The influence of diabetes on gingival crevicular fluid <i>β</i>‐glucuronidase and interleukin‐8

Engebretson, Steven P.; Vossughi, Faranak; Hey-Hadavi, Judith; Emingil, Gülnur; Grbic, John T.

doi:10.1111/j.1600-051x.2006.00984.x

Cited by 53 publications

(59 citation statements)

References 60 publications

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“…Although the dogma is that neutrophil function in periodontitis and diabetes is defective, the evidence obtained has been variable likely due to the variety of assays employed and the technical challenges in quantifying neutrophil function ex vivo (Engebretson et al 2006, Chapple & Matthews 2007. Also, these studies have without exception investigated the activity of peripheral and not gingival neutrophils.…”

Section: Immune Cell Functionmentioning

confidence: 99%

“…Also, these studies have without exception investigated the activity of peripheral and not gingival neutrophils. Importantly, levels of the neutrophil-derived enzyme b-glucuronidase and the neutrophil chemotactic factor IL-8 are depressed in chronic periodontitis patients with T2DM as compared to systemically healthy chronic periodontitis patients which might suggest compromised gingival neutrophil-mediated immune responses in diabetes (Engebretson et al 2006).…”

Section: Immune Cell Functionmentioning

confidence: 99%

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

Taylor

Preshaw

Lalla

2013

Journal of Periodontology

205

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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Section: Immune Cell Functionmentioning

confidence: 99%

Section: Immune Cell Functionmentioning

confidence: 99%

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

Taylor

Preshaw

Lalla

2013

Journal of Periodontology

205

258

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“…Inflammation is significantly pronounced in the presence of diabetes, insulin resistance and hyperglycemia (7). Several inflammatory biomarkers such as cytokines, chemokines and bone-related factors have been found to play a very important role in the pathogenesis of both chronic periodontitis (CP) and type 2 DM (8,9). Studies of the links between periodontal disease and cardiovascular disease have indicated that C-reactive protein (CRP) is one the inflam matory biomarkers involved (10).…”

Section: Introductionmentioning

confidence: 99%

Association of stem cell factor and high-sensitivity C reactive protein concentrations in crevicular fluid and serum in patients with chronic periodontitis with and without type 2 diabetes

et al. 2013

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Abstract:The aim of the present study was to clarify whether there is any correlation between the levels of high-sensitivity C reactive protein (hs-CRP) and stem cell factor (SCF) in serum and gingival crevicular fluid (GCF) of patients with chronic periodontitis (CP) with and without type 2 diabetes mellitus (DM). A total of 40 subjects were divided into 3 groups: 10 periodontally healthy subjects (Group 1), 15 CP patients (Group 2), and 15 type 2 DM patients with CP (Group 3). Levels of hs-CRP and SCF in GCF and serum were quantified using different techniques. The clinical outcomes evaluated were gingival index (GI), probing depth (PD) and clinical attachment level (CAL), and the correlations of the two inflammatory mediators with clinical parameters were evaluated. The levels of these inflammatory mediators increased continuously from group 1 to group 2, and to group 3. The serum levels of both hs-CRP and SCF were correlated with PD in patients with CP (P < 0.05). SCF levels were correlated with PD in Group 3 (P < 0.05). The fact that the levels of hs-CRP and SCF were highest in DM patients with CP suggests that the presence of a systemic condition has a profound effect on the levels of inflammatory mediators, both locally at sites of periodontal disease, and elsewhere. (J Oral Sci 55, 57-62, 2013)

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“…Certaines études animales et cliniques semblent montrer que l'adhérence, le chimiotactisme (diminution de l'IL-8) et la phagocytose des neutrophiles tant périphériques que gingivaux sont altérés chez les patients diabétiques de type 2 [8]. De même, le rôle des monocytes dits « hyper répondants » ou « hyper inflammatoires » est soulevé dans la susceptibilité des patients diabétiques aux maladies parodontales.…”

Section: Rôle De La Dysfonction Immunitaire Et De La Réaction Inflammunclassified

Diabète et maladies parondontales

Dagorne¹,

Rangé²

2014

Actual. Odonto-Stomatol.

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The influence of diabetes on gingival crevicular fluid β‐glucuronidase and interleukin‐8

Abstract: These data suggest that an inadequate local response by PMN, partially explained by an altered chemokine gradient, may contribute to periodontal disease in patients with type 2 DM.

Cited by 53 publications

References 60 publications

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

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

Association of stem cell factor and high-sensitivity C reactive protein concentrations in crevicular fluid and serum in patients with chronic periodontitis with and without type 2 diabetes

Diabète et maladies parondontales

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