scholarly journals Bifidobacterium Strains Present Distinct Effects on the Control of Alveolar Bone Loss in a Periodontitis Experimental Model

2021 ◽  
Vol 12 ◽  
Author(s):  
Natali Shimabukuro ◽  
Amália C. de S. Cataruci ◽  
Karin H. Ishikawa ◽  
Bruna E. de Oliveira ◽  
Dione Kawamoto ◽  
...  
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Microbial Consortium ◽  
Bone Destruction ◽  
Experimental Period ◽  
Serum Levels ◽  
Alveolar Bone Loss ◽  
Oral Microbiome ◽  
Host Cells ◽  
Tnf Α

Periodontitis is an inflammatory disease induced by a dysbiotic oral microbiome. Probiotics of the genus Bifidobacterium may restore the symbiotic microbiome and modulate the immune response, leading to periodontitis control. We evaluated the effect of two strains of Bifidobacterium able to inhibit Porphyromonas gingivalis interaction with host cells and biofilm formation, but with distinct immunomodulatory properties, in a mice periodontitis model. Experimental periodontitis (P+) was induced in C57Bl/6 mice by a microbial consortium of human oral organisms. B. bifidum 1622A [B+ (1622)] and B. breve 1101A [B+ (1101)] were orally inoculated for 45 days. Alveolar bone loss and inflammatory response in gingival tissues were determined. The microbial consortium induced alveolar bone loss in positive control (P + B-), as demonstrated by microtomography analysis, although P. gingivalis was undetected in oral biofilms at the end of the experimental period. TNF-α and IL-10 serum levels, and Treg and Th17 populations in gingiva of SHAM and P + B- groups did not differ. B. bifidum 1622A, but not B. breve 1101A, controlled bone destruction in P+ mice. B. breve 1101A upregulated transcription of Il-1β, Tnf-α, Tlr2, Tlr4, and Nlrp3 in P-B+(1101), which was attenuated by the microbial consortium [P + B+(1101)]. All treatments downregulated transcription of Il-17, although treatment with B. breve 1101A did not yield such low levels of transcripts as seen for the other groups. B. breve 1101A increased Th17 population in gingival tissues [P-B+ (1101) and P + B+ (1101)] compared to SHAM and P + B-. Administration of both bifidobacteria resulted in serum IL-10 decreased levels. Our data indicated that the beneficial effect of Bifidobacterium is not a common trait of this genus, since B. breve 1101A induced an inflammatory profile in gingival tissues and did not prevent alveolar bone loss. However, the properties of B. bifidum 1622A suggest its potential to control periodontitis.

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 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.

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 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 The roles of osteocytes in alveolar bone destruction in periodontitis

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Xiaofei Huang ◽  
Mengru Xie ◽  
Yanling Xie ◽  
Feng Mei ◽  
Xiaofeng Lu ◽  
...  
Keyword(s):  
Bone Loss ◽  
Bone Remodeling ◽  
Alveolar Bone ◽  
Bone Cells ◽  
Bone Destruction ◽  
Alveolar Bone Loss ◽  
Receptor Activator ◽  
Local Destruction ◽  
Underlying Mechanisms

AbstractPeriodontitis, a bacterium-induced inflammatory disease that is characterized by alveolar bone loss, is highly prevalent worldwide. Elucidating the underlying mechanisms of alveolar bone loss in periodontitis is crucial for understanding its pathogenesis. Classically, bone cells, such as osteoclasts, osteoblasts and bone marrow stromal cells, are thought to dominate the development of bone destruction in periodontitis. Recently, osteocytes, the cells embedded in the mineral matrix, have gained attention. This review demonstrates the key contributing role of osteocytes in periodontitis, especially in alveolar bone loss. Osteocytes not only initiate physiological bone remodeling but also assist in inflammation-related changes in bone remodeling. The latest evidence suggests that osteocytes are involved in regulating bone anabolism and catabolism in the progression of periodontitis. The altered secretion of receptor activator of NF-κB ligand (RANKL), sclerostin and Dickkopf-related protein 1 (DKK1) by osteocytes affects the balance of bone resorption and formation and promotes bone loss. In addition, the accumulation of prematurely senescent and apoptotic osteocytes observed in alveolar bone may exacerbate local destruction. Based on their communication with the bloodstream, it is noteworthy that osteocytes may participate in the interaction between local periodontitis lesions and systemic diseases. Overall, further investigations of osteocytes may provide vital insights that improve our understanding of the pathophysiology of periodontitis.

