scholarly journals Effects of Jixueteng on Experimental Periodontitis During Orthodontic Tooth Movement in Rats

2021 ◽  
Vol 16 (4) ◽  
pp. 1934578X2110024
Author(s):  
Taira Katayama ◽  
Takenori Sato ◽  
Nobushiro Hamada ◽  
Seiji Goda ◽  
Tetsutaro Yamaguchi ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Orthodontic Treatment ◽  
Alveolar Bone ◽  
Tooth Movement ◽  
Orthodontic Tooth Movement ◽  
Bone Destruction ◽  
Infected Group ◽  
Tartrate Resistant Acid Phosphatase ◽  
Micro Computed Tomography ◽  
Experimental Periodontitis

Recently, natural ingredients have focused on the inhibition of bacteria-induced alveolar bone resorption in orthodontic treatment. Jixueteng (Jix), a Chinese traditional medicine, contains several kinds of flavonoids given their biological properties. We evaluated the effects of Jix on experimental periodontitis during orthodontic tooth movement (OTM) in rats. To this end, 9-week-old male Wistar rats, which were equipped with orthodontic appliance, were orally infected with Porphyromonas gingivalis (Pg), while Jix was administered in their drinking water. A total of 28 days after the beginning of OTM, alveolar bone resorption on the right side of the upper jaws was scanned with micro-computed tomography. These were also used as histological specimens and underwent tartrate-resistant acid phosphatase (TRAP) staining. TRAP-positive multinucleated cells were counted as osteoclasts. As a result, the distance of tooth movement in the OTM and Pg infection with Jix administration (OTM + Pg + Jix) group was the same as that of the sham-infected group. The amount of bone resorption and number of osteoclasts in the OTM + Pg + Jix group was more significantly decreased than that in the OTM and Pg-infected group ( P < 0.05). Hence, Jix had little effect on OTM and inhibited Pg-induced alveolar bone destruction. We suggested that the administration of Jix can support tooth movement and contribute to the prevention of periodontitis during orthodontic treatment.

scholarly journals Single Local Injection of Epigallocatechin Gallate-Modified Gelatin Attenuates Bone Resorption and Orthodontic Tooth Movement in Mice

Polymers ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 1384 ◽  
Author(s):  
Yuta Katsumata ◽  
Hiroyuki Kanzaki ◽  
Yoshitomo Honda ◽  
Tomonari Tanaka ◽  
Yuuki Yamaguchi ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Alveolar Bone ◽  
Tooth Movement ◽  
Orthodontic Tooth Movement ◽  
Epigallocatechin Gallate ◽  
Bone Destruction ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Liquid Form

Osteoclastic bone resorption enables orthodontic tooth movement (OTM) in orthodontic treatment. Previously, we demonstrated that local epigallocatechin gallate (EGCG) injection successfully slowed the rate of OTM; however, repeat injections were required. In the present study, we produced a liquid form of EGCG-modified gelatin (EGCG-GL) and examined the properties of EGCG-GL with respect to prolonging EGCG release, NF-E2-related factor 2 (Nrf2) activation, osteoclastogenesis inhibition, bone destruction, and OTM. We found EGCG-GL both prolonged the release of EGCG and induced the expression of antioxidant enzyme genes, such as heme oxygenase 1 (Hmox1) and glutamate-cysteine ligase (Gclc), in the mouse macrophage cell line, RAW264.7. EGCG-GL attenuated intracellular reactive oxygen species (ROS) levels were induced by the receptor activator of nuclear factor-kB ligand (RANKL) and inhibited RANKL-mediated osteoclastogenesis in vitro. An animal model of bone destruction, induced by repeat Lipopolysaccharide (LPS)-injections into the calvaria of male BALB/c mice, revealed that a single injection of EGCG-GL on day-1 could successfully inhibit LPS-mediated bone destruction. Additionally, experimental OTM of maxillary first molars in male mice was attenuated by a single EGCG-GL injection on day-1. In conclusion, EGCG-GL prolongs the release of EGCG and inhibits osteoclastogenesis via the attenuation of intracellular ROS signaling through the increased expression of antioxidant enzymes. These results indicate EGCG-GL would be a beneficial therapeutic approach both in destructive bone disease and in controlling alveolar bone metabolism.

scholarly journals The role of inhibition of osteocyte apoptosis in mediating orthodontic tooth movement and periodontal remodeling: a pilot study

