scholarly journals Akkermansia muciniphila and Its Pili-Like Protein Amuc_1100 Modulate Macrophage Polarization in Experimental Periodontitis

2020 ◽  
Vol 89 (1) ◽  
pp. e00500-20
Author(s):  
Hannah Mulhall ◽  
Jeanne M. DiChiara ◽  
Matthew Deragon ◽  
Radha Iyer ◽  
Olivier Huck ◽  
...  
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Macrophage Polarization ◽  
Alveolar Bone Loss ◽  
Oral Microbiome ◽  
Content Type ◽  
Akkermansia Muciniphila ◽  
Periodontal Inflammation ◽  
Experimental Periodontitis ◽  
Anti Inflammatory

ABSTRACTPeriodontitis is a chronic inflammatory disease triggered by dysbiosis of the oral microbiome. Porphyromonas gingivalis is strongly implicated in periodontal inflammation, gingival tissue destruction, and alveolar bone loss through sustained exacerbation of the host response. Recently, the use of other bacterial species, such as Akkermansia muciniphila, has been suggested to counteract inflammation elicited by P. gingivalis. In this study, the effects of A. muciniphila and its pili-like protein Amuc_1100 on macrophage polarization during P. gingivalis infection were evaluated in a murine model of experimental periodontitis. Mice were gavaged with P. gingivalis alone or in combination with A. muciniphila or Amuc_1100 for 6 weeks. Morphometric analysis demonstrated that the addition of A. muciniphila or Amuc_1100 significantly reduced P. gingivalis-induced alveolar bone loss. This decreased bone loss was associated with a proresolutive phenotype (M2) of macrophages isolated from submandibular lymph nodes as observed by flow cytometry. Furthermore, the expression of interleukin 10 (IL-10) at the RNA and protein levels was significantly increased in the gingival tissues of the mice and in macrophages exposed to A. muciniphila or Amuc_1100, confirming their anti-inflammatory properties. This study demonstrates the putative therapeutic interest of the administration of A. muciniphila or Amuc_1100 in the management of periodontitis through their anti-inflammatory properties.

3,4,5-Trihydroxybenzoic acid attenuates ligature-induced periodontal disease in Wistar rats.

2020 ◽  
Vol 19 ◽  
Author(s):  
Ozkan Karatas ◽  
Fikret Gevrek
Keyword(s):  
Bone Loss ◽  
Gallic Acid ◽  
Wistar Rats ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Collagenase Activity ◽  
Osteoblastic Activity ◽  
Cell Counts ◽  
Experimental Periodontitis ◽  
Anti Inflammatory

Background: 3,4,5-Trihydroxybenzoic acid, which is also known as gallic acid, is an anti-inflammatory agent who could provide beneficial effects in preventing periodontal inflammation. The present study aimed to evaluate the anti-inflammatory effects of gallic acid on experimental periodontitis in Wistar rats. Alveolar bone loss, osteoclastic activity, osteoblastic activity, and collagenase activity were also determined. Methods: 32 Wistar rats were used in the present study. Study groups were created as following: Healthy control (C,n=8) group; periodontitis (P,n=8) group; periodontitis and 30 mg/kg gallic acid administered group (G30,n=8); periodontitis and 60 mg/kg gallic acid administered group (G60,n=8). Experimental periodontitis was created by placing 4-0 silk sutures around the mandibular right first molar tooth. Morphological changes in alveolar bone were determined by stereomicroscopic evaluation. Mandibles were undergone histological evaluation. Matrix metalloproteinase (MMP)-8, tissue inhibitor of MMPs (TIMP)-1, bone morphogenetic protein (BMP)-2 expressions, tartrate-resistant acid phosphatase (TRAP) positive osteoclast cells, osteoblast, and inflammatory cell counts were determined. Results: Highest alveolar bone loss was observed in the periodontitis group. Both doses of gallic acid decreased alveolar bone loss compared to the P group. TRAP-positive osteoclast cell counts were higher in the P group, and gallic acid successfully lowered these counts. Osteoblast cells also increased in gallic acid administered groups. Inflammation in the P group was also higher than those of C, G30, and G60 groups supporting the role of gallic acid in preventing inflammation. 30 and 60 mg/kg doses of gallic acid decreased MMP-8 levels and increased TIMP-1 levels. BMP levels increased in gallic acid administered groups, similar to several osteoblasts. Conclusion: Present results revealed an anti-inflammatory effect of gallic acid, which was indicated by decreased alveolar bone loss and collagenase activity and increased osteoblastic activity.

