scholarly journals Reveromycin A Administration Prevents Alveolar Bone Loss in Osteoprotegerin Knockout Mice with Periodontal Disease

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Manami Mizuno ◽  
Ken Miyazawa ◽  
Masako Tabuchi ◽  
Miyuki Tanaka ◽  
Mamoru Yoshizako ◽  
...  
Keyword(s):  
Bone Loss ◽  
Periodontal Disease ◽  
Knockout Mice ◽  
Alveolar Bone ◽  
Alveolar Bone Loss

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 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

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 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.

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 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.

Sign in / Sign up

Export Citation Format

Share Document