Association between periodontitis and anti‐cardiolipin antibodies in Buerger disease

Chen, Yi-Wen; Nagasawa, Toshiyuki; Wara-aswapati, Nawarat; Ushida, Yuka; Wang, Dongqing; Takeuchi, Yasuo; Kobayashi, Hiroaki; Umeda, Makoto; Inoue, Yasuhiro; Iwai, Takehisa; Ishikawa, Isao; Izumi, Yuichi

doi:10.1111/j.1600-051x.2009.01467.x

Cited by 42 publications

(39 citation statements)

References 36 publications

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“…We have previously observed that GAgP patients demonstrate elevated levels of anti-phospholipid antibodies such as anti-phosphorylcholine and β2-glycoproteindependent anti-cardiolipin (aCL), and that GAgP patients with elevated aCL also demonstrate elevated systemic markers of vascular inflammation (Schenkein et al, 2003(Schenkein et al, , 2007. The sources of such antibodies are unknown; they may be genuine autoantibodies, or they may be produced via molecular mimicry following exposure to cross-reactive periodontal bacterial pathogens (Chen et al, 2007(Chen et al, , 2009). The involvement of such antibodies in the pathogenesis of AgP is also not known.…”

Section: Discussionmentioning

confidence: 99%

IL-17 in Sera from Patients with Aggressive Periodontitis

Schenkein¹,

Koertge²,

Brooks

et al. 2010

J Dent Res

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Interleukin-17 (IL-17), the prototype cytokine produced by the Th17 subset of T-helper cells, plays a role in inflammatory responses, autoimmunity, and antimicrobial responses in a variety of infectious and inflammatory diseases. In view of the inflammatory nature and severity of aggressive periodontitis, we hypothesized that IL-17 might be detected in sera from patients with aggressive periodontitis. We used ELISA to measure IL-17 serum concentrations from 67 periodontally healthy (NP) individuals and from 53 patients with localized (LAgP) and 49 patients with generalized (GAgP) aggressive periodontitis. IL-17 was barely detectable in sera from periodontally healthy individuals (1.9 ± 2.0 pg/mL), but was present at significantly higher concentrations in sera from those with LAgP (7.6 ± 2.2 pg/mL) and GAgP (17.1 ± 2.3 pg/mL). Multivariate analyses demonstrated associations of IL-17 concentrations with periodontal attachment loss, but not with current smoking. Therefore, Th17 responses may be characteristic of AgP, and IL-17 may play a role in the pathogenesis of aggressive periodontitis.

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Section: Discussionmentioning

confidence: 99%

IL-17 in Sera from Patients with Aggressive Periodontitis

Schenkein¹,

Koertge²,

Brooks

et al. 2010

J Dent Res

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“…Chen et al reported that molecular mimicry between TLRVYK peptides on β2GPI and periodontopathic bacteria was also associated with Buerger's disease [35].…”

Section: Molecular Mimicrymentioning

confidence: 99%

Host–microbial co-evolution in periodontitis associated with Aggregatibacter actinomycetemcomitans infection

Nagasawa

Shimizu

Kato

et al. 2014

Journal of Oral Biosciences

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“…They therefore argue that A. actinomycetemcomitans induces antibodies that mimic β2GPI. Additionally, this group has demonstrated a strong association between α-CL and periodontitis in individuals with the thrombotic Buerger's disease (Chen et al, 2009).…”

Section: Anti-cardiolipin (α-Cl)mentioning

confidence: 99%