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.

Cinnamic acid decreases periodontal inflammation and alveolar bone loss in experimental periodontitis

2020 ◽  
Vol 55 (5) ◽  
pp. 676-685
Author(s):  
Ozkan Karatas ◽  
Hatice Balci Yuce ◽  
Mehmet Murat Taskan ◽  
Fikret Gevrek ◽  
Cemil Alkan ◽  
...  
Keyword(s):  
Bone Loss ◽  
Cinnamic Acid ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Periodontal Inflammation ◽  
Experimental Periodontitis

scholarly journals Anti-inflammatory effect of rosuvastatin decreases alveolar bone loss in experimental periodontitis

2017 ◽  
Vol 59 (2) ◽  
pp. 247-255 ◽  
Author(s):  
Fatma Y. Kırzıoğlu ◽  
Memduha Tözüm Bulut ◽  
Burak Doğan ◽  
Özlem Fentoğlu ◽  
Özlem Özmen ◽  
...  
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Experimental Periodontitis ◽  
Anti Inflammatory ◽  
Inflammatory Effect

scholarly journals SOCS-3 Regulates Alveolar Bone Loss in Experimental Periodontitis

2016 ◽  
Vol 95 (9) ◽  
pp. 1018-1025 ◽  
Author(s):  
E. Papathanasiou ◽  
A. Kantarci ◽  
A. Konstantinidis ◽  
H. Gao ◽  
T.E. Van Dyke
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Experimental Periodontitis

Angiopoietin‐like protein 2 deficiency promotes periodontal inflammation and alveolar bone loss

2021 ◽  
Author(s):  
Chenxi Jiang ◽  
Siqi Yao ◽  
Yi Guo ◽  
Li Ma ◽  
Xiaoxuan Wang ◽  
...  
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Periodontal Inflammation

Humic Acid, a Polyphenolic Substance, Decreases Alveolar Bone Loss in Experimental Periodontitis in Rats

2019 ◽  
Vol 36 (4) ◽  
pp. 257-265
Author(s):  
Metin Çalışır ◽  
Aysun Akpınar ◽  
Ömer Poyraz ◽  
Fahrettin Göze ◽  
Ziynet Çınar
Keyword(s):  
Humic Acid ◽  
Bone Loss ◽  
Inflammatory Cell ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Inflammatory Cell Infiltration ◽  
Cell Infiltration ◽  
Enzyme Linked Immunosorbent Assay ◽  
Local Administration ◽  
Experimental Periodontitis

The purpose of this study was to evaluate the biochemical, morphometric, and histopathological changes associated with experimental periodontitis in rats in response to local administration of humic acid. Thirty-eight Wistar rats were divided into 5 experimental groups: nonligated (NL) group, ligature-only (LO) group, and ligature + local administration of humic acid (20, 80, and 150 mg/kg body weight per day for 15 days, respectively; L-20, L-80, and L-150 groups). Changes in alveolar bone levels were clinically measured as the distance from the cementoenamel junction to the alveolar bone crest with a stereomicroscope. Tissues were histopathologically examined to assess the osteoclast numbers, osteoblastic activity, and inflammatory cell infiltration among the study groups. Enzyme-linked immunosorbent assay interleukin1β (IL-1β) and IL-10 levels in serum and gingival homogenates were evaluated. At the end of 15 days, the alveolar bone loss was significantly higher in the LO group compared to the NL, L-20, and L-150 groups ( P < .05). The osteoclast number in the LO group was significantly higher than the NL, L-20, and L-150 groups ( P < .05). Inflammatory cell infiltration was significantly higher in the LO and L-80 groups than the other groups ( P < .05). The highest serum and gingival homogenate IL-10 levels were determined in the NL group ( P < .05). The serum and gingival homogenate IL-1β levels in LO group were significantly higher than the NL, L-20, and L-150 groups ( P < .05). Within the limits of this study, it can be suggested that humic acid, when administered locally at 20 and 80 mg/kg doses, may prevent alveolar bone loss in the rat model.

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