scholarly journals Telmisartan Prevents Alveolar Bone Loss by Decreasing the Expression of Osteoclasts Markers in Hypertensive Rats With Periodontal Disease

2020 ◽  
Vol 11 ◽  
Author(s):  
Victor Gustavo Balera Brito ◽  
Mariana Sousa Patrocinio ◽  
Maria Carolina Linjardi de Sousa ◽  
Ayná Emanuelli Alves Barreto ◽  
Sabrina Cruz Tfaile Frasnelli ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Bone Loss ◽  
Bone Formation ◽  
Periodontal Disease ◽  
Alveolar Bone ◽  
Renin Angiotensin System ◽  
Alveolar Bone Loss ◽  
Hypertensive Rats ◽  
Bone Formation Markers ◽  
Tnf Α

Periodontal disease (PD) is a prevalent inflammatory disease with the most severe consequence being the loss of the alveolar bone and teeth. We therefore aimed to evaluate the effects of telmisartan (TELM), an angiotensin II type 1 receptor (Agtr1) antagonist, on the PD-induced alveolar bone loss, in Wistar (W) and Spontaneous Hypertensive Rats (SHRs). PD was induced by ligating the lower first molars with silk, and 10 mg/kg TELM was concomitantly administered for 15 days. The hemimandibles were subjected to microtomography, ELISA was used for detecting tumor necrosis factor (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), CXCL3, and CCL2, while qRT-PCR was used for analyzing expression of components of renin-angiotensin system (RAS) (Agt, Ace, Agt1r, Agt2r, Ace2, and Masr), and bone markers (Runx2, Osx, Catnb, Alp, Col1a1, Opn, Ocn, Bsp, Bmp2, Trap, Rank, Rankl, CtsK, Mmp-2, Mmp-9, and osteoclast-associated receptor (Oscar)). The SHR + PD group showed greater alveolar bone loss than the W + PD group, what was significantly inhibited by treatment with TELM, especially in the SHR group. Additionally, TELM reduced the production of TNF-α, IL-1β, and CXCL3 in the SHR group. The expression of Agt increased in the groups with PD, while Agtr2 reduced, and TELM reduced the expression of Agtr1 and increased the expression of Agtr2, in W and SHRs. PD did not induce major changes in the expression of bone formation markers, except for the expression of Alp, which decreased in the PD groups. The bone resorption markers expression, Mmp9, Ctsk, and Vtn, was higher in the SHR + PD group, compared to the respective control and W + PD group. However, TELM attenuated these changes and increased the expression of Runx2 and Alp. Our study suggested that TELM has a protective effect on the progression of PD, especially in hypertensive animals, as evaluated by the resorption of the lower alveolar bone. This can be partly explained by the modulation in the expression of Angiotensin II receptors (AT1R and AT2R), reduced production of inflammatory mediators, the reduced expression of resorption markers, and the increased expression of the bone formation markers.

scholarly journals Mast cells contribute to alveolar bone loss in Spontaneously Hypertensive Rats with periodontal disease regulating cytokines production

PLoS ONE ◽  
2021 ◽  
Vol 16 (3) ◽  
pp. e0247372
Author(s):  
Victor Gustavo Balera Brito ◽  
Mariana Sousa Patrocinio ◽  
Maria Carolina Linjardi Sousa ◽  
Ayná Emanuelli Alves Barreto ◽  
Sabrina Cruz Tfaile Frasnelli ◽  
...  
Keyword(s):  
Mast Cells ◽  
Bone Loss ◽  
Periodontal Disease ◽  
Spontaneously Hypertensive Rats ◽  
Alveolar Bone ◽  
Inflammatory Responses ◽  
Alveolar Bone Loss ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Inflammatory Status

