scholarly journals Osteoprotegerin-Deficient Male Mice as a Model for Severe Alveolar Bone Loss: Comparison With RANKL-Overexpressing Transgenic Male Mice

Endocrinology ◽  
2013 ◽  
Vol 154 (2) ◽  
pp. 773-782 ◽  
Author(s):  
Masanori Koide ◽  
Yasuhiro Kobayashi ◽  
Tadashi Ninomiya ◽  
Midori Nakamura ◽  
Hisataka Yasuda ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Alveolar Bone ◽  
Nuclear Factor Κb ◽  
Alveolar Bone Loss ◽  
Male Mice ◽  
Periodontal Tissues ◽  
Cortical Areas ◽  
Immunohistochemical Analyses ◽  
Transgenic Male

Periodontitis, an inflammatory disease of periodontal tissues, is characterized by excessive alveolar bone resorption. An increase in the receptor activator of nuclear factor-κB ligand (RANKL) to osteoprotegerin (OPG) ratio is thought to reflect the severity of periodontitis. Here, we examined alveolar bone loss in OPG-deficient (OPG−/−) mice and RANKL-overexpressing transgenic (RANKL-Tg) mice. Alveolar bone loss in OPG−/− mice at 12 weeks was significantly higher than that in RANKL-Tg mice. OPG−/− but not RANKL-Tg mice exhibited severe bone resorption especially in cortical areas of the alveolar bone. An increased number of osteoclasts was observed in the cortical areas in OPG−/− but not in RANKL-Tg mice. Immunohistochemical analyses showed many OPG-positive signals in osteocytes but not osteoblasts. OPG-positive osteocytes in the cortical area of alveolar bones and long bones were abundant in both wild-type and RANKL-Tg mice. This suggests the resorption in cortical bone areas to be prevented by OPG produced locally. To test the usefulness of OPG−/− mice as an animal model for screening drugs to prevent alveolar bone loss, we administered an antimouse RANKL antibody or risedronate, a bisphosphonate, to OPG−/− mice. They suppressed alveolar bone resorption effectively. OPG−/− mice are useful for screening therapeutic agents against alveolar bone loss.

scholarly journals Effects of cigarette smoking on periodontium

2002 ◽  
Vol 55 (5-6) ◽  
pp. 229-232 ◽  
Author(s):  
Marija Bokor-Bratic
Keyword(s):  
Bone Loss ◽  
Oral Hygiene ◽  
Dental Plaque ◽  
Alveolar Bone ◽  
Gingival Recession ◽  
Tobacco Consumption ◽  
Alveolar Bone Loss ◽  
Age Difference ◽  
Periodontal Tissues ◽  
Periodontal Condition

Introduction The exact mechanisms by which smoking effects the periodontal tissues are not known. Studies in which plaque or calculus are taken into consideration come to conflicting conclusions regarding effects of smoking. Aim The aim of this study was to examine the oral hygiene and periodontal status in smokers and compare them with nonsmokers. Material and methods The study group comprised 83 smokers and 83 nonsmokers. The mean age (SD) of smokers and nonsmokers was 42,4?7,0 years and 43,7?6,4 years, respectively. The age difference was not statistically significant. The average tobacco consumption of the smokers at the time of investigation was 14 cigarettes a day and they had been regular smokers for 21 years on average. Results The amount of dental plaque was evaluated in accordance with the criteria of Green-Vermillion by using disclosing solution. The periodontal condition was evaluated by Ramfjord Periodontal Disease Index. For gingival recession the distance from the cemento-enamel junction to the gingival margin was determined on mid-buccal and mid-lingual surfaces of all teeth. Each subject was radiographically examined with a full mouth intraoral survey. Alveolar bone loss was determined as the distance from the cemento-enamel junction to the point where lamina dura became continuous with the compact bone of the interdental septum. Mean alveolar bone loss based on all mesial and distal measurements was calculated for each subject. The amount of dental plaque was high in both smokers (2,60,60) and nonsmokers (1,50,70), whereas the differences were statistically significant (p<0.001). Conclusion Periodontal destruction, alveolar bone loss and gingival recession were significantly increased in smokers compared to nonsmokers (p<0.001). It is concluded that differences observed between smokers and nonsmokers with regard to periodontal condition are attributable to differences in oral hygiene. Smoking is a risk factor for periodontal health.

