Periodontal Disease: The sixth complication of diabetes mellitus

Löe, Harald

doi:10.2337/diacare.16.1.329

Cited by 1,203 publications

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“…Periodontitis is the sixth complication of diabetes mellitus [2]. Recently reactive oxygen species have been identified as a potential factor causing periodontal tissue destruction [3].…”

Section: Introductionmentioning

confidence: 99%

Effect of Non-Surgical Therapy on Salivary Nitric Oxide and Lipid Peroxidation Levels in Type Ii Diabetic and Non Diabetic Patients With Periodontal Disease

Latha

Uppoor

Nayak

et al. 2018

Asian J Pharm Clin Res

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Objective: Reactive oxygen species have been identified as potential factors causing periodontal tissue destruction. Elevated levels of these in patients with chronic periodontitis and diabetes may aggravate the oxidative stress burden thereby accelerating the tissue damage associated with diabetes. The present study aimed to assess the effect of diabetes and periodontal disease on the oxidative stress markers and the effect of non-surgical therapy on these markers.Methods: A total of 50 participants were divided into four groups based on the selection criteria. In addition to clinical parameters and biochemical parameters (salivary nitric oxide [NO] and malondialdehyde [MDA] levels) were assessed using spectrophotometric method at baseline and 3 months after non-surgical periodontal therapy.Result: There was a statistically significant difference in the clinical parameters as well as NO and MDA levels in patients with type 2 diabetes and chronic periodontitis than other three groups at baseline and at 3 months after non-surgical periodontal therapy. Conclusion:Diabetes mellitus and periodontitis have a compounding effect on the oxidative stress. Periodontal therapy is essential for diabetic patients as it can lower the levels of oxidative damage.

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“…Periodontitis is the sixth complication of diabetes mellitus [2]. Recently reactive oxygen species have been identified as a potential factor causing periodontal tissue destruction [3].…”

Section: Introductionmentioning

confidence: 99%

Effect of Non-Surgical Therapy on Salivary Nitric Oxide and Lipid Peroxidation Levels in Type Ii Diabetic and Non Diabetic Patients With Periodontal Disease

Latha

Uppoor

Nayak

et al. 2018

Asian J Pharm Clin Res

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“…These findings may have direct implications for inflammatory processes that characterize certain complications of diabetes and renal failure, for example, such as atherosclerosis, impaired wound healing, aggressive and inflammatory periodontal disease, and dialysis-related amyloidosis (DRA) (6,(35)(36).…”

mentioning

confidence: 99%

N ε-(Carboxymethyl)Lysine Adducts of Proteins Are Ligands for Receptor for Advanced Glycation End Products That Activate Cell Signaling Pathways and Modulate Gene Expression

Kislinger

Huber

et al. 1999

Journal of Biological Chemistry

840

695

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Recent studies suggested that interruption of the interaction of advanced glycation end products (AGEs), with the signal-transducing receptor receptor for AGE (RAGE), by administration of the soluble, extracellular ligand-binding domain of RAGE, reversed vascular hyperpermeability and suppressed accelerated atherosclerosis in diabetic rodents. Since the precise molecular target of soluble RAGE in those settings was not elucidated, we tested the hypothesis that predominant specific AGEs within the tissues in disorders such as diabetes and renal failure, N ⑀ -(carboxymethyl)lysine (CML) adducts, are ligands of RAGE. We demonstrate here that physiologically relevant CML modifications of proteins engage cellular RAGE, thereby activating key cell signaling pathways such as NF-B and modulating gene expression. Thus, CML-RAGE interaction triggers processes intimately linked to accelerated vascular and inflammatory complications that typify disorders in which inflammation is an established component.Receptor for AGE 1 (RAGE), a member of the immunoglobulin superfamily, was first described as a cell surface interaction site for advanced glycation end products (AGEs), products of glycation and oxidation of proteins and lipids (1-2). AGEs are a heterogeneous class of compounds, whose accumulation in disorders such as diabetes, renal failure, Alzheimer's disease, and, indeed, natural aging, albeit to a lesser degree, has suggested their potential contribution to the pathogenesis of complications that typify these conditions (3-7). Our previous studies demonstrated that both in vitro and in vivo derived heterogeneous AGEs ligate cell surface RAGE on endothelium (ECs), mononuclear phagocytes (MPs), vascular smooth muscle (VSMC), and neurons to activate cell signaling pathways such as ERK1/ERK2 kinases and NF-B (8 -9), thereby redirecting cellular function in a manner linked to expression of inflammatory and prothrombotic genes important in the pathogenesis of chronic disorders as apparently diverse as diabetic macrovascular disease and amyloidosis (10 -20).Our recent studies suggested that interruption of the interaction of AGEs with RAGE in vivo, by administration of soluble RAGE (sRAGE), the extracellular ligand-binding domain of RAGE, reversed vascular hyperpermeability and suppressed accelerated atherosclerotic lesion development and complexity in diabetic rodents (19 -20). In the latter studies, analysis of plasma demonstrated evidence of an sRAGE⅐AGE complex; immunoprecipitation of plasma obtained from diabetic sRAGEtreated mice with anti-RAGE IgG yielded species immunoreactive with both anti-RAGE IgG or affinity purified anti-AGE IgG, suggesting that sRAGE might bind up AGEs and limit their interaction with and activation of cell surface RAGE. The beneficial effects of sRAGE were independent of alterations in other risk factors, such as hyperglycemia and hyperlipidemia, implicating a role for AGE-RAGE interaction in the development of vascular dysfunction in diabetes (20).These past studies, however, did not elucidate ...