Mast cells (MCs) play a pivotal role in inflammatory responses and had been studied in inflammatory bone disorders, however, their role in alveolar bone loss induced by periodontal disease (PD) is not yet fully understood. We, therefore, aimed to evaluate the effects of MCs depletion in the PD-induced alveolar bone loss in Wistar (W) and Spontaneously Hypertensive Rats (SHRs). PD was induced by ligating the lower first molars with silk thread one day after the MCs depletion, by the pre-treatment with compound 48/80 for 4 days. After 15 days of PD induction, the hemi-mandibles were surgically collected for qRT-PCR, histological analyses, immunostaining, and ELISA. Systolic blood pressure (SBP) was verified by tail plethysmography to confirm the hypertensive status, and SHR presented SBP >150 mmHg, and previous MC depletion alone or associated with PD did not alter this parameter. SHRs showed a more severe alveolar bone loss compared to W, and MC depletion significantly inhibited this response in both strains, with a more significant response in SHRs. MCs were less abundant in 48/80+PD groups, thus validating the previous MCs depletion in our model. PD increased the number of MC in the gingival tissue of SHR. Cytokine production (TNF-α, IL-6, IL-1β, and CXCL3) was constitutively higher in SHR and increased further after PD, which was also significantly reduced in the MCs-depleted animals. PD led to an increased expression of Opn, Rankl, Rank, Vtn, Itga5, Itgb5, Trap, and Ctsk in the mandible of W and SHRs, which was reversed in MCs-depleted animals. These results suggest that MCs significantly contributes to the PD-induced alveolar bone resorption, especially in the SHR, which is associated with a more severe PD progression compared to Wistar, partly explained by these cells contribution to the inflammatory status and mediator production, stimulating osteoclast-related response markers, which were reduced after MC depletion in our experimental model.

scholarly journals Corrigendum: Telmisartan Prevents Alveolar Bone Loss by Decreasing the Expression of Osteoclasts Markers in Hypertensive Rats With Periodontal Disease

2021 ◽  
Vol 11 ◽  
Author(s):  
Victor Gustavo Balera Brito ◽  
Mariana Sousa Patrocinio ◽  
Maria Carolina Linjardi ◽  
Ayná Emanuelli Alves Barreto ◽  
Sabrina CT Frasnelli ◽  
...  
Keyword(s):  
Bone Loss ◽  
Periodontal Disease ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Hypertensive Rats

scholarly journals Does systemic oral administration of curcumin effectively reduce alveolar bone loss associated with periodontal disease? A systematic review and meta-analysis of preclinical in vivo studies

2020 ◽  
Vol 75 ◽  
pp. 104226
Author(s):  
Juliana Simeão Borges ◽  
Luiz Renato Paranhos ◽  
Gabriela Leite de Souza ◽  
Felipe de Souza Matos ◽  
Ítalo de Macedo Bernardino ◽  
...  
Keyword(s):  
Systematic Review ◽  
Bone Loss ◽  
Periodontal Disease ◽  
Oral Administration ◽  
Alveolar Bone ◽  
Meta Analysis ◽  
Alveolar Bone Loss ◽  
In Vivo Studies

scholarly journals Effect of inhaled corticosteroid on TNF-α production and alveolar bone loss in Wistar rats

2011 ◽  
Vol 56 (11) ◽  
pp. 1398-1403 ◽  
Author(s):  
Luciana Dondonis Daudt ◽  
Juliano Cavagni ◽  
Eduardo José Gaio ◽  
Andressa Souza ◽  
Iraci Lucena da Silva Torres ◽  
...  
Keyword(s):  
Bone Loss ◽  
Wistar Rats ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Inhaled Corticosteroid ◽  
Tnf Α

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.

Periodontal Disease Morbidity Quantification. II. Validation of Alveolar Bone Loss Measurements and Vertical Defect Diagnosis From Digital Bite-Wing Images

1990 ◽  
Vol 61 (10) ◽  
pp. 623-632 ◽  
Author(s):  
Charles F. Hildebolt ◽  
Michael W. Vannier ◽  
Michael K. Shrout,‡ ◽  
Thomas K. Pilgram ◽  
Michael Province ◽  
...  
Keyword(s):  
Bone Loss ◽  
Periodontal Disease ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Defect Diagnosis

Alpha 2-macroglobulin in gingival fluid: correlation with alveolar bone loss in periodontal disease