scholarly journals Antiperiodontitis Effects of Magnolia biondii Extract on Ligature-Induced Periodontitis in Rats

Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 934 ◽  
Author(s):  
Hae Jin Lee ◽  
Dong-Ryung Lee ◽  
Bong-Keun Choi ◽  
Seung Hwan Yang
Keyword(s):  
Bone Loss ◽  
Tissue Damage ◽  
Alveolar Bone ◽  
Histopathological Examination ◽  
Nuclear Factor Κb ◽  
Alveolar Bone Loss ◽  
Gingival Tissue ◽  
Protective Effects ◽  
Tissue Destruction ◽  
Commercial Kits

Over the past decades, periodontitis has become a rising health problem and caused various diseases. In the many studies shows that some extracts and compound to the prevention and treatment of periodontitis. This study focuses on the effects of inhibition of gingival damage and alveolar bone loss. The aim of this study was to evaluate the protective effects of Magnolia biondii extract (MBE) against ligature-induced periodontitis in rats. A ligature was placed around the molar teeth for 8 weeks, and MBE was administered for 8 weeks. Gingival tissue damage and alveolar bone loss were measured by microcomputed tomography (CT) analysis and histopathological examination. Serum Interluekin-1 β (IL-1β), tumor necrosis factor-α (TNF-α), cyclooxygenases-2 (COX-2), and receptor activator of nuclear factor–κB ligand (RANKL) levels were investigated using commercial kits to confirm the antiperiodontitis effects of MBE. We confirmed that ligature-induced periodontitis resulted in gingival tissue damage and alveolar bone loss. However, treatment for 8 weeks with MBE protected from periodontal tissue damage and downregulated serum inflammatory cytokine factors and RANKL levels. These results suggest that MBE exerts antiperiodontitis effects by inhibiting gingival tissue destruction and alveolar bone loss through regulation of anti-inflammatory cytokines in periodontitis-induced rats.

Involvement of Cot/Tp12 in Bone Loss during Periodontitis

2010 ◽  
Vol 89 (2) ◽  
pp. 192-197 ◽  
Author(s):  
T. Ohnishi ◽  
A. Okamoto ◽  
K. Kakimoto ◽  
K. Bandow ◽  
N. Chiba ◽  
...  
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Periodontal Tissue ◽  
Rankl Expression ◽  
Periodontal Tissues ◽  
Tnf Α ◽  
Experimental Periodontitis ◽  
Deficient Mice

Periodontitis causes resorption of alveolar bone, in which RANKL induces osteoclastogenesis. The binding of lipopolysaccharide to Toll-like receptors causes phosphorylation of Cot/Tp12 to activate the MAPK cascade. Previous in vitro studies showed that Cot/Tp12 was essential for the induction of RANKL expression by lipopolysaccharide. In this study, we examined whether Cot/Tp12 deficiency reduced the progression of alveolar bone loss and osteoclastogenesis during experimental periodontitis. We found that the extent of alveolar bone loss and osteoclastogenesis induced by ligature-induced periodontitis was decreased in Cot/Tp12-deficient mice. In addition, reduction of RANKL expression was observed in periodontal tissues of Cot/Tp12-deficient mice with experimental periodontitis. Furthermore, we found that Cot/Tp12 was involved in the induction of TNF-α mRNA expression in gingiva of mice with experimental periodontitis. Our observations suggested that Cot/Tp12 is essential for the progression of alveolar bone loss and osteoclastogenesis in periodontal tissue during experimental periodontitis mediated through increased RANKL expression.

