Porphyromonas gingivalis may play an important role in the pathogenesis of periodontitis-associated rheumatoid arthritis

Liao, Feng; Li, Zubing; Shi, Bin; Gong, Zhongcheng; Cheng, Xiang‐Rong

doi:10.1016/j.mehy.2008.12.040

Cited by 98 publications

(84 citation statements)

References 38 publications

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“…31,60 Recently, the focus has been turned to other periodontopathogens, such as P. gingivalis, which are supposed to have a major function in PD/RA interaction through active peptide citrullination, which could be involved in loss of self-tolerance and RA development. 61 However, even with the substitution of the infectious agent of ePD to P. gingivalis, no alterations in the severity of experimental RA were observed, whereas the increase of ePD was similar to that of A. actinomycetemcomitans. One possibility to this lack of association is that ePD presents a lower or narrow systemic effect than PIA, possibly insufficient to module RA severity.…”

Section: Experimental Periodontitis and Arthritis Interaction Ap Trommentioning

confidence: 89%

“…7,29,30 In addition, although early studies suggested a potential link between the periodontal pathogen A. actinomycetemcomitans and RA, 31,32 recent studies point to a possible causal function for Porphyromonas gingivalis in RA pathogenesis. 33,34 However, the exact molecular mechanisms underlying such putative functional interferences remain unknown.…”

Section: Introductionmentioning

confidence: 99%

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Periodontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype and functional immunological interferences

Trombone¹,

Claudino²,

Colavite³

et al. 2010

Genes Immun

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Periodontitis (PD) and rheumatoid arthritis (RA) have been found to be clinically associated and to share the chronic nature of the inflammatory reaction associated with bone resorption activity. However, the mechanisms underlying such association are unknown. Therefore, we examined the basis of Actinobacillus actinomycetemcomitans-and Porphyromonas gingivalis-induced PD and pristane-induced arthritis (PIA) interaction in mice. Higher severity PD in the genetically inflammation prone acute inflammatory reactivity maximum (AIRmax) mice strain was associated with higher levels of TNF-a, IL-1b, IL-17, matrix metalloproteinase (MMP)-13, and RANKL, whereas PD/PIA co-induction resulted in even higher levels of IL-1b, IFN-g, IL-17, RANKL, and MMP-13 levels. Conversely, PD/PIA co-induction in AIRmin strain did not alter the course of both pathologies. PIA/PD co-induction resulted in altered expression of T-cell subsets transcription factors expression, with T-bet and RORg levels being upregulated, whereas GATA-3 levels were unaltered. Interestingly, PIA induction resulted in alveolar bone loss, such response being highly dependent on the presence of commensal oral bacteria. No differences were found in PIA severity parameters by PD co-induction. Our results show that the interaction between experimental PD and arthritis in mice involves a shared hyper-inflammatory genotype and functional interferences in innate and adaptive immune responses.

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Section: Experimental Periodontitis and Arthritis Interaction Ap Trommentioning

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Periodontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype and functional immunological interferences

Trombone¹,

Claudino²,

Colavite³

et al. 2010

Genes Immun

View full text Add to dashboard Cite

show abstract

“…Elevated levels of P. gingivalis are detected in periodontal lesions, and these can be significantly reduced following successful periodontal therapy (Cappelli et al, 2009;Salvi et al, 1997;Socransky et al, 2002;Ximenez-Fyvie et al, 2000;Yamazaki et al, 2004). Apart from its well accepted role as an oral pathogen in the establishment of chronic inflammation at the site of infection, there is increasing evidence of a link between P. gingivalis-associated periodontal disease and systemic inflammatory conditions, such as diabetes, preterm birth, aspiration pneumonia and atherosclerotic cardiovascular disease (Brodala et al, 2005;Liao et al, 2009;Lin et al, 2003;Maekawa et al, 2011;Pussinen and Mattila, 2004). On the cellular level, a convincing body of evidence indicates that P. gingivalis possesses unique signalling properties, which enable it to evade, subvert or manipulate the host immune defences by exploiting the toll-like receptor (TLR) family, in particular TLR2 (Burns et al, 2006;Hajishengallis et al, 2002;Hajishengallis et al, 2008b;Harokopakis et al, 2006;Wang et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Involvement of the TREM-1/DAP12 pathway in the innate immune responses to Porphyromonas gingivalis

