Immunoregulatory control of Th1/Th2 cytokine profiles in periodontal disease

Gemmell, E.; Seymour, G. J.

doi:10.1111/j.0906-6713.2004.003557.x

Cited by 218 publications

(265 citation statements)

References 205 publications

(242 reference statements)

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“…1,2 Pathogenic bacteria constitute the primary extrinsic agent in the aetiology of AgP; however, the risk of developing periodontal disease is not the same for all individuals, suggesting that host factors are involved in determining susceptibility to the disease. 3,4 The role of genes and their variants in determining the host response in both 'chronic' and 'aggressive' forms of periodontitis, as well as in the progression of the disease, has been largely investigated.…”

Section: Introductionmentioning

confidence: 99%

Gene–gene interaction among cytokine polymorphisms influence susceptibility to aggressive periodontitis

et al. 2011

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Aggressive periodontitis (AgP) is a multifactorial disease. The distinctive aspect of periodontitis is that this disease must deal with a large number of genes interacting with one another and forming complex networks. Thus, it is reasonable to expect that gene-gene interaction may have a crucial role. Therefore, we carried out a pilot case-control study to identify the association of candidate epistatic interactions between genetic risk factors and susceptibility to AgP, by using both conventional parametric analyses and a higher order interactions model, based on the nonparametric Multifactor Dimensionality Reduction algorithm. We analyzed 122 AgP patients and 246 appropriate periodontally healthy individuals, and genotyped 28 polymorphisms, located within 14 candidate genes, chosen among the principal genetic variants pointed out from literature and having a role in inflammation and immunity. Our analyses provided significant evidence for gene-gene interactions in the development of AgP, in particular, present results: (a) indicate a possible role of two new polymorphisms, within SEPS1 and TNFRSF1B genes, in determining host individual susceptibility to AgP; (b) confirm the potential association between of IL-6 and Fc g-receptor polymorphisms and the disease; (c) exclude an essential contribution of IL-1 cluster gene polymorphisms to AgP in our Caucasian-Italian population.

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Section: Introductionmentioning

confidence: 99%

Gene–gene interaction among cytokine polymorphisms influence susceptibility to aggressive periodontitis

et al. 2011

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“…In the oral cavity, immune-mediated destruction of the supporting tissues surrounding the dentition is a characteristic feature of chronic inflammatory periodontal disease, 3,4 one of the most prevalent of infectious diseases. The infectious component central to the etiology of periodontal disease entails colonization of the oral niche with Gram-negative bacteria, including Porphyromonas gingivalis, a nonspore forming, nonmotile, obligate anaerobe strongly implicated in the pathogenic sequelae.…”

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confidence: 99%

Rapid Myeloid Cell Transcriptional and Proteomic Responses to Periodontopathogenic Porphyromonas gingivalis

Nares

Moutsopoulos

Angelov

et al. 2009

The American Journal of Pathology

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Long-lived monocytes, macrophages, and dendritic cells (DCs) are Toll-like receptor-expressing, antigenpresenting cells derived from a common myeloid lineage that play key roles in innate and adaptive immune responses. Based on immunohistochemical and molecular analyses of inflamed tissues from patients with chronic destructive periodontal disease, these cells, found in the inflammatory infiltrate, may drive the progressive periodontal pathogenesis. To investigate early transcriptional signatures and subsequent proteomic responses to the periodontal pathogen, Porphyromonas gingivalis, donor-matched human blood monocytes, differentiated DCs, and macrophages were exposed to P. gingivalis lipopolysaccharide (LPS) and gene expression levels were measured by oligonucleotide microarrays. In addition to striking differences in constitutive transcriptional profiles between these myeloid populations, we identify a P. gingivalis LPS-inducible convergent, transcriptional core response of more than 400 annotated genes/ESTs among these populations, reflected by a shared, but quantitatively distinct, proteomic response. Nonetheless, clear differences emerged between the monocytes, DCs, and macrophages. The finding that long-lived myeloid inflammatory cells, particularly DCs, rapidly and aggressively respond to P. gingivalis LPS by generating chemokines, proteases, and cytokines capable of driving T-helper cell lineage polarization without evidence of corresponding immunosuppressive pathways highlights their prominent role in host defense and progressive tissue pathogenesis. The shared, unique, and/or complementary transcriptional and proteomic profiles may frame the context of the host response to P. gingivalis, contributing to the destructive nature of periodontal inflammation.

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“…Despite the fact that the majority of cases are well controlled by conventional periodontal therapy, some cases are still a therapeutic challenge particularly because we do not know how some mild forms of periodontal disease evolve into more severe forms 2 . Diabetes Mellitus is a metabolic disease characterized by hyperglycemia due to deficient insulin production type 1 or type 2, that is preceded by systemic inflammation, leading to reduced pancreatic β-cell function, apoptosis and insulin resistence 3 , the latter being more prevalent in adults.…”

Section: Introductionmentioning

confidence: 99%

Glycemic control and the production of cytokines in diabetic patients with chronic periodontal disease

Franco

Moraes

Duarte

et al. 2017

RGO, Rev. Gaúch. Odontol.

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ObjectiveTo evaluate the association of glycemic control and cytokine production in type 2 diabetic subjects with chronic periodontitis Methods Gingival biopsies were performed in 40 patients, divided into four groups: systemically healthy subjects without periodontal disease (S); systemically healthy patients with chronic periodontitis (P); patients with well-controlled type 2 diabetes mellitus (DM) with chronic periodontitis (C); poorly controlled type 2 diabetes mellitus with chronic periodontitis (D). The production of interleukin (IL) -4, -6, -10, -17 and interferon (IFN) -γ was quantified by ELISA. Results The production of IL-4, IL-10, IL-17 and INF-γ was higher on group D when compared to other groups (p <0.05), which in turn were similar (p ≥0.05). In addition, there was no difference in the production of IL-6 in any of the evaluated groups (p≥0.05). ConclusionWere observed significantly elevated levels of pro-inflammatory and anti-inflammatory cytokines in patients with poorly controlled type 2 diabetes and chronic periodontitis, demonstrating that glycemic control may be associated to the immune inflammatory response of sites with chronic periodontitis.

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Immunoregulatory control of Th1/Th2 cytokine profiles in periodontal disease

Cited by 218 publications

References 205 publications

Gene–gene interaction among cytokine polymorphisms influence susceptibility to aggressive periodontitis

Gene–gene interaction among cytokine polymorphisms influence susceptibility to aggressive periodontitis

Rapid Myeloid Cell Transcriptional and Proteomic Responses to Periodontopathogenic Porphyromonas gingivalis

Glycemic control and the production of cytokines in diabetic patients with chronic periodontal disease

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