scholarly journals Protective Effect of Resveratrol against the Alveolar Bone Loss in Rats with Experimental Periodontitis and Acts Positively on the IL-17

2021 ◽  
pp. 162-173
Author(s):  
JordanaHeidemann Pandini ◽  
Lais Fernanda Pasqualotto ◽  
Pedro Henrique de Carli Rodrigues ◽  
João Paulo Gonçalves De Paivaa ◽  
Patricia Oehlmeyer Nassar ◽  
...  
Keyword(s):  
Bone Loss ◽  
Protective Effect ◽  
Alveolar Bone ◽  
Experimental Period ◽  
Alveolar Bone Loss ◽  
Control Group ◽  
Interleukin 17 ◽  
Periodontal Tissues ◽  
Male Wistar Rats ◽  
Experimental Periodontitis

The resveratrol is a polyphenol known for its health benefits, which includes the ability to interfere in the osteoblastogenesis, which may foster adverse immunomodulators effects in the host response to periodontal disease. In the present study we evaluated the appearance of periodontal tissues of rats with experimentally induced periodontitis, by using resveratrol. Twenty-four male Wistar rats were used, in which half of the animals received a ligature around the first lower molars, then forming the groups with experimental periodontitis. Next, four groups were created: 1) Control Group (CON); 2) The Ligature Group (LIG); 3) Group Resveratrol (RSV); 4) Ligature-Resveratrol Group (LIG-RSV). The animals of the Resveratrol groups were daily dosed with 10 mg/kg of body weight of polyphenol orally, during four weeks. After 105 days of experimental period, euthanasia was performed. The results showed a significantly lower alveolar bone loss (p<0.05) in animals that received resveratrol, and still, the polyphenol was able to reduce concentration of interleukin 17 (IL-17) in the groups dosed with it. Our conclusion is that dosing rats with experimental periodontitis with resveratrol could cause a protective effect on the alveolar bone loss, in addition to act positively on the IL-17.

scholarly journals Inflammasomes in Alveolar Bone Loss

2021 ◽  
Vol 12 ◽  
Author(s):  
Yang Li ◽  
Junqi Ling ◽  
Qianzhou Jiang
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Bone Remodeling ◽  
Host Defense ◽  
Alveolar Bone ◽  
Bone Destruction ◽  
Alveolar Bone Loss ◽  
Fine Tuning ◽  
Inflammasome Activation ◽  
Dependent Manner

Bone remodeling is tightly controlled by osteoclast-mediated bone resorption and osteoblast-mediated bone formation. Fine tuning of the osteoclast–osteoblast balance results in strict synchronization of bone resorption and formation, which maintains structural integrity and bone tissue homeostasis; in contrast, dysregulated bone remodeling may cause pathological osteolysis, in which inflammation plays a vital role in promoting bone destruction. The alveolar bone presents high turnover rate, complex associations with the tooth and periodontium, and susceptibility to oral pathogenic insults and mechanical stress, which enhance its complexity in host defense and bone remodeling. Alveolar bone loss is also involved in systemic bone destruction and is affected by medication or systemic pathological factors. Therefore, it is essential to investigate the osteoimmunological mechanisms involved in the dysregulation of alveolar bone remodeling. The inflammasome is a supramolecular protein complex assembled in response to pattern recognition receptors and damage-associated molecular patterns, leading to the maturation and secretion of pro-inflammatory cytokines and activation of inflammatory responses. Pyroptosis downstream of inflammasome activation also facilitates the clearance of intracellular pathogens and irritants. However, inadequate or excessive activity of the inflammasome may allow for persistent infection and infection spreading or uncontrolled destruction of the alveolar bone, as commonly observed in periodontitis, periapical periodontitis, peri-implantitis, orthodontic tooth movement, medication-related osteonecrosis of the jaw, nonsterile or sterile osteomyelitis of the jaw, and osteoporosis. In this review, we present a framework for understanding the role and mechanism of canonical and noncanonical inflammasomes in the pathogenesis and development of etiologically diverse diseases associated with alveolar bone loss. Inappropriate inflammasome activation may drive alveolar osteolysis by regulating cellular players, including osteoclasts, osteoblasts, osteocytes, periodontal ligament cells, macrophages, monocytes, neutrophils, and adaptive immune cells, such as T helper 17 cells, causing increased osteoclast activity, decreased osteoblast activity, and enhanced periodontium inflammation by creating a pro-inflammatory milieu in a context- and cell type-dependent manner. We also discuss promising therapeutic strategies targeting inappropriate inflammasome activity in the treatment of alveolar bone loss. Novel strategies for inhibiting inflammasome signaling may facilitate the development of versatile drugs that carefully balance the beneficial contributions of inflammasomes to host defense.

