Expression of periodontal interleukin-6 protein is increased across patients with neither periodontal disease nor diabetes, patients with periodontal disease alone and patients with both diseases

Ross, Jonathan H.; Hardy, D. C.; Schuyler, Corinne A.; Slate, Elizabeth H.; Mize, T. W.; Huang, Yan

doi:10.1111/j.1600-0765.2010.01286.x

Cited by 31 publications

(30 citation statements)

References 25 publications

(35 reference statements)

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“…An increase in periodontal interleukin‐6 protein levels in periodontal tissue across healthy patients to systemically healthy patients with periodontitis to patients with type 2 diabetes mellitus and periodontitis ( P = 0.006) was found by Ross et al. . Cytokine expression in gingival tissue from patients with type 1 diabetes mellitus and chronic periodontitis was also investigated by Duarte et al.…”

Section: Changes In the Periodontal Tissuesmentioning

confidence: 85%

“…Many studies have investigated the differences in cytokine profiles of gingival crevicular fluid or gingival tissue samples from patients with type 2 diabetes mellitus and periodontitis , whereas very few studies have analyzed the cytokine profiles in individuals with gingivitis and type 2 diabetes mellitus or type 1 diabetes mellitus and in individuals with type 1 diabetes mellitus and chronic periodontitis . The main sources and functions of these cytokines are summarized in Table .…”

Section: Alterations In Gingival Crevicular Fluidmentioning

confidence: 99%

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Local inflammatory reactions in patients with diabetes and periodontitis

Sonnenschein¹,

Meyle²

2015

Periodontology 2000

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The impact of diabetes mellitus on the prevalence, severity and progression of periodontal disease has been known for many years and intense efforts have been made to elucidate the underlying mechanisms. It is widely reported that hyperglycemia causes numerous systemic changes, including altered innate immune‐cell function and metabolic changes. The aim of this review was to summarize and discuss the evidence for mechanisms that probably play a role in the altered local inflammatory reactions in the periodontium of patients with diabetes, focusing on local changes in cytokine levels, matrix metalloproteinases, reactive oxygen species, advanced glycation end‐products, immune‐cell functions, the RANKL/osteoprotegerin axis and toll‐like receptors. Apart from the systemic effects of diabetes, recent evidence suggests that local changes in the periodontal tissues are characterized by enhanced interactions between leukocytes and endothelial cells and by altered leukocyte functions [resulting in increased levels of reactive oxygen species and of proinflammatory cytokines (interleukin‐1β, interleukin‐6 and tumor necrosis factor‐α)]. These local changes are amplified by the enhanced accumulation of advanced glycation end‐products and their interaction with receptors for advanced glycation end‐products. Furthermore, the increased levels of proinflammatory cytokines lead to an up‐regulation of RANKL in periodontal tissues, stimulating further periodontal tissue breakdown.

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Section: Changes In the Periodontal Tissuesmentioning

confidence: 85%

Section: Alterations In Gingival Crevicular Fluidmentioning

confidence: 99%

Local inflammatory reactions in patients with diabetes and periodontitis

Sonnenschein¹,

Meyle²

2015

Periodontology 2000

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“…However, other studies of IL-8 expression in gingival tissue and in GCF did not replicate these findings (Duarte et al 2007a, Ross et al 2010, Salvi et al 2010. Studies in diabetic rats have provided evidence of compromised gingival neutrophil function in vivo and in vitro (Ramamurthy et al 1979, Golub et al 1982 and studies in diabetic mice also suggest changes in gingival neutrophil function (Gyurko et al 2006, Sima et al 2010.…”

Section: Immune Cell Functionmentioning

confidence: 98%

“…The role of TNF-a (and IL-6) in the enhanced immune responses to periodontal bacteria in diabetic mouse models has also been highlighted (Graves et al 2005, Nishihara et al 2009, Takano et al 2010). However, evidence for any association between levels of TNF-a in oral fluids or gingival tissues and T2DM in chronic periodontitis is inconsistent (Duarte et al 2007b, Navarro-Sanchez et al 2007, Ross et al 2010, Santos et al 2010b. The majority of studies have focused on single or a limited number of mediators and most have investigated pro-inflammatory cytokines (Table 2).…”

Section: Cytokines and Adipokinesmentioning

confidence: 99%

A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes

Taylor

Preshaw

Lalla

2013

Journal of Periodontology

211

258

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A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes Taylor JJ, Preshaw PM, Lalla E. A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes.Abstract Aims: To review the evidence for the molecular and cellular processes that may potentially link periodontal disease and diabetes. The pathogenic roles of cytokines and metabolic molecules (e.g. glucose, lipids) are explored and the role of periodontal bacteria is also addressed. Paradigms for bidirectional relationships between periodontitis and diabetes are discussed and opportunities for elaborating these models are considered. Methods: Database searches were performed using MeSH terms, keywords, and title words. Studies were evaluated and summarized in a narrative review. Results: Periodontal microbiota appears unaltered by diabetes and there is little evidence that it may influence glycaemic control. Small-scale clinical studies and experiments in animal models suggest that IL-1b, TNF-a, IL-6, OPG and RANKL may mediate periodontitis in diabetes. The AGE-RAGE axis is likely an important pathway of tissue destruction and impaired repair in diabetesassociated periodontitis. A role for locally activated pro-inflammatory factors in the periodontium, which subsequently impact on diabetes, remains speculative. Conclusion: There is substantial information on potential mechanistic pathways which support a close association between diabetes and periodontitis, but there is a real need for longitudinal clinical studies using larger patient groups, integrated with studies of animal models and cells/tissues in vitro.

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“…They are responsible for diabetic collagen cross‐links, which lead to microvascular complications. AGEs bind also to macrophage receptors and induce the upregulation of cytokines (interleukin‐1, interleukin‐6, and tumor necrosis factor‐α) which in turn results in the increased expression of matrix metalloproteinases (MMPs) in the periodontal tissue (Yalda et al , 1994; Nishimura et al , 1998; Ross et al , 2010; Sima et al , 2010; Aspriello et al , 2011). These collagenases are responsible for the excessive degradation of major components of the extracellular matrix (e.g.…”

Section: Introductionmentioning

confidence: 99%