scholarly journals Selective cyclooxygenase-2 inhibition prevents bone resorption

2005 ◽  
Vol 19 (1) ◽  
pp. 36-40 ◽  
Author(s):  
Carlos Augusto Nassar ◽  
Patrícia Oehlmeyer Nassar ◽  
Patrícia Maria Nassar ◽  
Luis Carlos Spolidorio
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Experimental Period ◽  
Root Surface ◽  
Negative Control ◽  
Alveolar Bone Loss ◽  
Cyclooxygenase 2 ◽  
The Other ◽  
Cox 2 ◽  
Experimentally Induced

The aim of the present work was to evaluate the effect of a selective cyclooxygenase-2 (COX-2) inhibitor (meloxicam) on the alveolar bone loss progression in experimentally induced periodontitis. Forty (40) Wistar rats were separated into 8 experimental groups (n = 5). Cotton ligatures were placed at the gingival margin level of the lower right first molars of some rats. Four groups were treated for 5 or 15 days with an oral dose of 15 mg/kg of body weight/day of the selective COX-2 inhibitor. The other groups were used as positive control (sham) or negative control in each experimental period. Standardized digital radiographs were taken after sacrifice at 5 and 15 days to measure the amount of bone loss at the mesial root surface of the first molar tooth in each rat. The treatment with meloxicam did not induce weight alteration or other visible systemic manifestations. One way analysis of variance (ANOVA) indicated that groups treated with meloxicam, after 5 days, had significantly less alveolar bone loss (p < 0.05) when compared with control groups. On the other hand, no significant differences in bone loss were observed after 15 days of treatment with meloxicam. These data provide evidence that systemic therapy with meloxicam can modify the progression of experimentally induced periodontitis in rats during the initial experimental period.

scholarly journals Gingival solitary chemosensory cells are immune sentinels for periodontitis

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Xin Zheng ◽  
Marco Tizzano ◽  
Kevin Redding ◽  
Jinzhi He ◽  
Xian Peng ◽  
...  
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Bacterial Load ◽  
Alveolar Bone Loss ◽  
Oral Microbiome ◽  
Oral Microbiota ◽  
Naturally Occurring ◽  
Promising Target ◽  
Solitary Chemosensory Cells ◽  
Signaling Components

Abstract Solitary chemosensory cells (SCCs) are epithelial sentinels that utilize bitter Tas2r receptors and coupled taste transduction elements to detect pathogenic bacterial metabolites, triggering host defenses to control the infection. Here we report that SCCs are present in mouse gingival junctional epithelium, where they express several Tas2rs and the taste signaling components α-gustducin (Gnat3), TrpM5, and Plcβ2. Gnat3−/− mice have altered commensal oral microbiota and accelerated naturally occurring alveolar bone loss. In ligature-induced periodontitis, knockout of taste signaling molecules or genetic absence of gingival SCCs (gSCCs) increases the bacterial load, reduces bacterial diversity, and renders the microbiota more pathogenic, leading to greater alveolar bone loss. Topical treatment with bitter denatonium to activate gSCCs upregulates the expression of antimicrobial peptides and ameliorates ligature-induced periodontitis in wild-type but not in Gnat3−/− mice. We conclude that gSCCs may provide a promising target for treating periodontitis by harnessing innate immunity to regulate the oral microbiome.

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