Bostancı

Thurnheer

Belibasakis

2011

Molecular Immunology

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Porphyromonas gingivalis, is a Gram-negative obligate oral anaerobic bacterium highly implicated in periodontal disease, the most prevalent chronic inflammatory disease, but recent evidence also indicates a potential contribution to systemic inflammation. The Triggering Receptor Expressed on Myeloid cells 1 (TREM-1) is a cell surface receptor of the immunoglobulin superfamily, which, along with its adaptor signalling molecule DAP12, is involved in immune response to bacterial and fungal infections, particularly by amplifying the production of pro-inflammatory cytokines by the host. The aim of the present study was to investigate the effect of P. gingivalis on the expression of the TREM-1/DAP12 pathway, as well as its engagement in pro-inflammatory cytokine production, by the myelomonocytic cell line MonoMac-6. P. gingivalis enhanced TREM-1 gene expression by the cells, concomitantly to an increase of soluble TREM-1 secretion. Engagement of TREM-1, by introducing anti-TREM-1 to the experimental system, resulted in further potentiation of the pro-inflammatory responses to P. gingivalis, as evaluated by a further enhancement of interleukin (IL)-1 and IL-6 secretion. On the contrary, the synthetic TREM-1 antagonist LP17 reduced the P. gingivalis-induced IL-1 and IL-6 secretion by approximately 50%. In conclusion, the putative periodontal pathogen P. gingivalis can positively regulate the expression of the TREM-1/DAP12 pathway in monocytic cells. Moreover, engagement of TREM-1 can further potentiate the pro-inflammatory responses to P. gingivalis infection. This effect may contribute not only to the pathogenesis of inflammatory periodontal disease, but also to the enhancement of systemic inflammation.

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“…При тяжелом течении ПД отмечена тенденция к повышению частоты РА [7,43], ДНК бактерий периодонта обнаруживают в сыворотке крови и синовиальной жидкости больных РА, страдающих ПД [44]. Некоторые исследователи рассматривают хрони-ческий ПД в качестве ФР РА [1], в то же время, по данным крупного американского проспективного исследования у женщин с ПД, осложненным потерей зубов или опера-тивными вмешательствами, не установлено последующее повышение заболеваемости РА [45].…”

unclassified

“…Решающую роль в ассоциации РА и ПД может играть Porphyromonas gingivalis, единственный прокариот, выделя-ющий пептидил-аргинин деиминазу -фермент, катализи-рующий процесс расщепления аргинина до цитруллина [44]. Колонизация полости рта P. gingivalis может нарушать иммунную толерантность к цитруллинированным антиге-нам или усиливать аутоиммунный ответ и способствовать развитию РА у генетически предрасположенных больных.…”

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Anti‐Tumor Necrosis Factor‐Alpha Therapy and Periodontal Parameters in Patients With Rheumatoid Arthritis

Mayer

Balbir‐Gurman

Machtei

2009

Journal of Periodontology

144

138

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Background: The aim of this study was to evaluate the influence of anti‐tumor necrosis factor‐alpha (TNF‐α) therapy on the clinical and immunologic parameters of the periodontium. Methods: Ten patients with rheumatoid arthritis (RA) who routinely received infusions of infliximab, 200 mg (RA+), 10 patients with RA without anti‐TNF‐α therapy (RA−), and 10 healthy controls (C) were included. Clinical parameters, including the plaque index (PI), gingival index (GI), probing depth (PD), clinical attachment loss (AL), and bleeding on probing (BOP), were assessed, and total gingival crevicular fluid (GCF) TNF‐α level was determined using enzyme‐linked immunosorbent assay. Analysis of variance with Scheffe modification and the Pearson correlation test were used for statistical analysis. Results: The ages of the patients ranged from 22 to 76 years (mean, 50.73 ± 9.1 years). The mean PI was similar among the groups. However, mean inflammatory parameters in the three groups varied significantly; GI was greater in the RA− group compared to RA+ and C groups (P = 0.0042). The RA+ group exhibited less BOP than RA− and C groups (21.1% ± 3.0%, 45.9% ± 6.2%, and 39.1% ± 7.2%, respectively; P = 0.0146). The mean PD in the RA+ group was shallower than in RA− and C groups (3.22 ± 0.13 mm, 3.85 ± 0.22 mm, and 3.77 ± 0.20 mm, respectively; P = 0.055). Clinical AL in the RA+ group was lower than in RA− and C groups (3.68 ± 0.11 mm, 4.52 ± 0.26 mm, and 4.35 ± 0.24 mm, respectively; P = 0.0273). TNF‐α levels in the GCF of the RA+ group were the lowest compared to RA− and C groups (0.663, 1.23, and 0.949 ng/site, respectively; P = 0.0401). A significant positive correlation was found between TNF‐α levels in the GCF and clinical AL (r = 0.448; P = 0.0283). Conclusions: Patients with RA receiving anti‐TNF‐α medication had lower periodontal indices and GCF TNF‐α levels. Thus, suppression of proinflammatory cytokines might prove beneficial in suppressing periodontal diseases.

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Porphyromonas gingivalis may play an important role in the pathogenesis of periodontitis-associated rheumatoid arthritis

Cited by 98 publications

References 38 publications

Periodontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype and functional immunological interferences

Periodontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype and functional immunological interferences

Involvement of the TREM-1/DAP12 pathway in the innate immune responses to Porphyromonas gingivalis

Anti‐Tumor Necrosis Factor‐Alpha Therapy and Periodontal Parameters in Patients With Rheumatoid Arthritis

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