Gingival Inflammation and Interleukin‐1 β and Tumor Necrosis Factor‐Alpha Levels in Gingival Crevicular Fluid During the Menstrual Cycle

Başer, Ülkü; Çekici, Ali; Tanrıkulu-Küçük, Sevda; Kantarcı, Alpdoğan; Ademoğlu, Evin; Yalçın, Funda

doi:10.1902/jop.2009.090076

Cited by 44 publications

(73 citation statements)

References 23 publications

(49 reference statements)

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“…Some studies hypothesized that estrogen therapy may be used in these periodontal pathologies [45]. However, this therapeutic strategy would be not applicable in gingivitis because it is spontaneously reversed after gingival plaque removing and/or menstrual cycle normalization [46]. Conversely, estrogen deficiency is considered a risk factor for periodontitis [19].…”

Section: Discussionmentioning

confidence: 99%

High-Fat Diet Induces Periodontitis in Mice through Lipopolysaccharides (LPS) Receptor Signaling: Protective Action of Estrogens

et al. 2012

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BackgroundA fat-enriched diet favors the development of gram negative bacteria in the intestine which is linked to the occurrence of type 2 diabetes (T2D). Interestingly, some pathogenic gram negative bacteria are commonly associated with the development of periodontitis which, like T2D, is characterized by a chronic low-grade inflammation. Moreover, estrogens have been shown to regulate glucose homeostasis via an LPS receptor dependent immune-modulation. In this study, we evaluated whether diet-induced metabolic disease would favor the development of periodontitis in mice. In addition, the regulatory role of estrogens in this process was assessed.MethodsFour-week-old C57BL6/J WT and CD14 (part of the TLR-4 machinery for LPS-recognition) knock-out female mice were ovariectomised and subcutaneously implanted with pellets releasing either placebo or 17β-estradiol (E2). Mice were then fed with either a normal chow or a high-fat diet for four weeks. The development of diabetes was monitored by an intraperitoneal glucose-tolerance test and plasma insulin concentration while periodontitis was assessed by identification of pathogens, quantification of periodontal soft tissue inflammation and alveolar bone loss.ResultsThe fat-enriched diet increased the prevalence of periodontal pathogenic microbiota like Fusobacterium nucleatum and Prevotella intermedia, gingival inflammation and alveolar bone loss. E2 treatment prevented this effect and CD14 knock-out mice resisted high-fat diet-induced periodontal defects.Conclusions/SignificanceOur data show that mice fed with a diabetogenic diet developed defects and microflora of tooth supporting-tissues typically associated with periodontitis. Moreover, our results suggest a causal link between the activation of the LPS pathway on innate immunity by periodontal microbiota and HFD-induced periodontitis, a pathophysiological mechanism that could be targeted by estrogens.

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Section: Discussionmentioning

confidence: 99%

High-Fat Diet Induces Periodontitis in Mice through Lipopolysaccharides (LPS) Receptor Signaling: Protective Action of Estrogens

et al. 2012

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“…It could also be argued that hormonal fluctuations, which were not monitored, may have influenced the results [38, 39]. While this is a possibility, the fact that all subjects had a similar systemic response to dental plaque suggests that such a variation was not a major factor in the present study.…”

Section: Discussionmentioning

confidence: 89%

Local and Systemic Inflammatory Responses to Experimentally Induced Gingivitis

2013

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This study profiled the local and systemic inflammatory responses to experimentally induced gingivitis. Eight females participated in a 21-day experimental gingivitis model followed by a 14-day resolution phase. Bleeding on probing and plaque index scores were assessed before, during, and after resolution of gingival inflammation, and samples of saliva, GCF, and plasma were collected. Samples were assessed for biomarkers of inflammation using the BioPlex platform and ELISA. There were no significant changes in GCF levels of cytokines during the experimental phase; however, individual variability in cytokine profiles was noted. During resolution, mean GCF levels of IL-2, IL-6, and TNF-α decreased and were significantly lower than baseline levels (P = 0.003, P = 0.025, and P = 0.007, resp.). Furthermore, changes in GCF levels of IL-2, IL-6, and TNF-α during resolution correlated with changes in plaque index scores (r = 0.88, P = 0.004; r = 0.72, P = 0.042; r = 0.79, P = 0.019, resp.). Plasma levels of sICAM-1 increased significantly during the experimental phase (P = 0.002) and remained elevated and significantly higher than baseline levels during resolution (P < 0.001). These results support the concept that gingivitis adds to the systemic inflammatory burden of an individual.

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“…Animal studies in mice have reported that subcutaneous infection of P. gingivalis, with the chamber model, increases maternal TNF-a and enhances adverse pregnancy outcomes (Collins et al 1994, Lin et al 2003. In non-pregnant women with low standardized PlI scores, Baser et al (2009) did not observed changes in TNF-a levels in the GCF throughout menstrual cycle stages. In non-pregnant women with low standardized PlI scores, Baser et al (2009) did not observed changes in TNF-a levels in the GCF throughout menstrual cycle stages.…”

Section: Gingival Index Exhaustive Chaid Analysismentioning

confidence: 97%

Gingival changes during pregnancy: III. Impact of clinical, microbiological, immunological and socio‐demographic factors on gingival inflammation

Albornoz

Figuero

Herrera

et al. 2011

J Clinic Periodontology

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Gingival Inflammation and Interleukin‐1 β and Tumor Necrosis Factor‐Alpha Levels in Gingival Crevicular Fluid During the Menstrual Cycle

Abstract: These results demonstrate that the fluctuation of sex steroid hormones impact gingival inflammation during menstruation.

Cited by 44 publications

References 23 publications

High-Fat Diet Induces Periodontitis in Mice through Lipopolysaccharides (LPS) Receptor Signaling: Protective Action of Estrogens

High-Fat Diet Induces Periodontitis in Mice through Lipopolysaccharides (LPS) Receptor Signaling: Protective Action of Estrogens

Local and Systemic Inflammatory Responses to Experimentally Induced Gingivitis

Gingival changes during pregnancy: III. Impact of clinical, microbiological, immunological and socio‐demographic factors on gingival inflammation

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