scholarly journals Gan-Lu-Yin (Kanroin), Traditional Chinese Herbal Extracts, Reduces Osteoclast Differentiation In Vitro and Prevents Alveolar Bone Resorption in Rat Experimental Periodontitis

2021 ◽  
Vol 10 (3) ◽  
pp. 386
Author(s):  
Yuji Inagaki ◽  
Jun-ichi Kido ◽  
Yasufumi Nishikawa ◽  
Rie Kido ◽  
Eijiro Sakamoto ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Alveolar Bone ◽  
Osteoclast Differentiation ◽  
Raw264.7 Cells ◽  
Tartrate Resistant Acid Phosphatase ◽  
Therapeutic Effects ◽  
Traditional Chinese Herbal Medicine ◽  
Chinese Herbal ◽  
Experimental Periodontitis

Gan-Lu-Yin (GLY), a traditional Chinese herbal medicine, shows therapeutic effects on periodontitis, but that mechanism is not well known. This study aims to clarify the precise mechanism by investigating the inhibitory effects of GLY extracts on osteoclastogenesis in vitro and on bone resorption in periodontitis in vivo. RAW264.7 cells are cultured with soluble receptor activator of nuclear factor-kappa B (sRANKL) and GLY extracts (0.01–1.0 mg/mL), and stained for tartrate-resistant acid phosphatase (TRAP) to evaluate osteoclast differentiation. Experimental periodontitis is induced by placing a nylon ligature around the second maxillary molar in rats, and rats are administered GLY extracts (60 mg/kg) daily for 20 days. Their maxillae are collected on day 4 and 20, and the levels of alveolar bone resorption and osteoclast differentiation are estimated using micro-computed tomography (CT) and histological analysis, respectively. In RAW264.7 cells, GLY extracts significantly inhibit sRANKL-induced osteoclast differentiation at a concentration of more than 0.05 mg/mL. In experimental periodontitis, administering GLY extracts significantly decreases the number of TRAP-positive osteoclasts in the alveolar bone on day 4, and significantly inhibits the ligature-induced bone resorption on day 20. These results show that GLY extracts suppress bone resorption by inhibiting osteoclast differentiation in experimental periodontitis, suggesting that GLY extracts are potentially useful for oral care in periodontitis.

Edgeworthia papyrifera Regulates Osteoblast and Osteoclast Differentiation In Vitro and Exhibits Anti-osteoporosis Activity in Animal Models of Osteoporosis

Planta Medica ◽  
2019 ◽  
Vol 85 (09/10) ◽  
pp. 766-773 ◽  
Author(s):  
Pansoo Kim ◽  
Yeon-Ju Nam ◽  
Woo Jung Kim ◽  
Jin Kyu Kim ◽  
Gyeongbeen Lee ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Animal Models ◽  
Osteoclast Differentiation ◽  
Raw 264.7 Cells ◽  
Tartrate Resistant Acid Phosphatase ◽  
Raw 264.7 ◽  
Treatment Of Osteoporosis ◽  
Increased Risk ◽  
Interesting Candidate

AbstractOsteoporosis is a clinical condition characterized by low bone strength that leads to an increased risk of fracture. Strategies for the treatment of osteoporosis involve inhibition of bone resorption by osteoclasts and an increase of bone formation by osteoblasts. Here, we identified the extract derived from the stem part of Edgeworthia papyrifera that enhanced differentiation of MC3T3-E1 cells to osteoblast-like cells and inhibited osteoclast differentiation of RAW 264.7 cells in vitro. In support of our observation, rutin and daphnoretin, which were previously reported to inhibit osteoclast differentiation, were identified in E. papyrifera extract. In an animal model of osteoporosis, the ovariectomy-induced increases in bone resorption biomarkers such as pyridinoline and tartrate-resistant acid phosphatase were significantly reduced by E. papyrifera extract administration at 25.6 and 48.1%, respectively. Furthermore, the ovariectomy-induced bone loss in animal models of osteoporosis was significantly prevented by the administration of E. papyrifera in our study. Taking these observations into account, we suggest that E. papyrifera is an interesting candidate for further exploration as an anti-osteoporotic agent.