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“…Periodontal diseases are a group of inflammatory, microbial-induced infections involving the supporting tissues of the teeth and mainly caused by gram-negative, anaerobic bacteria [1,2]. The American Society of Diabetes defined periodontal disease as the sixth complication of diabetes in 1997 [3]. Pathogens which are commonly involved in causing periodontitis are Porphyromonas gingivalis, Prevotella intermedia, Tannarella forsythia and Aggregatibacter actinomycetmcomintans, which lead to soft and hard tissue destruction, dental mobility, and the loss of dental elements [4,5].…”

Section: Introductionmentioning

confidence: 99%

Effect of Oral Azithromycin and Metronidazole as an Adjunct to Scaling and Root Planing on Glycemic Control in Type Ii Diabetic Patients With Chronic Periodontitis

Dhivya

Yogarajan²,

Shanmugarajan³

2017

Asian J Pharm Clin Res

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Objective: Periodontitis, a chronic inflammatory disease characterized by destruction of the periodontal ligament and alveolar bone is the sixth complication of diabetes mellitus. Periodontal treatment that reduces gingival inflammation aids in the control of hyperglycemia. Therefore, the present study was designed to determine the effect of treating chronic periodontitis with oral antibiotics azithromycin and metronidazole on the level of serum glycated hemoglobin in type-II diabetic patients.Methods: This prospective observational study was carried out in the dental department of a tertiary care hospital for 9 months. Clinical and biochemistry reports of 90 patients were collected in designed case report forms. All statistical analyses were performed using IBM Statistical Package for Social Sciences 17 and Graph Pad Prism 7.0.Results: Significant reduction in all the clinical and dental parameters was comparatively higher in patients who received azithromycin than in patients who received metronidazole and scaling and root planning alone. Conclusion:Periodontal therapy with oral azithromycin can be employed as a supportive strategy for the management of diabetes mellitus. Henceforth, prevention and control of periodontal disease along with antibiotics must be considered an integral part of glycemic control. However, due to the lesser sample size in this study, further investigations are required to confirm the effect of periodontal therapy on systemic diseases.

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Periodontal Disease: The sixth complication of diabetes mellitus

Cited by 1,203 publications

References 0 publications

Effect of Non-Surgical Therapy on Salivary Nitric Oxide and Lipid Peroxidation Levels in Type Ii Diabetic and Non Diabetic Patients With Periodontal Disease

Effect of Non-Surgical Therapy on Salivary Nitric Oxide and Lipid Peroxidation Levels in Type Ii Diabetic and Non Diabetic Patients With Periodontal Disease

N ε-(Carboxymethyl)Lysine Adducts of Proteins Are Ligands for Receptor for Advanced Glycation End Products That Activate Cell Signaling Pathways and Modulate Gene Expression

Effect of Oral Azithromycin and Metronidazole as an Adjunct to Scaling and Root Planing on Glycemic Control in Type Ii Diabetic Patients With Chronic Periodontitis

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