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Michele Kaplan ◽  
Zana Kalajzic ◽  
Thomas Choi ◽  
Imad Maleeh ◽  
Christopher L. Ricupero ◽  
...  
Keyword(s):  
Bone Density ◽  
Alveolar Bone ◽  
Tooth Movement ◽  
Orthodontic Tooth Movement ◽  
Tartrate Resistant Acid Phosphatase ◽  
Osteocyte Apoptosis ◽  
Saline Administration ◽  
Group 2 ◽  
Group 1

Abstract Background Orthodontic tooth movement (OTM) has been shown to induce osteocyte apoptosis in alveolar bone shortly after force application. However, how osteocyte apoptosis affects orthodontic tooth movement is unknown. The goal of this study was to assess the effect of inhibition of osteocyte apoptosis on osteoclastogenesis, changes in the alveolar bone density, and the magnitude of OTM using a bisphosphonate analog (IG9402), a drug that affects osteocyte and osteoblast apoptosis but does not affect osteoclasts. Material and methods Two sets of experiments were performed. Experiment 1 was used to specifically evaluate the effect of IG9402 on osteocyte apoptosis in the alveolar bone during 24 h of OTM. For this experiment, twelve mice were divided into two groups: group 1, saline administration + OTM24-h (n=6), and group 2, IG9402 administration + OTM24-h (n=6). The contralateral unloaded sides served as the control. The goal of experiment 2 was to evaluate the role of osteocyte apoptosis on OTM magnitude and osteoclastogenesis 10 days after OTM. Twenty mice were divided into 4 groups: group 1, saline administration without OTM (n=5); group 2, IG9402 administration without OTM (n=5); group 3, saline + OTM10-day (n=6); and group 4, IG9402 + OTM10-day (n=4). For both experiments, tooth movement was achieved using Ultra Light (25g) Sentalloy Closed Coil Springs attached between the first maxillary molar and the central incisor. Linear measurements of tooth movement and alveolar bone density (BVF) were assessed by MicroCT analysis. Cell death (or apoptosis) was assessed by terminal dUTP nick-end labeling (TUNEL) assay, while osteoclast and macrophage formation were assessed by tartrate-resistant acid phosphatase (TRAP) staining and F4/80+ immunostaining. Results We found that IG9402 significantly blocked osteocyte apoptosis in alveolar bone (AB) at 24 h of OTM. At 10 days, IG9402 prevented OTM-induced loss of alveolar bone density and changed the morphology and quality of osteoclasts and macrophages, but did not significantly affect the amount of tooth movement. Conclusion Our study demonstrates that osteocyte apoptosis may play a significant role in osteoclast and macrophage formation during OTM, but does not seem to play a role in the magnitude of orthodontic tooth movement.

scholarly journals Is Inflammation a Friend or Foe for Orthodontic Treatment?: Inflammation in Orthodontically Induced Inflammatory Root Resorption and Accelerating Tooth Movement

2021 ◽  
Vol 22 (5) ◽  
pp. 2388
Author(s):  
Masaru Yamaguchi ◽  
Shinichi Fukasawa
Keyword(s):  
Inflammatory Mediators ◽  
Orthodontic Treatment ◽  
Alveolar Bone ◽  
Tooth Movement ◽  
Root Resorption ◽  
Orthodontic Tooth Movement ◽  
Tnf Α ◽  
Orthodontic Forces ◽  
Necrosis Factor

The aim of this paper is to provide a review on the role of inflammation in orthodontically induced inflammatory root resorption (OIIRR) and accelerating orthodontic tooth movement (AOTM) in orthodontic treatment. Orthodontic tooth movement (OTM) is stimulated by remodeling of the periodontal ligament (PDL) and alveolar bone. These remodeling activities and tooth displacement are involved in the occurrence of an inflammatory process in the periodontium, in response to orthodontic forces. Inflammatory mediators such as prostaglandins (PGs), interleukins (Ils; IL-1, -6, -17), the tumor necrosis factor (TNF)-α superfamily, and receptor activator of nuclear factor (RANK)/RANK ligand (RANKL)/osteoprotegerin (OPG) are increased in the PDL during OTM. OIIRR is one of the accidental symptoms, and inflammatory mediators have been detected in resorbed roots, PDL, and alveolar bone exposed to heavy orthodontic force. Therefore, these inflammatory mediators are involved with the occurrence of OIIRR during orthodontic tooth movement. On the contrary, regional accelerating phenomenon (RAP) occurs after fractures and surgery such as osteotomies or bone grafting, and bone healing is accelerated by increasing osteoclasts and osteoblasts. Recently, tooth movement after surgical procedures such as corticotomy, corticision, piezocision, and micro-osteoperforation might be accelerated by RAP, which increases the bone metabolism. Therefore, inflammation may be involved in accelerated OTM (AOTM). The knowledge of inflammation during orthodontic treatment could be used in preventing OIIRR and AOTM.

