scholarly journals O009: A novel Bruton's kinase inhibitor acalabrutinib inhibits osteoclastogenesis and Porphyromonas gingivalis lipopolysaccharide-induced alveolar bone resorption

2018 ◽  
Vol 45 ◽  
pp. 8-8
Keyword(s):  
Bone Resorption ◽  
Porphyromonas Gingivalis ◽  
Alveolar Bone ◽  
Kinase Inhibitor ◽  
Porphyromonas Gingivalis Lipopolysaccharide

scholarly journals Role of Porphyromonas gingivalis Phosphoserine Phosphatase Enzyme SerB in Inflammation, Immune Response, and Induction of Alveolar Bone Resorption in Rats

2010 ◽  
Vol 78 (11) ◽  
pp. 4560-4569 ◽  
Author(s):  
Brian Bainbridge ◽  
Raj K. Verma ◽  
Christie Eastman ◽  
Bilal Yehia ◽  
Mercedes Rivera ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Epithelial Cells ◽  
Periodontal Disease ◽  
Porphyromonas Gingivalis ◽  
Rat Model ◽  
Alveolar Bone ◽  
Critical Role ◽  
Polymorphonuclear Neutrophil ◽  
Gingival Epithelial Cells ◽  
Phosphatase Enzyme

ABSTRACT Porphyromonas gingivalis secretes a serine phosphatase enzyme, SerB, upon contact with gingival epithelial cells in vitro. The SerB protein plays a critical role in internalization and survival of the organism in epithelial cells. SerB is also responsible for the inhibition of interleukin-8 (IL-8) secretion from gingival epithelial cells infected with P. gingivalis. This study examined the ability of a P. gingivalis SerB mutant to colonize the oral cavity and induce gingival inflammation, immune responses, and alveolar bone resorption in a rat model of periodontal disease. Both P. gingivalis ATCC 33277 and an isogenic ΔSerB mutant colonized the oral cavities of rats during the 12-week experimental period. Both of the strains induced significant (P < 0.05) systemic levels of immunoglobulin G (IgG) and isotypes IgG1, IgG2a, and IgG2b, indicating the involvement of both T helper type 1 (Th1) and Th2 responses to infection. Both strains induced significantly (P < 0.05) higher levels of alveolar bone resorption in infected rats than in sham-infected control rats. However, horizontal and interproximal alveolar bone resorption induced by the SerB mutant was significantly (P < 0.05) lower than that induced by the parental strain. Rats infected with the ΔSerB mutant exhibited significantly higher levels of apical migration of the junctional epithelium (P < 0.01) and polymorphonuclear neutrophil (PMN) recruitment (P < 0.001) into the gingival tissues than rats infected with the wild type. In conclusion, in a rat model of periodontal disease, the SerB phosphatase of P. gingivalis is required for maximal alveolar bone resorption, and in the absence of SerB, more PMNs are recruited into the gingival tissues.

scholarly journals Free Lipid A Isolated from Porphyromonas gingivalis Lipopolysaccharide Is Contaminated with Phosphorylated Dihydroceramide Lipids: Recovery in Diseased Dental Samples

2011 ◽  
Vol 80 (2) ◽  
pp. 860-874 ◽  
Author(s):  
Frank C. Nichols ◽  
Bekim Bajrami ◽  
Robert B. Clark ◽  
William Housley ◽  
Xudong Yao
Keyword(s):  
Porphyromonas Gingivalis ◽  
Lipid A ◽  
Alveolar Bone ◽  
Ionization Mass ◽  
Subgingival Plaque ◽  
Content Type ◽  
Free Lipid ◽  
The Matrix ◽  
Tlr2 Activation ◽  
Porphyromonas Gingivalis Lipopolysaccharide