1986 ◽  
Vol 13 (9) ◽  
pp. 833-836 ◽  
Author(s):  
Uroš Skalerič ◽  
Peter Zajšek ◽  
Erika Cvetko ◽  
Tamara Lah ◽  
Joža Babnik
Keyword(s):  
Bone Loss ◽  
Periodontal Disease ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Gingival Fluid

scholarly journals Effects of Colocasia antiquorum var. Esculenta Extract In Vitro and In Vivo against Periodontal Disease

Medicina ◽  
2021 ◽  
Vol 57 (10) ◽  
pp. 1054
Author(s):  
Seong-Hee Moon ◽  
Seong-Jin Shin ◽  
Hyun-Jin Tae ◽  
Seung-Han Oh ◽  
Ji-Myung Bae
Keyword(s):  
Bone Loss ◽  
Periodontal Disease ◽  
Pathogenic Bacteria ◽  
Alveolar Bone ◽  
Negative Control ◽  
Alveolar Bone Loss ◽  
Oral Microbiome ◽  
Control Group

Background and Objectives: Periodontal disease is a chronic inflammatory disease in which gradual destruction of tissues around teeth is caused by plaque formed by pathogenic bacteria. The purpose of this study was to evaluate the potential of 75% ethanol extract of Colocasia antiquorum var. esculenta (CA) as a prophylactic and improvement agent for periodontal disease in vitro and in vivo. Materials and Methods: The antimicrobial efficacy of CA against Porphyromonas gingivalis (P. gingivalis, ATCC 33277) was evaluated using minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) test, and cytotoxicity was confirmed by CCK-8 assay. For the in vivo study, P. gingivalis was applied by oral gavage to BALB/c mice. Forty-two days after the first inoculation of P. gingivalis, intraoral swabs were taken for microbiome analysis, and the mice were sacrificed to evaluate the alveolar bone loss. Results: The MIC of CA against P. gingivalis was 31.3 μg/mL, the MBC was 62.5 μg/mL, with no cytotoxicity. The diversity of the oral microbiome decreased in the positive control group, while those of the VA (varnish) and VCA (varnish added with CA) groups increased as much as in the negative control group, although the alveolar bone loss was not induced in the mouse model. Conclusions: CA showed antibacterial effects in vitro, and the VA and VCA groups exhibited increased diversity in the oral microbiome, suggesting that CA has potential for improving periodontal disease.

scholarly journals Resolution phase agonists &bone remodeling

2016 ◽  
Author(s):  
Ευάγγελος Παπαθανασίου
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Peritoneal Macrophages ◽  
Alveolar Bone Loss ◽  
Cytokine Signaling ◽  
Periodontal Inflammation ◽  
Oral Inoculation ◽  
Tnf Α ◽  
Socs Proteins ◽  
Anti Inflammatory

