Periodontal Treatment Decreases Levels of Antibodies to <i>Porphyromonas gingivalis</i> and Citrulline in Patients With Rheumatoid Arthritis and Periodontitis

Okada, Mihoko; Kobayashi, Tetsuo; Ito, Satoshi; Yokoyama, Tomoko; Abe, Asami; Murasawa, Akira; Yoshie, Hiromasa

doi:10.1902/jop.2013.130079

Cited by 117 publications

(130 citation statements)

References 46 publications

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“…The CD is composed of 377 proteins retrieved from six data sources (Data Sheet 1, Tables S1–S6): 1) RA genome-wide association studies (GWAS) gathered and integrated from five different databases (BioGPS (Wu et al, 2009), HuGE (Yu et al, 2008), NHGRI, OMIM, PharmGKB (Klein et al, 2001); see Data Sheet 1, Table S1 for the specific query processes);2) RA-associated proteins from the Universal Protein Resource (Uniprot) (Consortium, 2010), retrieved using as search parameters “ rheumatoid arthritis ” and “ human ” and then manually screened (Data Sheet 1, Table S2);3) Genes and proteins retrieved from a comprehensive review of the literature, in particular genes appearing in Tables 1, 2 of Review (Mcinnes and Schett, 2011) and cited references (Data Sheet 1, Table S3);4) Genes that show epigenetic changes in relation to RA, as specified in Trenkmann et al (2010); Karouzakis et al (2011) (Data Sheet 1, Table S4);5) Proteins that are at the interface between the host and the oral microbiome, in particular proteins experimentally known to be differentially expressed in presence of Porphyromonas Gingivalis (Zhou and Amar, 2006), a periodontitis-causing bacterium that has been strongly linked to the insurgence of RA (Mikuls et al, 2012; Scher et al, 2012; Smit et al, 2012; Bingham and Moni, 2013; Ogrendik, 2013; Okada et al, 2013) (Data Sheet 1, Table S5);6) The key elements of the NF-κB system, the master regulator of inflammation (Oeckinghaus et al, 2011; Smale, 2011; Hayden and Ghosh, 2012) at the center of a complex regulatory interactome (Tieri et al, 2012) prominently implicated in the onset and development of RA (Miagkov et al, 1998; Makarov, 2001; Feldmann et al, 2002; Okamoto, 2006; Roman-Blas and Jimenez, 2006, 2008; Simmonds and Foxwell, 2008; Van Loo and Beyaert, 2011): we included 16 “consensus” proteins that appear at the intersection of the three main NF-κB-related datasets described in Tieri et al (2012) (Data Sheet 1, Table S6). …”

Section: Methodsmentioning

confidence: 99%

Multi-omic landscape of rheumatoid arthritis: re-evaluation of drug adverse effects

Tieri

Zhou

Zhu

et al. 2014

Front. Cell Dev. Biol.

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Objective: To provide a frame to estimate the systemic impact (side/adverse events) of (novel) therapeutic targets by taking into consideration drugs potential on the numerous districts involved in rheumatoid arthritis (RA) from the inflammatory and immune response to the gut-intestinal (GI) microbiome.Methods: We curated the collection of molecules from high-throughput screens of diverse (multi-omic) biochemical origin, experimentally associated to RA. Starting from such collection we generated RA-related protein-protein interaction (PPI) networks (interactomes) based on experimental PPI data. Pharmacological treatment simulation, topological and functional analyses were further run to gain insight into the proteins most affected by therapy and by multi-omic modeling.Results: Simulation on the administration of MTX results in the activation of expected (apoptosis) and adverse (nitrogenous metabolism alteration) effects. Growth factor receptor-bound protein 2 (GRB2) and Interleukin-1 Receptor Associated Kinase-4 (IRAK4, already an RA target) emerge as relevant nodes. The former controls the activation of inflammatory, proliferative and degenerative pathways in host and pathogens. The latter controls immune alterations and blocks innate response to pathogens.Conclusions: This multi-omic map properly recollects in a single analytical picture known, yet complex, information like the adverse/side effects of MTX, and provides a reliable platform for in silico hypothesis testing or recommendation on novel therapies. These results can support the development of RA translational research in the design of validation experiments and clinical trials, as such we identify GRB2 as a robust potential new target for RA for its ability to control both synovial degeneracy and dysbiosis, and, conversely, warn on the usage of IRAK4-inhibitors recently promoted, as this involves potential adverse effects in the form of impaired innate response to pathogens.

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Section: Methodsmentioning

confidence: 99%

Multi-omic landscape of rheumatoid arthritis: re-evaluation of drug adverse effects

Tieri

Zhou

Zhu

et al. 2014

Front. Cell Dev. Biol.