scholarly journals Epigallocatechin gallate (EGCG) suppresses lipopolysaccharide-induced inflammatory bone resorption, and protects against alveolar bone loss in mice

FEBS Open Bio ◽  
2015 ◽  
Vol 5 (1) ◽  
pp. 522-527 ◽  
Author(s):  
Tsukasa Tominari ◽  
Chiho Matsumoto ◽  
Kenta Watanabe ◽  
Michiko Hirata ◽  
Florian M.W. Grundler ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Alveolar Bone ◽  
Epigallocatechin Gallate ◽  
Alveolar Bone Loss

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 Structural Dissection andIn VivoEffectiveness of a Peptide Inhibitor ofPorphyromonas gingivalisAdherence toStreptococcus gordonii

2010 ◽  
Vol 79 (1) ◽  
pp. 67-74 ◽  
Author(s):  
Carlo Amorin Daep ◽  
Elizabeth A. Novak ◽  
Richard J. Lamont ◽  
Donald R. Demuth
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Peptide Inhibitor ◽  
Dental Biofilm ◽  
Streptococcal Antigen ◽  
Α Helix

ABSTRACTThe interaction of the minor fimbrial antigen (Mfa) with streptococcal antigen I/II (e.g., SspB) facilitates colonization of the dental biofilm byPorphyromonas gingivalis.We previously showed that a 27-mer peptide derived from SspB (designated BAR) resembles the nuclear receptor (NR) box protein-protein interacting domain and potently inhibits this interactionin vitro. Here, we show that the EXXP motif upstream of the NR core α-helix contributes to the Mfa-SspB interaction and that BAR reducesP. gingivaliscolonization and alveolar bone lossin vivoin a murine model of periodontitis. Substitution of Gln for Pro1171or Glu1168increased the α-helicity of BAR and reduced its inhibitory activityin vitroby 10-fold and 2-fold, respectively. To determine if BAR preventsP. gingivalisinfectionin vivo, mice were first infected withStreptococcus gordoniiand then challenged withP. gingivalisin the absence and presence of BAR. Animals that were infected with either 109CFU ofS. gordoniiDL-1 or 107CFU ofP. gingivalis33277 did not show a statistically significant increase in alveolar bone resorption over sham-infected controls. However, infection with 109CFU ofS. gordoniifollowed by 107CFU ofP. gingivalisinduced significantly greater bone loss (P< 0.01) than sham infection or infection of mice with either organism alone.S. gordonii-infected mice that were subsequently challenged with 107CFU ofP. gingivalisin the presence of BAR exhibited levels of bone resorption similar to those of sham-infected animals. Together, these results indicate that both EXXP and the NR box are important for the Mfa-SspB interaction and that BAR peptide represents a potential therapeutic that may limit colonization of the oral cavity byP. gingivalis.

