Progression of Periodontal Destruction and the Roles of Advanced Glycation End Products in Experimental Diabetes

Chang, Ping-Chuan; Chien, Li-Ying; Yeo, Jin-Fei; Wang, Yi Ping; Chung, Maxey C.M.; Li, Chong; Kuo, Mark Yen‐Ping; Chen, Chun‐Hao; Chiang, Hsüch‐Ching; Ng, Benjamin N.; Lee, Qi Qi; Phay, Yong Kang; Ng, Jeffery R.; Erk, Kok Yong

doi:10.1902/jop.2012.120076

Cited by 62 publications

(72 citation statements)

References 42 publications

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“…The down-regulation of TNF-α (Fig. 4C) also confirmed that the activation of the AGE-RAGE axis was in parallel with the progression of inflammation (Chang et al, 2012(Chang et al, , 2013. However, without the infection from exogenous pathogens, inflammation was elicited only in the initial stages and gradually receded in the control group (Fig.…”

Section: Discussionsupporting

confidence: 60%

Soft-tissue Wound Healing by Anti-advanced Glycation End-products Agents

et al. 2014

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The blocking of advanced glycation end-products (AGE) has been shown to reduce diabetic complications and control periodontitis. This study investigated the pattern of palatal wound-healing after graft harvesting under the administration of aminoguanidine (AG), an AGE inhibitor, or N-phenacylthiazolium bromide (PTB), a glycated cross-link breaker. Full-thickness palatal excisional wounds (5.0 x 1.5 mm(2)) were created in 72 Sprague-Dawley rats. The rats received daily intraperitoneal injections of normal saline (control), AG, or PTB and were euthanized after 4 to 28 days. The wound-healing pattern was assessed by histology, histochemistry for collagen matrix deposition, immunohistochemistry for AGE and the AGE receptor (RAGE), and the expression of RAGE, as well as inflammation- and recovery-associated genes. In the first 14 days following AG or PTB treatments, wound closure, re-epithelialization, and collagen matrix deposition were accelerated, whereas AGE deposition, RAGE-positive cells, and inflammation were reduced. RAGE and tumor necrosis factor-alpha were significantly down-regulated at day 7, and heme oxygenase-1 was persistently down-regulated until day 14. The levels of vascular endothelial growth factor, periostin, type I collagen, and fibronectin were all increased at day 14. In conclusion, anti-AGE agents appeared to facilitate palatal wound-healing by reducing AGE-associated inflammation and promoting the recovery process.

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Section: Discussionsupporting

confidence: 60%

Soft-tissue Wound Healing by Anti-advanced Glycation End-products Agents

et al. 2014

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“…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 Stressmentioning

confidence: 66%

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

Taylor

Preshaw

Lalla

2013

Journal of Periodontology

210

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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“…Research indicates that T2DM has been associated with the formation and accumulation of advanced glycation end products (AGEs), which contribute to its pathogenesis and to abnormal periodontal wound healing. 6,7 These end products reduce the production of matrix proteins such as collagen and osteocalcin by gingival and periodontal fibroblasts. 8 It has also been suggested that T2DM patients present with persistent inflammatory response, significant attachment loss, and increased alveolar bone resorption.…”

Section: Introductionmentioning

confidence: 99%

Stability and bone loss around submerged and non-submerged implants in diabetic and non-diabetic patients: a 7-year follow-up

Zahrani

Mutairi

2018

Braz. oral res.

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Stability and bone loss around submerged and non-submerged implants in diabetic and non-diabetic patients: a 7-year follow-up Abstract: To evaluate peri-implant bone loss (PIBL) and stability around submerged and non-submerged dental implants in patients with and without type 2 diabetes mellitus (T2DM). Thirty-five T2DM and non-diabetic (NT2DM) patients were included in this study. Demographic data were recorded using a questionnaire and PIBL was measured on digital radiographs. Resonance frequency analysis (RFA) was carried out for each implant at the time of fixture placement and at 3 months in both groups. P values less than 0.05 were considered statistically significant. One hundred and eighteen dental implants with a mean height of 10 to 12 mm and 3.3 to 4.1 mm in diameter were placed. The comparison of the mean RFA values at baseline and at 3 months was statistically significant (p = 0.008) in T2DM patients. The inter-group mean RFA values at baseline and at 3 months were not significant (p > 0.05). PIBL was significantly high in T2DM as compared to NT2DM patients at each follow-up (p < 0.05). At 2, 3, and 7 years, non-submerged dental implants showed significantly high PIBL in T2DM patients as compared to NT2DM individuals (p<0.05). The results of the present clinical study demonstrate increased PIBL around non-submerged single-tooth implant-supported restorations in T2DM patients, which may be due to the immune inflammatory status.

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Progression of Periodontal Destruction and the Roles of Advanced Glycation End Products in Experimental Diabetes

Abstract: Diabetes augments periodontal destruction by reducing the proliferating capability and activating resorptive activities. Presence of the AGE-RAGE axis without diabetes implies that it is involved in the regulation of inflammation.

Cited by 62 publications

References 42 publications

Soft-tissue Wound Healing by Anti-advanced Glycation End-products Agents

Soft-tissue Wound Healing by Anti-advanced Glycation End-products Agents

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

Stability and bone loss around submerged and non-submerged implants in diabetic and non-diabetic patients: a 7-year follow-up

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