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 Magnolol Ameliorates Ligature-Induced Periodontitis in Rats and Osteoclastogenesis:In VivoandIn VitroStudy

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Sheng-Hua Lu ◽  
Ren-Yeong Huang ◽  
Tz-Chong Chou
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Periodontal Disease ◽  
Alveolar Bone ◽  
Morphological Changes ◽  
Osteoclast Differentiation ◽  
Alveolar Bone Loss ◽  
Tartrate Resistant Acid Phosphatase ◽  
Nuclear Factor ◽  
Raw264.7 Macrophages

Periodontal disease characterized by alveolar bone resorption and bacterial pathogen-evoked inflammatory response has been believed to have an important impact on human oral health. The aim of this study was to evaluate whether magnolol, a main constituent ofMagnolia officinalis, could inhibit the pathological features in ligature-induced periodontitis in rats and osteoclastogenesis. The sterile, 3–0 (diameter; 0.2 mm) black braided silk thread, was placed around the cervix of the upper second molars bilaterally and knotted medially to induce periodontitis. The morphological changes around the ligated molars and alveolar bone were examined by micro-CT. The distances between the amelocemental junction and the alveolar crest of the upper second molars bilaterally were measured to evaluate the alveolar bone loss. Administration of magnolol (100 mg/kg, p.o.) significantly inhibited alveolar bone resorption, the number of osteoclasts on bony surface, and protein expression of receptor activator of nuclear factor-κB ligand (RANKL), a key mediator promoting osteoclast differentiation, in ligated rats. Moreover, the ligature-induced neutrophil infiltration, expression of inducible nitric oxide synthase, cyclooxygenase-2, matrix metalloproteinase (MMP)-1 and MMP-9, superoxide formation, and nuclear factor-κB activation in inflamed gingival tissues were all attenuated by magnolol. In thein vitrostudy, magnolol also inhibited the growth ofPorphyromonas gingivalis and Aggregatibacter actinomycetemcomitansthat are key pathogens initiating periodontal disease. Furthermore, magnolol dose dependently reduced RANKL-induced osteoclast differentiation from RAW264.7 macrophages, tartrate-resistant acid phosphatase (TRAP) activity of differentiated cells accompanied by a significant attenuation of resorption pit area caused by osteoclasts. Collectively, we demonstrated for the first time that magnolol significantly ameliorates the alveolar bone loss in ligature-induced experimental periodontitis by suppressing periodontopathic microorganism accumulation, NF-κB-mediated inflammatory mediator synthesis, RANKL formation, and osteoclastogenesis. These activities support that magnolol is a potential agent to treat periodontal disease.

scholarly journals Effects of Isoliquiritigenin on Bone Metabolism and Uterus in Ovariectomized Rats

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 469-469
Author(s):  
Lara Sattgast ◽  
Carmen Wong ◽  
Daniel Doerge ◽  
William Helferich ◽  
Urszula Iwaniec ◽  
...  
Keyword(s):  
Gene Expression ◽  
Bone Resorption ◽  
Epithelial Cell ◽  
Osteoclast Differentiation ◽  
Ovariectomized Rats ◽  
Tartrate Resistant Acid Phosphatase ◽  
Uterine Weight ◽  
Uterine Epithelial Cell ◽  
Ovx Rats