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“…After controlling for a variety of confounding factors, including RA status, age, gender, education,114 smoking,111 115 alcohol consumption and body mass index (BMI), only RA status and age predict periodontal disease 114. In addition, patients with RA who receive treatment for periodontal disease show improvements in RA with concomitant decreases in APCAs, anti- P. gingivalis antibodies,116 and proinflammatory cytokines such as TNF-α 117…”

Section: Rheumatoid Arthritismentioning

confidence: 99%

Does the microbiota play a role in the pathogenesis of autoimmune diseases?

McLean

Dieguez

Miller

et al. 2014

Gut

184

112

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The microbiota of the human metaorganism is not a mere bystander. These microbes have coevolved with us and are pivotal to normal development and homoeostasis. Dysbiosis of the GI microbiota is associated with many disease susceptibilities, including obesity, malignancy, liver disease and GI pathology such as IBD. It is clear that there is direct and indirect crosstalk between this microbial community and host immune response. However, the precise mechanism of this microbial influence in disease pathogenesis remains elusive and is now a major research focus. There is emerging literature on the role of the microbiota in the pathogenesis of autoimmune disease, with clear and increasing evidence that changes in the microbiota are associated with some of these diseases. Examples include type 1 diabetes, coeliac disease and rheumatoid arthritis, and these contribute significantly to global morbidity and mortality. Understanding the role of the microbiota in autoimmune diseases may offer novel insight into factors that initiate and drive disease progression, stratify patient risk for complications and ultimately deliver new therapeutic strategies. This review summarises the current status on the role of the microbiota in autoimmune diseases.

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“…Observou-se que o grupo de indivíduos que receberam TP apresentou diminuição significativa na média DAS28 e na sorologia para TNF-α, em comparação àqueles pacientes que não foram tratados periodontalmente, embora a redução na média de ESR foi insignificante. 44 , realizaram a avaliação dos efeitos da terapia periodontal não-cirúrgica na evolução da artrite reumatoide com um aprimoramento metodológico. Esse autores utilizaram parâmetros periodontais e reumatológicos, bem como níveis séricos de citocinas e marcadores inflamatórios como citrulina e imunoglobulina (IG) G para Porphyromonas gingivalis no início do estudo e 8 semanas após a TP.…”

Section: Perda óSsea Inflamatória Na Artrite Reumatoide E Na Periodonunclassified

Efeito Da Terapia Periodontal Não Cirúrgica Na Redução Da Severidade Da Artrite Reumatoide

Sousa¹,

Figueiredo²,

Guimarães³

2017

RevBahianaOdonto

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A remodelação óssea é um processo contínuo que depende da atuação equilibrada entre osteoclastos e osteoblastos, responsáveis pela reabsorção e formação óssea, respectivamente. Situações inflamatórias persistentes podem alterar este processo, como a artrite reumatoide (AR) e a periodontite crônica. A patogênese destas duas doenças está associada às alterações nos níveis de mediadores inflamatórios que leva a um desequilíbrio imunológico associado à perda óssea. Estudos têm sugerido que tais doenças são bidirecionais, onde a presença de uma influencia a evolução da outra. Esse trabalho revisa os resultados de estudos de pesquisas científicas sobre o efeito da terapia periodontal não cirúrgica (TP) na redução da gravidade da AR. Para tanto, foi realizada uma busca por artigos científicos publicados a partir do ano 2006, no banco de dados PubMed, utilizando-se as palavras chaves: artrite reumatoide, periodontite e tratamento periodontal, nos idiomas inglês/português. Foram selecionados nove estudos com metodologia de pesquisa semelhante e que compuseram amostras de pacientes acometidos pelas duas doenças. Parâmetros como índice de sangramento gengival, profundidade de sondagem, sangramento à sondagem ou nível clínico de inserção avaliaram a condição periodontal de cada paciente, enquanto que questionários averiguando a qualidade de vida dos pacientes e os testes laboratoriais relacionados à atividade inflamatória sistêmica foram considerados parâmetros associados à severidade da artrite reumatoide. Em oito estudos, a TP reduziu significamente severidade inflamatória da AR. Assim, os últimos dados científicos indicam o benefício da realização do TP ao reduzir a gravidade da AR, considerando, ainda a facilidade e baixo custo deste tipo de terapia.

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Periodontal Treatment Decreases Levels of Antibodies to Porphyromonas gingivalis and Citrulline in Patients With Rheumatoid Arthritis and Periodontitis

Abstract: These results suggest that supragingival scaling decreases DAS28-CRP and serum levels of IgG to P. gingivalis HBP35 and citrulline in patients with RA. These observations may reflect a role of P. gingivalis in the protein citrullination, which is related to the pathogenesis of RA.

Cited by 117 publications

References 46 publications

Multi-omic landscape of rheumatoid arthritis: re-evaluation of drug adverse effects

Multi-omic landscape of rheumatoid arthritis: re-evaluation of drug adverse effects

Does the microbiota play a role in the pathogenesis of autoimmune diseases?

Efeito Da Terapia Periodontal Não Cirúrgica Na Redução Da Severidade Da Artrite Reumatoide

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