ABSTRACTRecent reports indicate thatPorphyromonas gingivalismediates alveolar bone loss or osteoclast modulation through engagement of Toll-like receptor 2 (TLR2), though the factors responsible for TLR2 engagement have yet to be determined. Lipopolysaccharide (LPS) and lipid A, lipoprotein, fimbriae, and phosphorylated dihydroceramides ofP. gingivalishave been reported to activate host cell responses through engagement of TLR2. LPS and lipid A are the most controversial in this regard because conflicting evidence has been reported concerning the capacity ofP. gingivalisLPS or lipid A to engage TLR2 versus TLR4. In the present study, we first preparedP. gingivalisLPS by the Tri-Reagent method and evaluated this isolate for contamination with phosphorylated dihydroceramide lipids. Next, the lipid A prepared from this LPS was evaluated for the presence of phosphorylated dihydroceramide lipids. Finally, we characterized the lipid A by the matrix-assisted laser desorption ionization mass spectrometry (MALDI-MS) and electrospray-MS methods in order to quantify recovery of lipid A in lipid extracts from diseased teeth or subgingival plaque samples. Our results demonstrate that both the LPS and lipid A derived fromP. gingivalisare contaminated with phosphorylated dihydroceramide lipids. Furthermore, the lipid extracts derived from diseased teeth or subgingival plaque do not contain free lipid A constituents ofP. gingivalisbut contain substantial amounts of phosphorylated dihydroceramide lipids. Therefore, the free lipid A ofP. gingivalisis not present in measurable levels at periodontal disease sites. Our results also suggest that the TLR2 activation of host tissues attributed to LPS and lipid A ofP. gingivaliscould actually be mediated by phosphorylated dihydroceramides.

scholarly journals Porphyromonas gingivalis GroEL Induces Osteoclastogenesis of Periodontal Ligament Cells and Enhances Alveolar Bone Resorption in Rats

PLoS ONE ◽  
2014 ◽  
Vol 9 (7) ◽  
pp. e102450 ◽  
Author(s):  
Feng-Yen Lin ◽  
Fung-Ping Hsiao ◽  
Chun-Yao Huang ◽  
Chun-Ming Shih ◽  
Nai-Wen Tsao ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Porphyromonas Gingivalis ◽  
Periodontal Ligament ◽  
Alveolar Bone ◽  
Periodontal Ligament Cells

scholarly journals Ginsenoside Rb3 Inhibits Pro-Inflammatory Cytokines via MAPK/AKT/NF-κB Pathways and Attenuates Rat Alveolar Bone Resorption in Response to Porphyromonas gingivalis LPS

Molecules ◽  
2020 ◽  
Vol 25 (20) ◽  
pp. 4815
Author(s):  
Minmin Sun ◽  
Yaoting Ji ◽  
Zhen Li ◽  
Rourong Chen ◽  
Shuhui Zhou ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Porphyromonas Gingivalis ◽  
Alveolar Bone ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Periodontal Ligament Cells ◽  
Dependent Manner ◽  
Experimental Periodontitis ◽  
Anti Inflammatory ◽  
Porphyromonas Gingivalis Lps

Conventional treatments for chronic periodontitis are less effective in controlling inflammation and often relapse. Therefore, it is necessary to explore an immunomodulatory medication as an adjuvant. Ginsenoside Rb3 (Rb3), one of the most abundant active components of ginseng, has been found to possess anti-inflammatory and immunomodulatory properties. Here, we detected the anti-inflammatory effect of Rb3 on Porphyromonas gingivalis LPS-stimulated human periodontal ligament cells and experimental periodontitis rats for the first time. We found that the expression of pro-inflammatory mediators, including IL-1β, IL-6 and IL-8, upregulated by lipopolysaccharide (LPS) stimulation was remarkably downregulated by Rb3 treatment in a dose-dependent manner at both transcriptional and translational levels. Network pharmacological analysis of Rb3 showed that the mitogen-activated protein kinase (MAPK) signaling pathway had the highest richness and that p38, JNK, and ERK molecules were potential targets of Rb3 in humans. Western blot analysis revealed that Rb3 significantly suppressed the phosphorylation of p38 MAPK and p65 NF-κB, as well as decreased the expression of total AKT. In experimental periodontitis rat models, reductions in alveolar bone resorption and osteoclast generation were observed in the Rb3 treatment group. Thus, we can conclude that Rb3 ameliorated Porphyromonas gingivalis LPS-induced inflammation by inhibiting the MAPK/AKT/NF-κB signaling pathways and attenuated alveolar bone resorption in experimental periodontitis rats.

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