Periodontitis is the 6th most prevalent disease in the world and the primary cause for tooth loss in adults. The host immune response plays a key role in bacteria-induced alveolar bone resorption. Endogenous control of the magnitude and duration of inflammatory signaling is considered an important determinant of the extent of periodontal pathology. Suppressor of cytokine signaling (SOCS) proteins are inhibitors of cytokine signaling pathways and may play a role in controlling periodontal inflammation. SOCS proteins are also considered crucial intracellular mediators of the anti-inflammatory actions of lipid mediator agonists including resolvins such as RvE1. We hypothesized that SOCS-3 regulates inflammatory cytokine signaling and alveolar bone loss in experimental periodontitis and that the anti-inflammatory actions of RvE1 are SOCS-3 dependent. Periodontal bone loss was induced in myeloid-specific SOCS-3-knockout (KO) and SOCS-3-wild-type (WT) C57Bl6-B.129 mice by oral inoculation with 1×109 colony-forming units (CFU) P. gingivalis A7436 using an oral gavage model for periodontitis. Sham controls for both types of mice received vehicle without bacteria. The mice were euthanized 6 weeks after the last oral inoculation. Morphometric, histomorphometric, and µCT analyses were performed to assess alveolar bone loss. Peritoneal macrophages were elicited with 4% thioglycolate broth and isolated from myeloid SOCS-3-KO and SOCS-3-WT mice by differential centrifugation. Macrophages were cultured at a concentration of 1.5×106 cells/ml in 6-well plates. After 2 hours, non-adherent cells were discarded and the remaining adherent cells were treated with either culture medium alone (control) or with 100 ng/ml P. gingivalis A7436 LPS or with culture medium and 100nM RvE1 or with 100 ng/ml P. gingivalis A7436 LPS and RvE1 100nM (n≥3 wells per group). Supernatants and cells were collected after 12 hours. Cytokine levels were assessed using Luminex multiplex bead immunoassay and RNA was extracted by Trizol and processed for qRT-PCR. Increased bone loss was demonstrated in P. gingivalis-infected SOCS-3- KO mice compared to P. gingivalis-infected WT mice by direct morphological measurements, µCT analyses and quantitative histology. Loss of SOCS-3 function resulted in increased number of alveolar bone osteoclasts and increased RANKL expression after P. gingivalis infection. SOCS-3 deficiency in myeloid cells also promoted a higher P. gingivalis LPS-induced inflammatory response by inducing a higher secretion of IL-1β, IL-6, TNF-α and KC (IL-8) by peritoneal macrophages from SOCS-3-KO mice. 100nM RvE1 resulted in a significant decrease in P. gingivalis LPS-induced secretion of IL-6, TNF-α and IL-8 by increasing mRNA expression of SOCS-3 and ERV1 in macrophages from SOCS-3-WT mice compared to macrophages from myeloid SOCS-3-KO ones. Our data implicate SOCS-3 as a critical negative regulator of alveolar bone loss in experimental periodontitis and P. gingivalis LPS-induced inflammatory response. SOCS-3 regulates the anti-inflammatory actions of RvE1 on P. gingivalis LPS-induced inflammatory cytokines in macrophages. Understanding further the role of SOCS proteins in regulating periodontal inflammation may provide novel pathways of host susceptibility to periodontitis and new therapeutic targets for modulating the immune response to achieve successful resolution of periodontal inflammation.

scholarly journals Annually and Cumulative Radiographic Alveolar Bone Loss Rates using Digital Scanning Image for the Periodontal Disease Groups before and after Periodontal Treatment

2021 ◽  
Vol 2 (3) ◽  
pp. 23-27
Author(s):  
Guey-Lin Hou
Keyword(s):  
Bone Loss ◽  
Periodontal Disease ◽  
Loss Rate ◽  
Alveolar Bone ◽  
Aggressive Periodontitis ◽  
Alveolar Bone Loss ◽  
University Hospital ◽  
Before And After ◽  
Digital Scanning ◽  
Bone Gain

The aim of the present study was to assess the cumulative radiographic alveolar bone loss (CRABL) and yearly radiographic periodontal attachment loss (YRABL) of periodontal disease groups over 5 years or more. A total of 53 subjects, who had taken two sets of full-mouth standardized paralleling radiographs with separated periods of 5 years or more in Kaohsiung Medical University Hospital during 1981-2001, were collected for the past 20 years. The radiographic alveolar bone levels at mesial and distal aspects of teeth were assessed by measuring the distance between cemento-enamel junction and alveolar bone crest using an electronic digimatic caliper (EDC) under a 3.5X magnified radiographs. The results revealed that 1) patients with a periodic recall (3-4 times/yr.) showed a significantly lower loss rate than patients without periodic recalls; 2) mean CRPAL was highest in the generalized aggressive periodontitis (GAgP) group (5.52±3.27mm), then the chronic periodontitis (CP) group (4.82±3.47mm), and the localized aggressive periodontitis (LAgP) group (4.47±3.47mm) followed, and lowest in the periodontal healthy (PH) group (1.05±0.59mm); 3) mean YRPAL was the highest in the LAgP group (0.26±0.25mm/yr.), then the GAgP group (0.20±0.13 mm/yr.), and the CP group (0.12±0.09 mm/yr.) followed, and lowest in the periodontal healthy group (0.07±0.06 mm/yr.). It was concluded that: 1) sites with more advanced alveolar bone loss are more likely to undergo further breakdown; 2) patients with a periodic recall showed a significantly lower alveolar bone loss rate and bone gain, irrespective disease groups; 3) mean CPBLs was highest in the GAgP group; mean YRABLs was highest in the LAgP.

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