Expression of the receptor of advanced glycation end products in gingival tissues of type 2 diabetes patients with chronic periodontal disease: a study utilizing immunohistochemistry and RT‐PCR

Katz, Joseph; Bhattacharyya, Indraneel; Farkhondeh-Kish, F.; Perez, Federico M.; Caudle, Robert M.; Heft, Marc W.

doi:10.1111/j.1600-051x.2004.00623.x

Cited by 152 publications

(137 citation statements)

References 22 publications

Supporting

Mentioning

127

Contrasting

Unclassified

Order By: Relevance

“…Importantly, the beneficial effects of RAGE blockade were paralleled by suppressed expression of the receptor and its ligands in gingival tissues and were independent of the level of glycaemia. Increased RAGE expression was subsequently reported in other experimental models of diabetes-associated periodontitis (Chang et al 2012a,b, Claudino et al 2012) and in gingival tissues of diabetic individuals with periodontitis, and its expression was correlated to that of NF-kB (Katz et al 2005, Abbass et al 2012, Yu et al 2012. These findings demonstrated that AGE-RAGE interaction may lead to the exaggerated inflammatory response and periodontal tissue destruction seen in diabetes.…”

Section: Hyperglycaemia and Cellular Stresssupporting

confidence: 57%

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

Taylor

Preshaw

Lalla

2013

Journal of Periodontology

217

258

View full text Add to dashboard Cite

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.

show abstract

Section: Hyperglycaemia and Cellular Stresssupporting

confidence: 57%

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

Taylor

Preshaw

Lalla

2013

Journal of Periodontology

217

258

View full text Add to dashboard Cite

show abstract

“…Conversely, the presence of MetS or any of its components in a previously periodontally healthy person could facilitate a prooxidant state which would diminish anti-oxidant capacity of the periodontal tissues, and the response of these tissues to bacterial challenge could be impaired. The presence of a high RAGE expression in periodontal tissues (Katz et al, 2005) is an important finding supporting the sensitivity of these tissues to products derived from oxidative damage. Moreover, AGE may promote apoptosis in osteoblasts (Alikhani et al, 2007a) and fibroblasts (Alikhani et al, 2007b), and this might have an influence on alveolar bone homeostasis and the progression of periodontitis.…”

Section: Resistin and Periodontitismentioning

confidence: 99%

Metabolic Syndrome and Periodontitis: Is Oxidative Stress a Common Link?

et al. 2009

View full text Add to dashboard Cite

A review of pathological mechanisms that can explain the relationship between periodontitis and cardiovascular disease (CVD) is necessary to improve the management of both conditions. Metabolic syndrome is a combination of obesity, hypertension, impaired glucose tolerance or diabetes, hyperinsulinemia, and dyslipidemia. All these have been examined in recent years in terms of their relationship to periodontitis. Reviewed data indicate an association between some of them (body mass index, high-density lipoprotein-cholesterol [HDL-C], triglycerides, high blood pressure, among others) and periodontitis. Oxidative stress may act as a potential common link to explain relationships between each component of metabolic syndrome and periodontitis. Both conditions show increased serum levels of products derived from oxidative damage, with a pro-inflammatory state likely influencing each other bidirectionally. Adipocytokines might modulate the oxidant/anti-oxidant balance in this relationship.

show abstract

“…The receptor for AGE (RAGE),an integral membrane protein, forming the central binding site on the cell surface for AGEs, is a multi ligand and signal transduction receptor belonging to immunoglobulin superfamily and can be unregulated under various pathological conditions (Katz et al 2005;Ziyadeh et al 1997;Park et al 2004;Schmidt et al 2000). The engagement of AGEs to RAGE leads to the activation of the transcription factor, nuclear factor kappa B (NFkB) and subsequent expression of NFkB regulated cytokines.…”

Section: Resultsmentioning

confidence: 99%

Dietary coconut kernel protein beneficially modulates NFκB and RAGE expression in streptozotocin induced diabetes in rats

et al. 2012

View full text Add to dashboard Cite

Previous studies showed that arginine rich coconut kernel protein (CKP) maintains glucose homeostasis in experimental diabetic rats. But the mechanism of this effect was not clear. This study investigated the effect of CKP on the expression of liver receptor for advance glycated end products (RAGE), inducible nitric oxide synthase (iNOS) and NFkB. Diabetes was induced by injecting a single dose of streptozotocin (75 mg/kg body weight) intraperitoneally. After inducing diabetes, CKP was administered to rats orally for 45 days. After the experimental period, serum glucose, insulin, liver glycogen, glucose metabolizing enzyme activities and the expression of liver RAGE, iNOS and NFkB was evaluated. The results showed that CKP beneficially modulated the levels of glucose and insulin as well as the metabolizing enzyme activities. Expression of RAGE and NFkB was found to be over expressed in diabetic rats but was found to be down regulated in CKP fed diabetic rats. iNOS expression was down regulated in diabetic rats, which was expressed normally in CKP fed diabetic rats.These results clearly demonstrated that anti diabetic activity of CKP is mediated through NFkB pathway.

show abstract

Expression of the receptor of advanced glycation end products in gingival tissues of type 2 diabetes patients with chronic periodontal disease: a study utilizing immunohistochemistry and RT‐PCR

Abstract: Although there was no change in the staining intensity for RAGE between both groups, the increase in the mRNA for RAGE in the type 2 diabetes gingival epithelium may indicate a possible involvement of this receptor in the periodontal destruction in type 2 diabetes.

Cited by 152 publications

References 22 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

Metabolic Syndrome and Periodontitis: Is Oxidative Stress a Common Link?

Dietary coconut kernel protein beneficially modulates NFκB and RAGE expression in streptozotocin induced diabetes in rats

Contact Info

Product

Resources

About