FSH Aggravates Periodontitis-related Bone Loss in Ovariectomized Rats

2010 ◽  
Vol 89 (4) ◽  
pp. 366-371 ◽  
Author(s):  
S. Liu ◽  
Y. Cheng ◽  
M. Fan ◽  
D. Chen ◽  
Z. Bian
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Clinical Features ◽  
Alveolar Bone ◽  
Follicle Stimulating Hormone ◽  
Alveolar Bone Loss ◽  
Ovariectomized Rats ◽  
Fsh Receptor ◽  
Histochemical Tests ◽  
Experimental Periodontitis

Alveolar bone loss is one of the prominent pathologic and clinical features of periodontitis. Recently, the direct effect of follicle-stimulating hormone (FSH) on bone resorption has been demonstrated. However, the effect of FSH on alveolar bone loss remains unknown. This study tested the hypothesis that FSH would exacerbate periodontitis-related alveolar bone loss. Experimental periodontitis was induced in ovariectomized rats, and the rats were treated with extrinsic FSH or its inhibitor, leuprorelin. After mandibles were collected, we performed morphological examinations to evaluate bone loss, enzyme histochemical tests for osteoclasts, and immunohistochemical examinations for FSH receptor (FSHR). The results showed that FSH significantly increased alveolar bone resorption compared with non-FSH-treated ovariectomized rats (P < 0.05), and the number of FSHR-positive cells was positively correlated with alveolar bone loss area (r = 0.682, P < 0.01). Our results suggested that FSH can aggravate alveolar bone loss by FSHR, independent of estrogen.

scholarly journals Comparative effects of riboflavin, nicotinamide and folic acid on alveolar bone loss: A morphometric and histopathologic study in rats

2016 ◽  
Vol 144 (5-6) ◽  
pp. 273-279 ◽  
Author(s):  
Aysun Akpınar ◽  
Nebı Karakan ◽  
Aysan Alpan ◽  
Suat Dogan ◽  
Fahrettin Goze ◽  
...  
Keyword(s):  
Folic Acid ◽  
Bone Loss ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Water Soluble ◽  
Control Group ◽  
Serum Samples ◽  
Osteoblastic Activity ◽  
Periodontal Tissues ◽  
Mandibular Molar

Introduction. Periodontitis is a chronic inflammatory and osteolytic disease. Vitamin B complex is a class of water-soluble vitamins that play important roles in cell metabolism. Objective. The aim of this study was to evaluate the effects of riboflavin (RBF), nicotinamide (NA), and folic acid (FA) on alveolar bone loss in experimental periodontitis rat model. Methods. Sixty-four male Wistar rats were randomly divided into the following eight groups: Control, Ligated, RBF50 (RBF, 50 mg/kg daily), NA50 (NA, 50 mg/kg daily), FA50 (FA, 50 mg/kg daily), RBF100 (RBF, 100 mg/kg daily), NA100 (NA, 100 mg/kg daily), and FA100 (FA, 100 mg/kg daily). Periodontitis was induced using silk ligature around the right first mandibular molar. After 11 days the rats were sacrificed. Mandible and serum samples were collected. Changes in alveolar bone levels were measured clinically, and periodontal tissues were examined histopathologically. Serum IL-1? (pg/ml) levels were analyzed by using ELISA. Results. Mean alveolar bone loss in the mandibular first molar tooth revealed to be significantly lower in RBF100 group than in the Control group. In the Ligated group, alveolar bone loss was significantly higher than in all other groups. The ratio of presence of inflammatory cell infiltration in the Ligated group was significantly higher than in the Control group. The differences in the serum IL-1? levels between the groups were not statistically significant. Osteoclasts that were observed in the Ligated group were significantly higher than those of the Control and FA100 groups. The osteoblastic activity in the Ligated group, RBF100, and NA100 groups were shown to be significantly higher than those in the Control group. Conclusion. This study has demonstrated that systemic administration of RBF, NA, and FA in different dosages (50-100 mg/kg) reduced alveolar bone loss in periodontal disease in rats.

Sign in / Sign up

Export Citation Format

Share Document