Abstract Objectives Isoliquiritigenin (ILQ) is a phenolic compound found in licorice and is a popular dietary supplement. ILQ exhibits model-specific antioxidant, anti-inflammatory, anti-tumor, and estrogenic activities. Limited data suggest the potential of ILQ to prevent or treat osteoporosis. Therefore, this study evaluated the effects of short-duration treatment with ILQ on bone and uterine tissue in estrogen-deplete ovariectomized (ovx) rats. The uterus was important to evaluate because ILQ stimulates proliferation of MCF7 breast cancer cells through an estrogen receptor-dependent mechanism. Methods Six-week-old rats (ovx'd at 4 weeks of age) were fed diets containing 0, 100, 250 or 750 ppm ILQ (n = 5/treatment) for 1 week and sacrificed. Gene expression in femur and uterus, blood markers of global bone turnover, body composition, and uterine weight and epithelial cell height were determined. In addition, the effect of ILQ on in vitro differentiation of osteoclasts derived from bone marrow was assessed. Results Treatment resulted in a dose-dependent increase in serum ILQ with levels reaching 2.4 ± 0.2 mM in rats receiving the highest dose. ILQ did not alter serum levels of osteocalcin, a global marker of bone formation, or osteocalcin gene expression in femur. Additionally, there was little or no effect of ILQ on genes related to osteoblast differentiation or activity in femur. These largely null findings contrast with a reduction in serum CTX, a global marker of bone resorption, at all dose levels of ILQ. At the gene level, ILQ resulted in lower mRNA for genes related to osteoclast differentiation and function in femur, including Acp5 (tartrate resistant acid phosphatase), Timp2 and Mmp2, and suppressed osteoclast differentiation in vitro. ILQ had no effect on the ovx-induced increase in body weight. Ovx resulted in lower uterine weight. Treatment with ILQ at 750 ppm resulted in development of severe uterine epithelial cell hyperplasia in two of five animals. Conclusions ILQ supplementation led to reduced biochemical and gene expression markers of bone resorption in vivo and reduced osteoclast differentiation in vitro without increasing estrogen-dependent gene expression. However, the potential benefits must be weighed against potential detrimental off-target effects, including uterine hypertrophy. Funding Sources NIH [P50AT006268].

scholarly journals Deferoxamine Reduces Inflammation and Osteoclastogenesis in Avulsed Teeth

2021 ◽  
Vol 22 (15) ◽  
pp. 8225
Author(s):  
Ko Eun Lee ◽  
Mijeong Jeon ◽  
Seunghan Mo ◽  
Hyo-Seol Lee ◽  
Je Seon Song ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Alveolar Bone ◽  
Root Surface ◽  
Tartrate Resistant Acid Phosphatase ◽  
Micro Ct ◽  
Sprague Dawley ◽  
Micro Computed Tomography ◽  
Model Cell

Replacement and inflammatory resorption are serious complications associated with the delayed replantation of avulsed teeth. In this study, we aimed to assess whether deferoxamine (DFO) can suppress inflammation and osteoclastogenesis in vitro and attenuate inflammation and bone resorption in a replanted rat tooth model. Cell viability and inflammation were evaluated in RAW264.7 cells. Osteoclastogenesis was confirmed by tartrate-resistant acid phosphatase staining, reactive oxygen species (ROS) measurement, and quantitative reverse transcriptase–polymerase chain reaction in teeth exposed to different concentrations of DFO. In vivo, molars of 31 six-week-old male Sprague–Dawley rats were extracted and stored in saline (n = 10) or DFO solution (n = 21) before replantation. Micro-computed tomography (micro-CT) imaging and histological analysis were performed to evaluate inflammation and root and alveolar bone resorption. DFO downregulated the genes related to inflammation and osteoclastogenesis. DFO also reduced ROS production and regulated specific pathways. Furthermore, the results of the micro-CT and histological analyses provided evidence of the decrease in inflammation and hard tissue resorption in the DFO group. Overall, these results suggest that DFO reduces inflammation and osteoclastogenesis in a tooth replantation model, and thus, it has to be further investigated as a root surface treatment option for an avulsed tooth.

scholarly journals 10-Gingerol Suppresses Osteoclastogenesis in RAW264.7 Cells and Zebrafish Osteoporotic Scales

2021 ◽  
Vol 9 ◽  
Author(s):  
Liqing Zang ◽  
Kazuhiro Kagotani ◽  
Hiroko Nakayama ◽  
Jacky Bhagat ◽  
Yuki Fujimoto ◽  
...  
Keyword(s):  
Transmembrane Protein ◽  
Osteoclast Differentiation ◽  
Hexane Extract ◽  
Scale Model ◽  
Raw264.7 Cells ◽  
Tartrate Resistant Acid Phosphatase ◽  
Nuclear Factor ◽  
Osteoclastic Activity

