Toll-Like Receptor-2 Plays a Fundamental Role in Periodontal Bacteria-Accelerated Abdominal Aortic Aneurysms

Aoyama, Norio; Suzuki, Jun–ichi; Ogawa, Masahito; Watanabe, Ryoji; Kobayashi, Naho; Hanatani, Tomoya; Ashigaki, Norihiko; Sekinishi, Asuka; Izumi, Yuichi; Isobe, Mitsuaki

doi:10.1253/circj.cj-12-1191

Cited by 35 publications

(40 citation statements)

References 43 publications

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“…The main sources of the inflammatory cytokines TNF and IL-1, in response to stimulatory bacterial molecules which are recognized by pattern-recognition receptors (PRR), are neutrophils and monocytes/macrophages (see Glossary) [38]. These phagocytic cells express innate immune receptors Toll-like receptor 2 (TLR2), C3aR and C5aR at high levels and mice lacking these proteins exhibit reduction of alveolar bone loss in experimental periodontitis models [39–42]. C3aR and C5aR are the receptors for processed complement factors that are produced through activation of bacteria-stimulated classical and alternative complement pathways as well as the lectin-dependent pathway [28].…”

Section: Induction Of Inflammatory Responses Results In Alveolar Bonementioning

confidence: 99%

Emerging roles of immunostimulatory oral bacteria in periodontitis development

Jiao

Hasegawa

Inohara

2014

Trends in Microbiology

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Periodontitis is a common dental disease which results in irreversible alveolar bone loss around teeth, and subsequent tooth loss. Previous studies have focused on bacteria that damage the host and the roles of commensals to facilitate their colonization. Although some immune responses targeting oral bacteria protect the host from alveolar bone loss, recent studies show that particular host defense responses to oral bacteria can induce alveolar bone loss. Host damaging and immunostimulatory oral bacteria cooperatively induce bone loss by inducing gingival damage followed by immunostimulation. In mouse models of experimental periodontitis induced by either Porphyromonas gingivalis or ligature, γ-proteobacteria accumulate and stimulate host immune responses to induce host damage. Here we review the differential roles of individual bacterial groups in promoting bone loss through the induction of host damage and immunostimulation.

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Section: Induction Of Inflammatory Responses Results In Alveolar Bonementioning

confidence: 99%

Emerging roles of immunostimulatory oral bacteria in periodontitis development

Jiao

Hasegawa

Inohara

2014

Trends in Microbiology

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“…Periodontal disease has been reported as a significant independent risk factor for BD mainly due to transit bacteremia, either directly through their cytotoxicity or indirectly by inducing or exacerbating inflammation (14, 15). The oral cavity represents a potentially large reservoir of Gram-negative bacteria that are responsible for periodontal disease.…”

Section: Resultsmentioning

confidence: 99%

Periodontitis and Buerger's Disease: Recent Advances

Pavlić¹,

Vujić-Aleksić²,

Zubović³

et al. 2013

Acta Inform Med

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Buerger’s disease (BD) is a relatively rare thrombotic, occlusive and non-atherosclerotic clinical syndrome of unknown etiology. In recent years, numerous epidemiological studies confirmed the strong association between chronic anaerobic periodontal infection and development of cardiovascular diseases, including BD. Therefore, the aim of this study is to clarify association between periodontal pathogens and Buerger’s disease. Confirmation of presence and identification of periopathogens in patients with BD can be considered crucial in developing novel therapies for BD. Further, periodontal therapy will lead to eventual improvement of BD patients’ condition.

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“…1) Recently, we demonstrated that P. gingivalis deteriorated AAA [8][9][10] and wire-injury induced arteriosclerosis 14) in animal models. Furthermore, we demonstrated that A. actinomycetemcomitans aggravated ventricular remodeling after myocardial ischemia 15) and pressure overload-induced myocardial hypertrophy.…”

Section: Discussionmentioning

confidence: 99%

“…8) We clarifi ed that P. gingivalis affected AAA progression through toll-like receptors (TLRs) and matrix metalloproteinases (MMPs). [8][9][10] P. intermedia is also known to be an important periodontal pathogen in cardiovascular diseases. 11) However, the clinical infl uence of specifi c periodontal bacterium on AAA has not been investigated.…”

mentioning

confidence: 99%

High Incidence of Periodontitis in Japanese Patients With Abdominal Aortic Aneurysm

et al. 2014

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SummaryPeriodontitis is known to be a risk factor for abdominal aortic aneurysm (AAA). However, the infl uence of periodontitis on AAA in Japanese patients has not yet been elucidated. The aim of this clinical investigation was to assess the relationship between periodontal bacterial burden in AAA patients.We studied 12 AAA patients and 24 age-and sex-matched non-AAA cardiovascular patients. We examined periodontitis and the presence of the periodontal pathogens Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, and Prevotella intermedia in oral samples using polymerase chain reaction assays.We found that the AAA patients had deeper pocket depth compared to the non-AAA patients (3.53 ± 0.38 mm versus 2.67 ± 0.17 mm, P < 0.05). However, the populations of periodontal bacteria were comparable between the two groups. Periodontitis may have a greater effect on aneurysm progression compared to other cardiovascular diseases. (Int Heart J 2014; 55: 268-270)

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Toll-Like Receptor-2 Plays a Fundamental Role in Periodontal Bacteria-Accelerated Abdominal Aortic Aneurysms

Cited by 35 publications

References 43 publications

Emerging roles of immunostimulatory oral bacteria in periodontitis development

Emerging roles of immunostimulatory oral bacteria in periodontitis development

Periodontitis and Buerger's Disease: Recent Advances

High Incidence of Periodontitis in Japanese Patients With Abdominal Aortic Aneurysm

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