Oxidative and inflammatory status in Type 2 diabetes patients with periodontitis

Allen, Edith; Matthews, J. B.; Halloran, Domhnall J. O'; Griffiths, Helen R.; Chapple, Iain

doi:10.1111/j.1600-051x.2011.01764.x

Cited by 107 publications

(100 citation statements)

References 36 publications

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“…Systemic reductions in TAOC were also detected in the above-mentioned studies by Masi et al [ 45 ] and Baltacioglu et al [ 41 ]. Using the same assay, TAC (renamed small molecule antioxidant capacity) was found to be lower in the plasma of diabetic patients with periodontitis compared to diabetic patients with healthy periodontia [ 51 ]. On the other hand, the antioxidant capacity of venous blood measured by reduction of NBT test was found to be higher in periodontitis patients compared to healthy subjects [ 60 ].…”

Section: Systemic Redox Balancesupporting

confidence: 60%

Periodontitis and Oxidative Stress: Human Studies

Nibali

Henderson

Volti

et al. 2013

Studies on Periodontal Disease

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Section: Systemic Redox Balancesupporting

confidence: 60%

Periodontitis and Oxidative Stress: Human Studies

Nibali

Henderson

Volti

et al. 2013

Studies on Periodontal Disease

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“…Tipping the scale on one side or the other can result either in resolution of the inflammation, or tissue destruction, since immune response to bacteria and/or their by-products can induce contradictory events by playing both protective and destructive roles. Other factors such as diabetes [38][39][40] ,smoking [6,41] and previous periodontitis history [16,42] also affect the occurrence of periimplantitis. In any case, regardless of the complex interplay, it is obvious that the common aetiology of peri-implant pathogens remains the microbial colonization of implant surfaces.…”

Section: Introductionmentioning

confidence: 98%

Bacterial adhesion mechanisms on dental implant surfaces and the influencing factors

Han

Tsoi

Rodrigues

et al. 2016

International Journal of Adhesion and Adhesives

101

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a b s t r a c tBacterial adhesion on dental implants may cause peri-implant disease including peri-implant mucositis and peri-implantitis. Peri-implantitis may lead to bone resorption and eventually loss of the implant. Therefore, the factors which influence bacterial adhesion are critical and revealed by many studies. The purpose of this review is to summarize the current knowledge of factors influencing the bacteria adhesion, including local factors of implant surface topography, abutment, cement and oral environment factors of saliva and protein. In addition, the corresponding strategies of surface modifications, coatings and challenges for implant materials as prevention and treatment approaches for bacteria adhesion on implant will also be discussed. We expect to give an overall picture of the bacteria adhesion on implant, and provide future perspectives, such as laser therapy, photocatalysis, plasma and bioelectric effect to inspire researchers to explore on this issue.

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“…Biochemical markers of systemic oxidative stress are elevated in both diabetes and periodontitis (Bullon et al 2009) and are positively correlated with CRP in periodontitis patients as compared to healthy controls (D'Aiuto et al 2010). It has been proposed that hyperactive neutrophils, possibly activated in the periodontium, may be an important source of reactive oxygen species which lead to an activation of pro-inflammatory pathways and promote insulin resistance in patients with periodontitis and diabetes (Allen et al 2011).…”

Section: Inflammatory Factorsmentioning

confidence: 99%

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

Taylor

Preshaw

Lalla

2013

Journal of Periodontology

217

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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Oxidative and inflammatory status in Type 2 diabetes patients with periodontitis

Abstract: Periodontitis is associated with increased oxidative stress and compromised glycaemic control in Type 2 diabetes patients.

Cited by 107 publications

References 36 publications

Periodontitis and Oxidative Stress: Human Studies

Periodontitis and Oxidative Stress: Human Studies

Bacterial adhesion mechanisms on dental implant surfaces and the influencing factors

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

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