scholarly journals Chitosan oligosaccharide inhibits skull resorption induced by lipopolysaccharides in mice

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Ke Guo ◽  
Zong Lin Liu ◽  
Wen Chao Wang ◽  
Wei Feng Xu ◽  
Shi Qi Yu ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Therapeutic Potential ◽  
Bone Destruction ◽  
Osteoclast Formation ◽  
Water Soluble ◽  
Tartrate Resistant Acid Phosphatase ◽  
Chitosan Oligosaccharide ◽  
Micro Computed Tomography ◽  
Bone Damage ◽  
Dose Dependent Decrease

Abstract Background Low-molecular-weight chitosan oligosaccharide (LMCOS), a chitosan degradation product, is water-soluble and easily absorbable, rendering it a popular biomaterial to study. However, its effect on bone remodelling remains unknown. Therefore, we evaluated the effect of LMCOS on lipopolysaccharide (LPS)-induced bone resorption in mice. Methods Six-week-old male C57BL/6 mice (n = five per group) were randomly divided into five groups: PBS, LPS, LPS + 0.005% LMCOS, LPS + 0.05% LMCOS, and LPS + 0.5% LMCOS. Then, the corresponding reagents (300 μL) were injected into the skull of the mice. To induce bone resorption, LPS was administered at 10 mg/kg per injection. The mice were injected three times a week with PBS alone or LPS without or with LMCOS and sacrificed 2 weeks later. The skull was removed for micro-computed tomography, haematoxylin-eosin staining, and tartrate-resistant acid phosphatase staining. The area of bone damage and osteoclast formation were evaluated and recorded. Results LMCOS treatment during LPS-induced skull resorption led to a notable reduction in the area of bone destruction; we observed a dose-dependent decrease in the area of bone destruction and number of osteoclasts with increasing LMCOS concentration. Conclusions Our findings showed that LMCOS could inhibit skull bone damage induced by LPS in mice, further research to investigate its therapeutic potential for treating osteolytic diseases is required.

scholarly journals Effects of Gold Nanoparticles Combined Human β-defensin 3 on The Alveolar Bone of Experimental Periodontitis

2021 ◽  
Author(s):  
Jing Zhou ◽  
Lingjun Li ◽  
Di Cui ◽  
Xiaoting Xie ◽  
Wenrong Yang ◽  
...  
Keyword(s):  
Gold Nanoparticles ◽  
Bone Resorption ◽  
Alveolar Bone ◽  
Ct Scanning ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tartrate Resistant Acid Phosphatase ◽  
Micro Ct ◽  
Tnf Α ◽  
Experimental Periodontitis ◽  
Masson Staining

Abstract Background Nanomaterials of biomedicine and tissue engineering have been proposed in the treatment of periodontitis recently. This study aimed to investigate the effect of gold nanoparticles (AuNPs) combined human β-defensin 3 (hBD3) on the repair of alveolar bone of experimental periodontitis in rats. Methods A model of experimental periodontitis was established by ligating of the maxillary second molars with silk thread in rats, which were treated with or without AuNPs combined hBD3. Micro-focus computerized tomography (micro-CT) scanning, enzyme-linked immunosorbent assay (ELISA) and histological and immunohistochemical staining, including alkaline phosphatase (ALP), osteoprotegerin (OPG) tartrate-resistant acid phosphatase (TRAP) and receptor activator of NF-κB Ligand (RANKL), were used to analyze. Results Micro-CT demonstrated that the alveolar bone resorption was significantly reduced after the treatment of AuNPs combined hBD3. Levels of TNF-α and IL-6 decreased markedly compared with the ligation group. HE and Masson staining showed that AuNPs combined hBD3 group had less inflammatory cell infiltration, collagen fibrosis and fracture, but higher calcification in the new bone tissue. Moreover, the administration of AuNPs combined hBD3 increased the expression of ALP and OPG (related to bone formation) expression, while decreased TRAP and RANKL (related to bone resorption) expression. Conclusions AuNPs combined hBD3 had a protective effect on the progress of experimental periodontitis in rats, and also played a certain role in promoting osteogenesis.

scholarly journals Cellular and Molecular Changes in Orthodontic Tooth Movement

2011 ◽  
Vol 11 ◽  
pp. 1788-1803 ◽  
Author(s):  
Shahrul Hisham Zainal Ariffin ◽  
Zulham Yamamoto ◽  
lntan Zarina Zainol Abidin ◽  
Rohaya Megat Abdul Wahab ◽  
Zaidah Zainal Ariffin
Keyword(s):  
Orthodontic Treatment ◽  
Alveolar Bone ◽  
Tooth Movement ◽  
Root Resorption ◽  
Orthodontic Tooth Movement ◽  
Biological Processes ◽  
Tissue Samples ◽  
Dental Tissues ◽  
Compression Region ◽  
Tissue Changes

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.