Osteoporosis is the most common aging-associated bone disease and is caused by hyperactivation of osteoclastic activity. We previously reported that the hexane extract of ginger rhizome [ginger hexane extract (GHE)] could suppress receptor activator of nuclear factor kappa-B ligand (RANKL)-induced osteoclastogenesis in RAW264.7 cells. However, the anti-osteoclastic components in GHE have not yet been identified. In this study, we separated GHE into several fractions using silica gel column chromatography and evaluated their effects on osteoclastogenesis using a RAW264.7 cell osteoclast differentiation assay (in vitro) and the zebrafish scale model of osteoporosis (in vivo). We identified that the fractions containing 10-gingerol suppressed osteoclastogenesis in RAW264.7 cells detected by tartrate-resistant acid phosphatase (TRAP) staining. In zebrafish, GHE and 10-gingerol suppressed osteoclastogenesis in prednisolone-induced osteoporosis regenerated scales to promote normal regeneration. Gene expression analysis revealed that 10-gingerol suppressed osteoclast markers in RAW264.7 cells [osteoclast-associated immunoglobulin-like receptor, dendrocyte-expressed seven transmembrane protein, and matrix metallopeptidase-9 (Mmp9)] and zebrafish scales [osteoclast-specific cathepsin K (CTSK), mmp2, and mmp9]. Interestingly, nuclear factor of activated T-cells cytoplasmic 1, a master transcription regulator of osteoclast differentiation upstream of the osteoclastic activators, was downregulated in zebrafish scales but showed no alteration in RAW264.7 cells. In addition, 10-gingerol inhibited CTSK activity under cell-free conditions. This is the first study, to our knowledge, that has found that 10-gingerol in GHE could suppress osteoclastic activity in both in vitro and in vivo conditions.

scholarly journals Beta-Cryptoxanthin Inhibits Lipopolysaccharide-Induced Osteoclast Differentiation and Bone Resorption via the Suppression of Inhibitor of NF-κB Kinase Activity

Nutrients ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 368 ◽  
Author(s):  
Narumi Hirata ◽  
Ryota Ichimaru ◽  
Tsukasa Tominari ◽  
Chiho Matsumoto ◽  
Kenta Watanabe ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Molecular Mechanism ◽  
Transcriptional Activation ◽  
Alveolar Bone ◽  
Biological Activities ◽  
Osteoclast Differentiation ◽  
Docking Simulation ◽  
Vitro Assay

Beta-cryptoxanthin (β-cry) is a typical carotenoid found abundantly in fruit and vegetables such as the Japanese mandarin orange, persimmon, papaya, paprika, and carrot, and exerts various biological activities (e.g., antioxidant effects). We previously reported that β-cry suppressed lipopolysaccharide (LPS)-induced osteoclast differentiation via the inhibition of prostaglandin (PG) E2 production in gingival fibroblasts and restored the alveolar bone loss in a mouse model for periodontitis in vivo. In this study, we investigated the molecular mechanism underlying the inhibitory effects of β-cry on osteoclast differentiation. In mouse calvarial organ cultures, LPS-induced bone resorption was suppressed by β-cry. In osteoblasts, β-cry inhibited PGE2 production via the downregulation of the LPS-induced mRNA expression of cyclooxygenase (COX)-2 and membrane-bound PGE synthase (mPGES)-1, which are PGE synthesis-related enzymes, leading to the suppression of receptor activator of NF-κB ligand (RANKL) mRNA transcriptional activation. In an in vitro assay, β-cry directly suppressed the activity of the inhibitor of NF-κB kinase (IKK) β, and adding ATP canceled this IKKβ inhibition. Molecular docking simulation further suggested that β-cry binds to the ATP-binding pocket of IKKβ. In Raw264.7 cells, β-cry suppressed RANKL-mediated osteoclastogenesis. The molecular mechanism underlying the involvement of β-cry in LPS-induced bone resorption may involve the ATP-competing inhibition of IKK activity, resulting in the suppression of NF-κB signaling.

