Porphyromonas gingivalis adopts intricate and unique molecular mechanisms to survive and persist within the host: a critical update

Chopra, Aditi; Bhat, Somashekara; Sivaraman, Karthik

doi:10.1080/20002297.2020.1801090

Cited by 35 publications

(44 citation statements)

References 217 publications

(801 reference statements)

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“…As a matter of fact, P. gingivalis has a wide range of virulence factors that impair the adaptive immune response 35 . The strong association between P. gingivalis and clinical signs of periodontal attachment loss and inflammation is well justified by the increased levels of components derived of tissue destruction and inflammatory mediators that make the periodontal pocket a perfect environment for this species 17,35 . However, the presence of P. gingivalis or other single pathogen is not sufficient to lead to periodontitis, for host‐related and environmental factors have a major impact on susceptibility to microbial immune subversion 32,35 .…”

Section: Discussionmentioning

confidence: 99%

Subgingival microbiota in overweight and obese young adults with no destructive periodontal disease

Andrade¹,

Silva²,

Colombo

et al. 2021

Journal of Periodontology

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Background This study analyzed the levels of a specific group of periodontal health/disease‐related oral bacteria in the subgingival biofilm of young adults with overweight (OW) and obesity (OB), and no destructive periodontal disease. Methods Full‐mouth periodontal assessment and subgingival biofilm sampling were performed in individuals with normal weight (NW) (BMI [body mass index] ≥18.5 to ≤24.9 kg/m2; n = 29), OW (BMI ≥25 to ≤29.9 kg/m2; n = 26), or OB (BMI ≥30 kg/m2; n = 22). BMI, waist (WC) and hip (HC) circumferences, and waist‐hip ratio (WHR) were established for every individual. Biofilm samples were analyzed by checkerboard. Spearman coefficient, linear, and logistic regression analyses were obtained. Results Gingivitis was detected in 45% NW, 65% OW, and 73% OB individuals. NW patients presented significantly less calculus and supragingival biofilm than OB. OW, and OB individuals had significantly higher levels of Porphyromonas gingivalis and Tannerella forsythia than NW patients (P <0.05). Treponema denticola correlated with BMI (rho = 0.31), WC (rho = 0.28), and HC (rho = 0.29), P≤0.01. Linear regression analysis showed significant (P <0.05) positive associations between BMI, WC, HC, and WHR indicators and Prevotella spp., Lactobacillus spp., V. parvula, and A. actinomycetemcomitans (Aa); negative associations were found between Capnocytophaga spp., WC, and HC (β = −0.29 and β = −0.37, respectively; P <0.01). However, the interaction of Prevotella spp. and T. forsythia decreased the likelihood of an individual to be diagnosed as OW/OB (OR 0.183 [95% CI, 0.062–0.540]). Conclusions Few periodontal pathogens differed in levels between NW and OW/OB individuals without destructive periodontal disease. Moreover, Aa, T. denticola, and Prevotella spp. were associated with clinical parameters of obesity.

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Section: Discussionmentioning

confidence: 99%

Subgingival microbiota in overweight and obese young adults with no destructive periodontal disease

Andrade¹,

Silva²,

Colombo

et al. 2021

Journal of Periodontology

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“…However, in one study, OMVs from P. gingivalis were found to increase lactate dehydrogenase (LDH) release from macrophages, indicating the occurrence of pyroptosis induced by inflammasome activation, whereas P. gingivalis alone did not promote LDH release; in another study, P. gingivalis was found to increase GSDMD-N expression and induce pyroptosis in macrophages ( 166 , 181 ). In addition, P. gingivalis can increase noncanonical caspase-11/4 expression in macrophages ( 166 , 167 ). Treponema denticola and Tannerella forsythia activate caspase-1 and caspase-4 and trigger pyroptosis in THP-1 macrophages ( 168 ).…”

Section: Inflammasomes In Inflammatory Osteolysis Of the Alveolar Bone And Jawsmentioning

confidence: 99%

Inflammasomes in Alveolar Bone Loss

Ling

Jiang

2021

Front. Immunol.

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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.

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“…In addition, independent of APC activation in vitro , P. gingivalis -LPS promotes Th17 cell differentiation directly through TLR2 signalling. It also enhances IL-17-mediated bone resorption by the up-regulation of transcription factors such as RORC as well ( 133 , 134 ).…”

Section: Th17 Cell Involvement In Periodontitis Pathogenesismentioning

confidence: 99%

Th17 Cells in Periodontitis and Its Regulation by A20

et al. 2021

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Periodontitis is a prevalent chronic disease that results in loss of periodontal ligament and bone resorption. Triggered by pathogens and prolonged inflammation, periodontitis is modulated by the immune system, especially pro-inflammatory cells, such as T helper (Th) 17 cells. Originated from CD4+ Th cells, Th17 cells play a central role for they drive and regulate periodontal inflammation. Cytokines secreted by Th17 cells are also major players in the pathogenesis of periodontitis. Given the importance of Th17 cells, modulators of Th17 cells are of great clinical potential and worth of discussion. This review aims to provide an overview of the current understanding of the effect of Th17 cells on periodontitis, as well as a brief discussion of current and potential therapies targeting Th17 cells. Lastly, we highlight this article by summarizing the causal relationship between A20 (encoded by TNFAIP3), an anti-inflammatory molecule, and Th17 cell differentiation.

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Porphyromonas gingivalis adopts intricate and unique molecular mechanisms to survive and persist within the host: a critical update

Cited by 35 publications

References 217 publications

Subgingival microbiota in overweight and obese young adults with no destructive periodontal disease

Subgingival microbiota in overweight and obese young adults with no destructive periodontal disease

Inflammasomes in Alveolar Bone Loss

Th17 Cells in Periodontitis and Its Regulation by A20

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