Expression of HMGB1 and HMGN2 in gingival tissues, GCF and PICF of periodontitis patients and peri-implantitis

Luo, Lin; Xie, Ping; Gong, Ping; Tang, Xiaohai; Ding, Yi; Deng, Lijing

doi:10.1016/j.archoralbio.2011.03.020

Cited by 42 publications

(41 citation statements)

References 27 publications

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“…In the ligature model, HMGB1 expression could be compared to the expression profile of TNF- α and IL-6 from our previous study in which higher expression of these genes occurred at days 7 and 15 followed by a reduction at 30 days [29]. These in vivo results corroborate also with a clinical study that have demonstrated high levels of HMGB1 in gingival tissues and gingival crevicular fluid of chronic periodontitis patients compared to control [30]. In addition, this clinical study showed that HMGB1 responds in a similar way to other cytokines during disease progression.…”

Section: Discussionsupporting

confidence: 75%

HMGB1 Localization during Experimental Periodontitis

Nogueira

Souza

Molon

et al. 2014

Mediators of Inflammation

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Aim. This study sought to investigate the in vitro expression profile of high mobility group box 1 (HMGB1) in murine periodontal ligament fibroblasts (mPDL) stimulated with LPS or IL-1β and in vivo during ligature- or LPS-induced periodontitis in rats. Material and Methods. For the in vivo study, 36 rats were divided into experimental and control groups, and biopsies were harvested at 7–30 d following disease induction. Bone loss and inflammation were evaluated. HMGB1 expression was assessed by immunohistochemistry, qPCR, and Western blot. Results. Significant increases in mPDL HMGB1 mRNA occurred at 4, 8, and 12 h with protein expression elevated by 24 h. HMGB1 mRNA expression in gingival tissues was significantly increased at 15 d in the LPS-PD model and at 7 and 15 d in the ligature model. Immunohistochemical staining revealed a significant increase in the number of HMGB1-positive cells during the experimental periods. Conclusion. The results show that PDL cells produce HMGB1, which is increased and secreted extracellularly after inflammatory stimuli. In conclusion, this study demonstrates that HMGB1 may be associated with the onset and progression of periodontitis, suggesting that further studies should investigate the potential role of HMGB1 on periodontal tissue destruction.

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Section: Discussionsupporting

confidence: 75%

HMGB1 Localization during Experimental Periodontitis

Nogueira

Souza

Molon

et al. 2014

Mediators of Inflammation

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“…In addition, P. gingivalis is associated with oral squamous cell carcinomas and other chronic diseases [3, 52]. Our findings also support studies showing that HMGB1 is another possible candidate for an early inflammatory disease marker [53, 54]. Collectively, these results suggest that P. gingivalis NDK dampens the host-immune response by decreasing release of pro-inflammatory cytokine, IL-1β, and the pro-inflammatory danger signal, HMGB1, from infected GECs.…”

Section: Discussionsupporting

confidence: 87%

Porphyromonas gingivalis attenuates ATP-mediated inflammasome activation and HMGB1 release through expression of a nucleoside-diphosphate kinase

Johnson

Atanasova

Bui

et al. 2015

Microbes and Infection

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Many intracellular pathogens evade the innate immune response in order to survive and proliferate within infected cells. We show that Porphyromonas gingivalis, an intracellular opportunistic pathogen, uses a nucleoside-diphosphate kinase (NDK) homolog to inhibit innate immune responses due to stimulation by extracellular ATP, which acts as a danger signal that binds to P2X7 receptors and induces activation of an inflammasome and caspase-1. Thus, infection of gingival epithelial cells (GECs) with wild-type P. gingivalis results in inhibition of ATP-induced caspase-1 activation. However, ndk-deficient P. gingivalis is less effective than wild-type P. gingivalis in reducing ATP-mediated caspase-1 activation and secretion of the proinflammatory cytokine, IL-1β, from infected GECs. Furthermore, P. gingivalis NDK modulates release of high-mobility group protein B1 (HMGB1), a pro-inflammatory danger signal, which remains associated with chromatin in healthy cells. Unexpectedly, infection with either wild-type or ndk-deficient P. gingivalis causes release of HMGB1 from the nucleus to the cytosol. But HMGB1 is released to the extracellular space when uninfected GECs are further stimulated with ATP, and there is more HMGB1 released from the cells when ATP-treated cells are infected with ndk-deficient mutant than wild-type P. gingivalis. Our results reveal that NDK plays a significant role in inhibiting P2X7-dependent inflammasome activation and HMGB1 release from infected GECs.

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“…Thirteen studies showed higher levels of IL-1β in PICF than healthy implant sites [7,21,22,30,35,36,41-47]. Of the 10 studies assessed TNF-α, 3 of them showed no relationship with this cytokine with peri-implant inflammation [7,25,43], while other 7 studies showed significant relationship with this cytokine [23,24,36,41,46-48]. These findings suggest that pro-inflammatory cytokines such as IL-1β and TNF-α are up to date, the most promising proteins to be used as markers in PICF for differentiation between peri-implantitis and healthy implants.…”

Section: Discussionmentioning

confidence: 99%

Peri-Implant Crevicular Fluid Analysis, Enzymes and Biomarkers: a Systemetic Review

Dursun

Tözüm

2016

JOMR

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ObjectivesTo review the current understanding of the biomarkers and enzymes associated with different forms peri-implant diseases and how their level changes influence the pathogenesis of the inflammatory diseases around dental implants.Material and MethodsAn electronic search in two different databases was performed including MEDLINE (PubMed) and EMBASE between 1996 to 2016. Human studies analyse peri-implant crevicular fluid (PICF) biomarker and enzyme levels of implants having peri-implant mucositis and peri-implantitis published in English language, were evaluated. A systematic review was performed to assess which biomarkers and enzymes in PICF were used to identify the inflammatory conditions around dental implants.ResultsFifty-one articles were identified of which 41 were further evaluated and included in the analysis. Due to significant heterogeneity between included studies, a meta-analysis could not be performed. Instead, a systematic descriptive review was performed.ConclusionsBiomarkers and enzymes in peri-implant crevicular fluid have shown promising results in differentiating from peri-implant disease condition to health. However, due to inconsistent results and acquiring much evidence from cross-sectional studies, additional evidence supported by randomized-controlled trials is needed to validate the links reported.

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Expression of HMGB1 and HMGN2 in gingival tissues, GCF and PICF of periodontitis patients and peri-implantitis

Cited by 42 publications

References 27 publications

HMGB1 Localization during Experimental Periodontitis

HMGB1 Localization during Experimental Periodontitis

Porphyromonas gingivalis attenuates ATP-mediated inflammasome activation and HMGB1 release through expression of a nucleoside-diphosphate kinase

Peri-Implant Crevicular Fluid Analysis, Enzymes and Biomarkers: a Systemetic Review

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