Effects of Prostaglandin E2 on Alveolar Bone Resorption during Orthodontic Tooth Movement

1988 ◽  
Vol 132 (4) ◽  
pp. 304-309 ◽  
Author(s):  
Chung-Fu Chao ◽  
Chung Shih ◽  
Teen-Meei Wang ◽  
Tai-Hua Lo
Keyword(s):  
Bone Resorption ◽  
Alveolar Bone ◽  
Tooth Movement ◽  
Orthodontic Tooth Movement ◽  
Prostaglandin E

scholarly journals Increasing the amount of corticotomy does not affect orthodontic tooth movement or root resorption, but accelerates alveolar bone resorption in rats

2016 ◽  
pp. cjw038 ◽  
Author(s):  
Takeshi Kurohama ◽  
Hitoshi Hotokezaka ◽  
Megumi Hashimoto ◽  
Takako Tajima ◽  
Kotaro Arita ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Alveolar Bone ◽  
Tooth Movement ◽  
Root Resorption ◽  
Orthodontic Tooth Movement

scholarly journals Raloxifene administration enhances retention in an orthodontic relapse model

2020 ◽  
Vol 42 (4) ◽  
pp. 371-377
Author(s):  
Niloufar Azami ◽  
Po-Jung Chen ◽  
Shivam Mehta ◽  
Zana Kalajzic ◽  
Eliane H Dutra ◽  
...  
Keyword(s):  
Alveolar Bone ◽  
Tooth Movement ◽  
Volume Fraction ◽  
Orthodontic Tooth Movement ◽  
Bone Volume ◽  
Resin Cement ◽  
Control Group ◽  
Tartrate Resistant Acid Phosphatase ◽  
Bone Volume Fraction ◽  
Tissue Density

Abstract Background and objectives Orthodontic relapse is a physiologic process that involves remodelling of the alveolar bone and principle periodontal ligament fibres. Raloxifene is an Food and Drug Administration (FDA)-approved selective oestrogen receptor modulator that inhibits systemic bone loss. In our study, we examined the effects of Raloxifene on alveolar bone modelling and orthodontic relapse in a rodent model. Materials and methods The efficacy of raloxifene was evaluated in 15-week-old male Wistar rats, 8 in each group (Control, Raloxifene, Raloxifene + 7-day relapse, Raloxifene + 14-day relapse) for a total of 42 days. All animals had 14 days of orthodontic tooth movement with a closed nickel–titanium coil spring tied from incisors to right first molar applying 5–8 gm of force. On the day of appliance removal, impression was taken with silicon material and the distance between first molar and second molar was filled with light-cured adhesive resin cement for retention phase. Raloxifene Retention, Raloxifene Retention + 7D, Raloxifene Retention + 14D groups received 14 daily doses of raloxifene (2.0 mg/kg/day) subcutaneously after orthodontic tooth movement during retention. After 14 days of retention, the retainer was removed and right first molar was allowed to relapse for a period of 14 days. Raloxifene injection continued for the Raloxifene + 14-day relapse group during relapse phase too. Control group received saline injections during retention. Animals were euthanized by CO2 inhalation. The outcome measure included percentage of relapse, bone volume fraction, tissue density, and histology analysis using tartrate-resistant acid phosphatase staining and determining receptor activator of nuclear factor-кB-ligand (RANKL) and osteoprotegerin expression. Results Raloxifene Retention + 14D group had significantly less (P &lt; 0.05) orthodontic relapse when compared with other groups. There was a significant increase (P &lt; 0.05) in bone volume fraction and tissue density in the Raloxifene Retention + 14D group when compared with other groups. Similarly, there was significant decrease in number of osteoclasts and RANKL expression in Raloxifene Retention + 14D group when compared with Raloxifene Retention + 7D group (P &lt; 0.05). Conclusion Raloxifene could decrease post-orthodontic treatment relapse by decreasing bone resorption and indirectly enhancing bone formation.

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