation and bone resorption in vitro. We hypothesized that a bisphosphonate derivative of enoxacin, bis-enoxacin (BE), which was previously studied as a bone-directed antibiotic, might have similar activities. BE shared a number of characteristics with enoxacin: It blocked binding between the recombinant B-subunit and microfilaments and inhibited osteoclastogenesis in cell culture with IC50s of about 10 µM in each case. BE did not alter the relative expression levels of various osteoclast-specific proteins. Even though tartrate-resistant acid phosphatase 5b was expressed, proteolytic activation of the latent pro-enzyme was inhibited. However, unlike enoxacin, BE stimulated caspase-3 activity. BE bound to bone slices and inhibited bone resorption by osteoclasts on BE-coated bone slices in cell culture. BE reduced the amount of orthodontic tooth movement achieved in rats after 28 days. Analysis of these data suggests that BE is a novel anti-resorptive molecule that is active both in vitro and in vivo and may have clinical uses.AbbreviationsBE, bis-enoxacin; V-ATPase, vacuolar H(+)-ATPase; TRAP, tartrate-resistant acid phosphatase; ?MEM D10, minimal essential media, alpha modification with 10% fetal bovine serum; SDS-PAGE, sodium dodecyl sulfate-polyacrylamide gel electrophoresis; RANKL, receptor activator of nuclear factor kappa B-ligand; NFATc1, nuclear factor of activated T-cells; ADAM, a disintegrin and metalloprotease domain; OTM, orthodontic tooth movement.
| S-EPMC3775373 | biostudies-literature
Project description:Recently, involvement of the sympathetic nervous system in bone metabolism has attracted attention. β2-Adrenergic receptor (β2-AR) is presented on osteoblastic and osteoclastic cells. We previously demonstrated that β-AR blockers at low dose improve osteoporosis with hyperactivity of the sympathetic nervous system via β2-AR blocking, while they may have a somewhat inhibitory effect on osteoblastic activity at high doses. In this study, the effects of butoxamine (BUT), a specific β2-AR antagonist, on tooth movement were examined in spontaneously hypertensive rats (SHR) showing osteoporosis with hyperactivity of the sympathetic nervous system. We administered BUT (1 mg/kg) orally, and closed-coil springs were inserted into the upper-left first molar. After sacrifice, we calculated the amount of tooth movement and analyzed the trabecular microarchitecture and histomorphometry. The distance in the SHR control was greater than that in the Wistar-Kyoto rat group, but no significant difference was found in the SHR treated with BUT compared with the Wistar-Kyoto rat control. Analysis of bone volume per tissue volume, trabecular number, and osteoclast surface per bone surface in the alveolar bone showed clear bone loss by an increase of bone resorption in SHR. In addition, BUT treatment resulted in a recovery of alveolar bone loss. Furthermore, TH-immunoreactive nerves in the periodontal ligament were increased by tooth movement, and BUT administration decreased TH-immunoreactive nerves. These results suggest that BUT prevents alveolar bone loss and orthodontic tooth movement via β2-AR blocking.
| S-EPMC4293756 | biostudies-literature
Project description:Objectives: Myeloid p38α/MAPK regulate and coordinate osteoclastogenesis. The present study was conducted to investigate the role of myeloid p38α/MAPK during orthodontic tooth movement. Methods: Orthodontic tooth movement was performed in wildtype and p38αΔmyel mice lacking p38α/MAPK expression in myeloid cells. First, bone parameter as well as osteoblast and osteoclast number were determined in tibiae. RNA was isolated from the untreated and orthodontically treated maxillary jaw side and expression of genes involved in inflammation and bone remodelling were analysed. Finally, periodontal bone loss, alveolar bone density and extent of orthodontic tooth movement were assessed. Results: Bone density was increased in p38αΔmyel mice compared to wildtype mice in tibiae (p = 0.043) and alveolar bone (p = 0.003). This was accompanied by a reduced osteoclast number in tibiae (p = 0.005) and TRAP5b in serum (p = 0.015). Accordingly, expression of osteoclast-specific genes was reduced in p38αΔmyel mice. Extent of tooth movement was reduced in p38αΔmyel mice (p = 0.024). This may be due to the higher bone density of the p38αΔmyel mice. Conclusions: Myeloid p38α/MAPK thus appears to play a regulatory role during orthodontic tooth movement by regulating osteoclastogenesis.
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Project description:BACKGROUND This study was performed to investigate the effect of local injection of asperosaponin VI (ASA VI) on the orthodontic tooth movement in rats. MATERIAL AND METHODS A total of 64 healthy female Sprague-Dawley rats were selected and divided into 2 groups randomly: the ASA VI group and the control group. For the ASA VI group, 10 mg/kg ASA VI solution was injected into buccal submucoperiosteal of bilaterally first maxillary molars, and the same volume of normal saline was given to the control group. The orthodontic force was applied to the maxillary first molars. All rats were sacrificed on days 3, 7, or 14. Tooth movement effects on the periodontium were analyzed through hematoxylin and eosin (H&E) staining, tartrate-resistant acid phosphatase (TRAP) staining and immunohistochemistry analysis. Tooth movement measurements and alveolar bone volumetric changes were analyzed using a micro-computed tomography (CT) scan. Molecular changes were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. RESULTS The ASA VI group presented with a significant increase of tooth movement, osteoclast number, and the expression of osteoclast differentiation factor (ODF) compared with the control group. ASA VI also induced a significant decrease in bone volume and density and an increase in trabecular spacing and RANKL (receptor activator of nuclear factor kappa-B ligand) expression at the compression side. Furthermore, ASA VI stimulated bone formation on the tension side by enhancing OCN (osteocalcin) expression and RUNX2 (runt-related transcription factor 2) expression, increasing bone volume and density and decreasing in trabecular spacing. CONCLUSIONS Injection of ASA VI may accelerate tooth movement via increasing the activity of osteoclasts, stimulating bone resorption at the compression side. Furthermore, ASA VI has a positive effect on bone formation at the tension side.
| S-EPMC7193222 | biostudies-literature
Project description:An OTM-related healing model was established where a maxillary second premolar was protracted into the critical-sized defect for 6 weeks (Group DT6). As controls, natural healing models without OTM were set at 2 weeks (Group D2) and at 6 weeks (Group D6) after surgery. Total RNAs were extracted from dissected regenerated tissues and additionally from sound alveolar bone as a baseline (Group C). mRNA profiling was performed using microarray analysis.
2017-08-01 | GSE85459 | GEO