Detection of oral bacterial <scp>DNA</scp> in synovial fluid

Reichert, Stefan; Haffner, Maximilian; Keyßer, Gernot; Schäfer, Christoph; Stein, J.; Schaller, Hans-Guenter; Wienke, Andreas; STRAUSS, H; Heide, S.; Schulz, Susanne

doi:10.1111/jcpe.12102

Cited by 97 publications

(93 citation statements)

References 46 publications

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“…Moreover, P. gingivalis -derived LPS was also detected in the brains of AD patients (Poole, et al, 2013). It is accepted that periodontal bacteria can be found at distant sites (Cavrini, et al, 2005, Haraszthy, et al, 2000, Okuda, et al, 2001, Reichert, et al, 2013). These data indicate that peripheral inflammation/infections can lead to infection/inflammation in the brain and promote amyloid accumulation.…”

Section: Discussionmentioning

confidence: 99%

Periodontal disease associates with higher brain amyloid load in normal elderly

Kamer¹,

Pirraglia²,

Tsui³

et al. 2015

Neurobiology of Aging

202

150

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Background The accumulation of amyloid β plaques (Aβ) is a central feature of Alzheimer’s disease (AD). First reported in animal models, it remains uncertain if peripheral inflammatory/infectious conditions in humans can promote Aβ brain accumulation. Periodontal disease, a common chronic infection, has been previously reported to be associated with AD. Methods Thirty-eight cognitively normal, healthy, community residing elderly (mean age 61; 68% female) were examined in an Alzheimer’s Disease research center and a University-based Dental School. Linear regression models (adjusted for age, ApoE and smoking) were used to test the hypothesis that periodontal disease assessed by clinical attachment loss was associated with brain Aβ load using 11C-PIB PET imaging. Results After adjusting for confounders, clinical attachment loss (≥ 3mm), representing a history of periodontal inflammatory/infectious burden, was associated with increased 11C-PIB uptake in Aβ vulnerable brain regions (p=0.002). Conclusion We show for the first time in humans an association between periodontal disease and brain Aβ load. These data are consistent with prior animal studies showing that peripheral inflammation/infections are sufficient to produce brain Aβ accumulations.

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Section: Discussionmentioning

confidence: 99%

Periodontal disease associates with higher brain amyloid load in normal elderly

Kamer¹,

Pirraglia²,

Tsui³

et al. 2015

Neurobiology of Aging

202

150

View full text Add to dashboard Cite

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“…A growing body of evidence has implicated periodontal pathogens in the development and progression of RA (de Pablo, Chapple, Buckley, & Dietrich, ). Interestingly, increased antibody titers against P. gingivalis (Mikuls et al., ) and the DNA of oral bacterial, including P. gingivalis, have been detected in the serum and synovial fluid of RA patients (Martinez‐Martinez et al., ; Moen et al., ; Reichert et al., ). Case‐control studies found a more prevalent and severe periodontal disease (PD) status in RA patients (Al‐Shammari, Al‐Khabbaz, Al‐Ansari, Neiva, & Wang, ; Bozkurt, Yetkin Ay, Berker, Tepe, & Akkus, ), as well as a reduction in the clinical parameters of active RA following effective periodontal treatment and control of periodontal infection (Al‐Katma, Bissada, Bordeaux, Sue, & Askari, ; Bıyıkoğlu et al., ; Ortiz et al., ).…”

Section: Introductionmentioning

confidence: 99%

The aggravation of arthritis by periodontitis is dependent of IL‐17 receptor A activation

Aquino

Talbot

Sônego

et al. 2017

J Clinic Periodontology

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“…P. gingivalis DNA was significantly more likely to be found in the synovial fluid of patients with RA than in controls (116), and interestingly the severity of periodontal disease (quantified by the number of missing teeth) in patients with RA was positively correlated with the number of affected joints. However, another study found only an association between P. gingivalis and the likelihood of developing and severity of periodontitis but no association with RA (117), and a third study found that P. gingivalis was more abundant in the oral cavity of controls compared to cases (113).…”

Section: Musculoskeletalmentioning

confidence: 99%

Clinical Evidence for the Microbiome in Inflammatory Diseases

et al. 2017

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Clinical evidence is accumulating for a role of the microbiome in contributing to or modulating severity of inflammatory diseases. These studies can be organized by various organ systems involved, as well as type of study approach utilized, whether investigators compared the microbiome of cases versus controls, followed patients longitudinally, or intervened with antibiotics, prebiotics, or bacterial introduction. In this review, we summarize the clinical evidence supporting the microbiome as an important mechanism in the onset and maintenance of inflammation.

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Detection of oral bacterial DNA in synovial fluid

Abstract: DNA of periodontopathogens can be found in synovial fluid and oral bacteria may play a role in the pathogenesis of arthritis.

Cited by 97 publications

References 46 publications

Periodontal disease associates with higher brain amyloid load in normal elderly

Periodontal disease associates with higher brain amyloid load in normal elderly

The aggravation of arthritis by periodontitis is dependent of IL‐17 receptor A activation

Clinical Evidence for the Microbiome in Inflammatory Diseases

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