scholarly journals VEGF Expression in Diabetic Rats Promotes Alveolar Bone Resorption by Porphyromonas gingivalis LPS

2016 ◽  
Vol 25 (1) ◽  
pp. 41-48
Author(s):  
Norimasa Tsumori ◽  
Tomoo Kono ◽  
Nobuhiro Shigematsu ◽  
Hiromasa Morita ◽  
Makoto Umeda
2010 ◽  
Vol 78 (11) ◽  
pp. 4560-4569 ◽  
Author(s):  
Brian Bainbridge ◽  
Raj K. Verma ◽  
Christie Eastman ◽  
Bilal Yehia ◽  
Mercedes Rivera ◽  
...  

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.


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 ◽  
...  

Molecules ◽  
2020 ◽  
Vol 25 (20) ◽  
pp. 4815
Author(s):  
Minmin Sun ◽  
Yaoting Ji ◽  
Zhen Li ◽  
Rourong Chen ◽  
Shuhui Zhou ◽  
...  

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.


2000 ◽  
Vol 68 (6) ◽  
pp. 3103-3107 ◽  
Author(s):  
Pamela J. Baker ◽  
Lisa DuFour ◽  
Mark Dixon ◽  
Derry C. Roopenian

ABSTRACT Alveolar bone resorption can be induced in specific-pathogen-free mice by oral infection with Porphyromonas gingivalis(P. J. Baker, R. T. Evans, and D. C. Roopenian, Arch. Oral Biol. 39:1035–1040, 1994). Here we used a mouse strain, C57BL/6J, which is relatively resistant to P. gingivalis-induced bone loss to examine whether partial or complete deletion of various adhesion molecules would increase susceptibility. Complete deletion of P-selectin or nearly complete lack of expression of intercellular adhesion molecule 1 (ICAM-1) led to increased susceptibility to bone resorption after oral infection, while a hypomorphic defect in β2-integrins did not. Both the total amount of bone lost and the number of sites at which there was significant loss were increased in mice deficient in either ICAM-1 or P-selectin. Each of the three adhesion molecule deficiencies was sufficient to decreaseP. gingivalis-specific serum immunoglobulin G responses, but lower antibody titers did not lead to increased bone loss in partially β2-integrin-deficient mice. In conclusion, P-selectin and ICAM-1 deficiencies increase susceptibility to and severity of alveolar bone loss after P. gingivalisinfection. This finding underscores the importance of innate immunity in protection against P. gingivalis-induced alveolar bone resorption.


2014 ◽  
Vol 49 (6) ◽  
pp. 801-809 ◽  
Author(s):  
Y. Nakatsuka ◽  
T. Nagasawa ◽  
Y. Yumoto ◽  
F. Nakazawa ◽  
Y. Furuichi

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