scholarly journals Inhibitory Effects of N-[2-(4-acetyl-1-piperazinyl) phenyl]-2-(2-chlorophenoxy) acetamide on Osteoclast Differentiation In Vitro via the Downregulation of TRAF6

2019 ◽  
Vol 20 (20) ◽  
pp. 5196 ◽  
Author(s):  
Zhihao Chen ◽  
Eunjin Cho ◽  
Jinkyung Lee ◽  
Sunwoo Lee ◽  
Tae-Hoon Lee
Keyword(s):  
Bone Resorption ◽  
Mononuclear Cells ◽  
Osteoclast Differentiation ◽  
Bone Diseases ◽  
Marker Genes ◽  
Tartrate Resistant Acid Phosphatase ◽  
Specific Marker ◽  
Potential Candidate ◽  
Dependent Manner

Osteoclasts are poly-nuclear cells that resorb mineral components from old or damaged bone tissue. Primary mononuclear cells are activated by receptor activator of nuclear factor kappa-Β ligand (RANKL) and differentiate into large multinucleated cells. Dysregulation of osteoclast differentiation can lead to pathological bone loss and destruction. Many studies have focused on the development of new molecules to regulate RANKL-mediated signaling. In this study, N-[2-(4-acetyl-1-piperazinyl)phenyl]-2-(2-chlorophenoxy) acetamide (PPOA-N-Ac-2-Cl) led to a significant decrease in the formation of multinucleated tartrate-resistant acid phosphatase (TRAP)-positive cells in a dose-dependent manner, without inducing significant cytotoxicity. PPOA-N-Ac-2-Cl affected the expression of osteoclast-specific marker genes, such as TRAF6, c-fos, DC-STAMP, NFATc1, MMP9, CtsK, and TRAP (Acp5), during RANKL-mediated osteoclastogenesis. Moreover, PPOA-N-Ac-2-Cl significantly attenuated the protein levels of CtsK, a critical protease involved in bone resorption. Accordingly, bone resorption activity and F-actin ring formation decreased in the presence of PPOA-N-Ac-2-Cl. In conclusion, this study shows that PPOA-N-Ac-2-Cl acts as an inhibitor of osteoclast differentiation and may serve as a potential candidate agent for the treatment of osteoclast-related bone diseases by virtue of attenuating bone resorption.

scholarly journals Effects of gold nanoparticles combined with human β-defensin 3 on the alveolar bone loss of periodontitis in rat

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Jing Zhou ◽  
Lingjun Li ◽  
Di Cui ◽  
Xiaoting Xie ◽  
Wenrong Yang ◽  
...  
Keyword(s):  
Gold Nanoparticles ◽  
Bone Resorption ◽  
Bone Repair ◽  
Alveolar Bone ◽  
Ct Scanning ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tartrate Resistant Acid Phosphatase ◽  
Micro Ct ◽  
Expression Levels ◽  
Experimental Periodontitis

Abstract Background Nanomaterials of biomedicine and tissue engineering have been proposed for the treatment of periodontitis in recent years. This study aimed to investigate the effects of gold nanoparticles (AuNPs) combined with human β-defensin 3 (hBD3) on the repair of the alveolar bones of experimental periodontitis in rats. Methods A model of experimental periodontitis was established by ligation of the maxillary second molars with silk thread in rats, which were treated with or without AuNPs combined with hBD3. Micro‐computerized tomography (micro-CT) scanning, enzyme-linked immunosorbent assay, 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 the samples. Results Micro-CT demonstrated that the alveolar bone resorption was significantly reduced after the treatment with AuNPs combined with hBD3. Levels of TNF-α and IL-6 were decreased markedly compared with the ligation group. H&E and Masson staining showed that AuNPs combined with 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 with hBD3 increased the expression levels of ALP and OPG (related to bone formation) while decreasing the expression levels of TRAP and RANKL (related to bone resorption) expression. Conclusions AuNPs combined with hBD3 had a protective effect on the progression of experimental periodontitis in rats and played a certain role in suppressing osteoclastogenesis and alleviating the inflammatory destruction of periodontitis along with the promotion of bone repair.

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