Effects of periodontal treatment on inflammation and oxidative stress markers in patients with metabolic syndrome

Torumtay, Gizem; Kırzıoğlu, Fatma Yeşim; Tonguç, Mine Öztürk; Kale, Banu; Calapoğlu, Mustafa; Orhan, Hikmet

doi:10.1111/jre.12328

Cited by 47 publications

(34 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…First, periodontal inflammatory conditions are associated with elevated systemic inflammation, which can in turn contribute to the development of MetS (Lee & Pratley, ; Montebugnoli et al., ). Second, periodontal disease is also known to be associated with increased oxidative stress (Torumtay et al., ). The presence of oxidative stress may alter the intracellular signalling pathway inducing insulin resistance, which result in a risk factor for MetS (Ceriello & Motz, ).…”

Section: Discussionmentioning

confidence: 99%

Relationship of toothbrushing to metabolic syndrome in middle‐aged adults

Tanaka

Takeuchi

Furuta

et al. 2018

J Clinic Periodontology

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Relationship of toothbrushing to metabolic syndrome in middle‐aged adults

Tanaka

Takeuchi

Furuta

et al. 2018

J Clinic Periodontology

View full text Add to dashboard Cite

show abstract

“…, Torumtay et al. ). Also to be noted in examining host responses in periodontitis is the clear role of adaptive immunity, and particularly humoral immune responses in the development of, or protection from, periodontitis (Ebersole et al.…”

Section: Discussionmentioning

confidence: 99%

Integrated biomarker profiling of smokers with periodontitis

Nagarajan

Al‐Sabbagh

Dawson

et al. 2017

J Clinic Periodontology

View full text Add to dashboard Cite

In the context of precision medicine, understanding patient-specific variation is an important step in developing targeted and patient-tailored treatment regimens for periodontitis. While several studies have successfully demonstrated the usefulness of molecular expression profiling in conjunction with single classifier systems in discerning distinct disease groups, the majority of these studies do not provide sufficient insights into potential variations within the disease groups. Aim The goal of the present study is to discern biological response profiles of periodontitis and non-periodontitis smoking subjects using an informed panel of biomarkers across multiple scales (salivary, oral microbiome, pathogens and other markers). Materials and Methods The investigation uses a novel ensemble classification approach (SVA-SVM) to differentiate disease groups and patient-specific biological variation of systemic inflammatory mediators and IgG antibody to oral commensal and pathogenic bacteria within the groups. Results Sensitivity of SVA-SVM is shown to be considerably higher than several traditional independent classifier systems. Patient-specific networks generated from SVA-SVM are also shown to reveal cross-talk between biomarkers in discerning the disease groups. High-confidence classifiers in these network abstractions comprised of host responses to microbial infection elucidated their critical role in discerning the disease groups. Conclusions Host adaptive immune responses to the oral colonization/infection contribute significantly to creating the profiles specific for periodontitis patients with potential to assist in defining patient-specific risk profiles and tailored interventions.

show abstract

“…Moreover, as differing from the upregulation of GPR40 by hyperlipidemia and hyperglycemia, it has been reported that CD36 expression is upregulated by proinflammatory cytokines such as IL‐1β, macrophage colony‐stimulating factor and granulocyte‐macrophage colony‐stimulating factor . Since proinflammatory cytokines in periodontal tissue are increased in patients with MetS, it is possible that CD36 is upregulated in periodontal tissues by increased proinflammatory cytokines. Our in vitro study showed that GPR40 and CD36 were upregulated by the palmitate and LPS, supporting the roles of dyslipidemia and inflammation in the upregulation of GPR40 and CD36 expression.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of free fatty acid receptors in periodontal tissues of patients with metabolic syndrome and periodontitis

Robles

et al. 2018

J of Periodontal Research

View full text Add to dashboard Cite

Background and objective Metabolic syndrome (MetS) exacerbates periodontitis. Since saturated fatty acid (SFA) is increased in MetS and enhances lipopolysaccharide (LPS)‐induced proinflammatory cytokine expression in macrophages, it has been considered to play a role in MetS‐exacerbated periodontitis. However, it remains unknown how fatty acid receptors, which mediate the interaction of cells with SFA and uptake of SFA, are expressed and regulated in the periodontal tissue. In this study, we tested our hypothesis that the periodontal expression of fatty acid receptors GPR40 and CD36 is increased in patients with both MetS and periodontitis. We also determined the effect of SFA and LPS on GPR40 and CD36 expression in vitro. Material and methods Periodontal tissue specimens were collected from 11 participants without MetS and periodontitis, 12 participants with MetS, 11 participants with periodontitis, and 14 participants with both MetS and periodontitis after surgeries. The tissues were processed, and GPR40 and CD36 were detected by immunohistochemistry. Furthermore, cultured macrophages and gingival fibroblasts were treated with LPS, palmitate, a major SFA, or LPS plus palmitate and the expression of GPR40 and CD36 was then quantified. Results Analysis of clinical data showed that age, smoker, gender, and race/ethnicity were not significantly different among 4 groups. Immunohistochemistry showed that GPR40 and CD36 were expressed by epithelial cells, fibroblasts, and immune cells. Quantitative data showed that GPR40 expression is increased in patients with periodontitis, MetS, or both periodontitis and MetS while CD36 expression is increased only in patients with both periodontitis and MetS. The in vitro studies showed that the expression of GPR40 and CD36 in macrophages and fibroblasts was upregulated by the combination of LPS and palmitate. Conclusion Periodontal expression of GPR40 and CD36 was upregulated in patients with both MetS and periodontitis, and GPR40 and CD36 in macrophages and fibroblasts were upregulated in vitro by the combination of LPS and palmitate, suggesting that GPR40 and CD36 may be involved in MetS‐exacerbated periodontitis.

show abstract

Effects of periodontal treatment on inflammation and oxidative stress markers in patients with metabolic syndrome

Cited by 47 publications

References 54 publications

Relationship of toothbrushing to metabolic syndrome in middle‐aged adults

Relationship of toothbrushing to metabolic syndrome in middle‐aged adults

Integrated biomarker profiling of smokers with periodontitis

Upregulation of free fatty acid receptors in periodontal tissues of patients with metabolic syndrome and periodontitis

Contact Info

Product

Resources

About