Bacterial modulators of bone remodeling in the periodontal pocket

Henderson, Brian E.; Kaiser, Frank J.

doi:10.1111/prd.12160

Cited by 32 publications

(23 citation statements)

References 94 publications

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“…The suppressed host immune response leads to a local immune response, which can enable periodontopathic bacteria to evade the host immune system. Furthermore, host immunological cells activated by bacteria produce various pro‐inflammatory mediators, eventually leading to periodontal tissues breakdown (Bosshardt, ; Henderson & Kaiser, ).…”

Section: Introductionmentioning

confidence: 99%

The role of autophagy in the pathogenesis of periodontal disease

Jiang

Zhu

2019

Oral Diseases

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Periodontal disease is a chronic inflammatory disease leading to destruction of periodontal tissues. As a local inflammation, periodontopathic bacterium, pro‐inflammatory mediators, and local immune response play pivotal role in the progress of periodontal disease. Besides, cigarette smoke has long been associated with periodontal disease and tooth loss. Autophagy is an intracellular degradation process highly conserved from yeast to humans. As a lysosomal degradation pathway of self‐digestion, it is critical for maintaining cells homeostasis and development. The role of autophagy has been investigated in oral diseases, such as oral cancer, periapical lesions, and oral candidiasis. Recently, increasing studies investigated the role of autophagy in periodontal disease. In this review, we try to illustrate the effect of autophagy on periodontal disease pathogenesis from 5 aspects: autophagy affects the intracellular infection and survival of bacteria; autophagy has an interaction with periodontal inflammation; autophagy is pivotal in periodontal cells biology and periodontal tissues destruction and reconstruction; autophagy can be induced by cigarette smoke; last but not least, autophagy may affect periodontal disease via endoplasmic reticulum stress.

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Section: Introductionmentioning

confidence: 99%

The role of autophagy in the pathogenesis of periodontal disease

Jiang

Zhu

2019

Oral Diseases

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“…In 2013, Basic National Health Research Department (RISKESDAS) reported the prevalence of periodontal disease as having reached 96.58 %, thereby representing the second most common oral and dental condition in Indonesia [2][3][4]. Numerous previous studies relating to dentistry have analyzed the relationship between bacterial activity and inflammation resulting from periodontal disease which lead to problematic alveolar bone defects [5]. To overcome these defects, numerous techniques such as hydroxyapatite [6,7] or Carbonate-apatite bone graft [8] have been developed to stimulate and enhance the regeneration of alveolar bone.…”

Section: Introductionmentioning

confidence: 99%

<i>In vitro</i> bone sialoprotein-I expression in combined gingival stromal cells and platelet rich fibrin during osteogenic differentiation

Nugraha¹,

Narmada²,

Ernawati³

et al. 2019

Trop. J. Pharm Res

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Purpose:To analyze the expression of bone sialoprotein -I (BSP -I) after the addition of platelet rich fibrin (PRF) in gingival somatic cell (GSC) culture medium during osteogenic differentiation in vitro. Methods: GSCs were extracted from healthy, 1-month-old, male Wistar rats (Rattus Novergicus), weighing 250 -300 g, and which had been randomly selected (n=4). These cells were cultured for 14 days and passaged every 4 days. Five subcultures of GSCs were cultured in three plates (M24) (N = 54; n = 6) for 7, 14 and 21 days in three preconditioned culture media (group I: plain culture media; group II: preconditioned osteogenic culture media, and group III: preconditioned osteogenic culture media with platelet rich fibrin). The expression of BSP-I was immunocytochemically (ICC) examined with monoclonal antibodies. Homogeneity and normality tests (p > 0.05) were then performed followed by an analysis of variance (ANOVA, p < 0.05). Results: The highest expression of BSP-I was found in group III (Day 21,13.00 ± 2.000), while the lowest expression of BSP-I was found in group I (Day 7, 7.33 ± 1.155). There were significant differences between the groups (p = 0.000, p < 0.05). Conclusion: PRF stimulates and significantly enhances the expression of BSP-I in GSC culture during osteogenic differentiation. Thus, PRF can be used to accelerate regeneration of alveolar bone defects. This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest

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“…In periodontitis, an intensified host inflammatory response against subgingival biofilms, consisting primarily of inflammophilic gram-negative species, causes the destruction of gingival tissue and alveolar bone (for reviews see refs. [4,5]) In this excessive inflammation neutrophils produce disproportionate amounts of reactive oxygen species (ROS) that take part in the tissue destruction (for review, see ref. [6]).…”

Section: Introductionmentioning

confidence: 99%

Interactions between the Aggregatibacter actinomycetemcomitans secretin HofQ and host cytokines indicate a link between natural competence and interleukin-8 uptake

et al. 2018

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Naturally competent bacteria acquire DNA from their surroundings to survive in nutrient-poor environments and incorporate DNA into their genomes as new genes for improved survival. The secretin HofQ from the oral pathogen Aggregatibacter actinomycetemcomitans has been associated with DNA uptake. Cytokine sequestering is a potential virulence mechanism in various bacteria and may modulate both host defense and bacterial physiology. The objective of this study was to elucidate a possible connection between natural competence and cytokine uptake in A. actinomycetemcomitans. The extramembranous domain of HofQ (emHofQ) was shown to interact with various cytokines, of which IL-8 exhibited the strongest interaction. The dissociation constant between emHofQ and IL-8 was 43 nM in static settings and 2.4 μM in dynamic settings. The moderate binding affinity is consistent with the hypothesis that emHofQ recognizes cytokines before transporting them into the cells. The interaction site was identified via crosslinking and mutational analysis. By structural comparison, relateda type I KH domain with a similar interaction site was detected in the Neisseria meningitidis secretin PilQ, which has been shown to participate in IL-8 uptake. Deletion of hofQ from the A. actinomycetemcomitans genome decreased the overall biofilm formation of this organism, abolished the response to cytokines, i.e., decreased eDNA levels in the presence of cytokines, and increased the susceptibility of the biofilm to tested β-lactams. Moreover, we showed that recombinant IL-8 interacted with DNA. These results can be used in further studies on the specific role of cytokine uptake in bacterial virulence without interfering with natural-competence-related DNA uptake.

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Bacterial modulators of bone remodeling in the periodontal pocket

Cited by 32 publications

References 94 publications

The role of autophagy in the pathogenesis of periodontal disease

The role of autophagy in the pathogenesis of periodontal disease

<i>In vitro</i> bone sialoprotein-I expression in combined gingival stromal cells and platelet rich fibrin during osteogenic differentiation

Interactions between the Aggregatibacter actinomycetemcomitans secretin HofQ and host cytokines indicate a link between natural competence and interleukin-8 uptake

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