Relationship Between Rheumatoid Arthritis and Periodontitis

Mercado, Faustino; Marshall, R. I.; Klestov, A.; Bartold, P. Mark

doi:10.1902/jop.2001.72.6.779

Cited by 371 publications

(406 citation statements)

References 39 publications

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“…Indeed, RA can increase the incidence and severity of PD (independently or only partially dependent) of oral hygiene status or modifying factors. [4][5][6][7]15,16,35 Accordingly, our results show that PIA increase the severity of ePD in AIRmax mice strain, whereas in AIRmin strain (resistant to PIA development), [25][26][27][28] the severity of ePD was not altered by pristane injection, showing that the development of PIA, and not the pristane injection, is involved in the modulation of ePD severity. Similarly, adjuvant-induced arthritis in rats also results in signs of periodontal destruction.…”

Section: Discussionmentioning

confidence: 65%

“…[1][2][3] Results from clinical studies point toward a co-morbidity association between chronic periodontitis (PD) and systemic rheumatic diseases, in particular rheumatoid arthritis (RA), described to increase the incidence and/or severity of PD, a chronic infectious inflammatory disease that leads to the destruction of the teeth attachment structures. [4][5][6][7] Chronic PD is the most prevalent chronic inflammatory disease in human beings, in which bacterial species that hosts periodontal biofilm trigger inflammatory and immune responses involved in tissue damage. 8,9 RA is a chronic autoimmune inflammatory disease that possibly arise because of a failure in thymic selection or a peripheral tolerance (the early mechanisms by which immune tolerance is breached and the subsequent event that triggers articular localization is poorly defined), characterized by persistent synovial inflammation and progressive destruction of cartilage and bone in the joints.…”

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: Discussionmentioning

confidence: 65%

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

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“…There is considerable evidence that the clinical impact of periodontal disease extends beyond the oral cavity (2). Strong associations have been found between periodontitis and a number of systemic conditions, including cardiovascular disease (3,4), preterm delivery and low-birth-weight babies (5), diabetes mellitus (6)(7)(8), and rheumatoid arthritis (9)(10)(11).…”

mentioning

confidence: 99%

Dysbiosis and Alterations in Predicted Functions of the Subgingival Microbiome in Chronic Periodontitis

Kirst

Alfant

et al. 2015

Appl Environ Microbiol

191

188

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Chronic periodontitis is an inflammatory disease of the periodontium affecting nearly 65 million adults in the United States. Changes in subgingival microbiota have long been associated with chronic periodontitis. Recent culture-independent molecular studies have revealed the immense richness and complexity of oral microbial communities. However, data sets across studies have not been directly compared, and whether the observed microbial variations are consistent across different studies is not known. Here, we used 16S rRNA sequencing to survey the subgingival microbiota in 25 subjects with chronic periodontal disease and 25 healthy controls and compared our data sets with those of three previously reported microbiome studies. Consistent with data from previous studies, our results demonstrate a significantly altered microbial community structure with decreased heterogeneity in periodontal disease. Comparison with data from three previously reported studies revealed that subgingival microbiota clustered by study. However, differences between periodontal health and disease were larger than the technical variations across studies. Using a prediction score and applying five different distance metrics, we observed two predominant clusters. One cluster was driven by Fusobacterium and Porphyromonas and was associated with clinically apparent periodontitis, and the second cluster was dominated by Rothia and Streptococcus in the majority of healthy sites. The predicted functional capabilities of the periodontitis microbiome were significantly altered. Genes involved in bacterial motility, energy metabolism, and lipopolysaccharide biosynthesis were overrepresented in periodontal disease, whereas genes associated with transporters, the phosphotransferase system, transcription factors, amino acid biosynthesis, and glycolysis/gluconeogenesis were enriched in healthy controls. These results demonstrate significant alterations in microbial composition and function in periodontitis and suggest genes and metabolic pathways associated with periodontal disease. P eriodontal disease is a common disease affecting many adults in the United States. If left untreated, chronic periodontitis (CP) can lead to serious problems such as tooth loss. Indeed, periodontal disease is the number one cause of tooth loss in the United States, accounting for half of all tooth loss in U.S. adults (1). There is considerable evidence that the clinical impact of periodontal disease extends beyond the oral cavity (2). Strong associations have been found between periodontitis and a number of systemic conditions, including cardiovascular disease (3, 4), preterm delivery and low-birth-weight babies (5), diabetes mellitus (6-8), and rheumatoid arthritis (9-11).The activity of periodontal disease is determined by a complex interplay between the immune system and periodontal pathogens (12, 13). Alterations in subgingival microbiota have long been associated with the development and progression of periodontitis (14). In susceptible individuals, perturbations in...

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“…Participants with RA had significant more missing teeth than participants without RA. Comparing periodontal status in 65 RA patients (according to the ACR criteria 1987) with an age-and gender-matched control group (age range 20e70 years) without RA, Mercado et al [42] found that individuals with RA are more likely to experience more periodontal disease (OR 2.2) compared to individuals without RA. Individuals in the RA group showed significant more missing teeth compared to the non-RA group, an observation that confirms previous findings [43,44].…”

Section: The Bradford Hill Approachmentioning

confidence: 99%

Rheumatoid arthritis and periodontitis; a possible link via citrullination

et al. 2011

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a b s t r a c tRheumatoid Arthritis (RA) and chronic and aggressive periodontitis are chronic inflammatory disorders characterized by deregulation of the host inflammatory response. Increased secretion of pro-inflammatory mediators results in soft and hard tissue destruction of the synovium and periodontium respectively. Both diseases share risk factors and have pathological pathways in common, resulting in loss of function and disability as a final clinical outcome. This article discusses possible interactions, particularly related to the periodontal pathogen Porphyromonas gingivalis, which could explain the observed association between these two prevalent diseases.

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Relationship Between Rheumatoid Arthritis and Periodontitis

Abstract: The results of this study provide further evidence of a significant association between periodontitis and rheumatoid arthritis. This association may be a reflection of a common underlying disregulation of the inflammatory response in these individuals.

Cited by 371 publications

References 39 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

Dysbiosis and Alterations in Predicted Functions of the Subgingival Microbiome in Chronic Periodontitis

Rheumatoid arthritis and periodontitis; a possible link via citrullination

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