Receptor Activator of Nuclear Factor‐Kappa B Ligand/Osteoprotegerin Ratio in Sites of Chronic Periodontitis of Subjects With Poorly and Well‐Controlled Type 2 Diabetes

Santos, Vanessa Renata; Lima, Jadson Almeida; Gonçalves, Tiago Eduardo Dias; Bastos, Marta Ferreira; Figueiredo, Luciene Cristina; Shibli, Jamil Awad; Duarte, Poliana Mendes

doi:10.1902/jop.2010.100125

Cited by 75 publications

(83 citation statements)

References 46 publications

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“…The majority of studies have focused on single or a limited number of mediators and most have investigated pro-inflammatory cytokines (Table 2). There is a possible role for T2DM in modulating the oral levels of receptor activator of nuclear factor-kappa B ligand (RANKL)/ osteoprotegerin (OPG) in chronic periodontitis (Santos et al 2010a, Vieira Ribeiro et al 2011. With the exception of IL-8 (CXCL8), few studies have investigated the role of chemokines.…”

Section: Cytokines and Adipokinesmentioning

confidence: 99%

“…However, although there is a substantial role for altered balance of Th1/Th2 cells in the pathogenesis and progression of periodontitis, there is no direct information about the role of specific T-cell subsets in periodontitis in patients with diabetes. Significantly, Th17 and Th1 cells have a role in regulation of bone resorption and are a source of cytokines such as RANKL and IL-17, which are elevated in periodontitis patients with diabetes (Santos et al 2010a, b, Vieira Ribeiro et al 2011; the role of these T-cell subsets in periodontal pathogenesis in diabetic patients is therefore worthy of investigation. In this regard, there is preliminary evidence for an association between glycaemic control and IL-4 (Th1 cytokine) and IL-17 levels in GCF from periodontitis patients with diabetes (Santos et al 2010b, Vieira Ribeiro et al 2011 and an immunohistochemical study recently provided evidence for elevated Th17 and T reg cells in patients with poorly controlled T2DM and periodontitis as compared to patients with periodontitis alone .…”

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

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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Section: Cytokines and Adipokinesmentioning

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

217

258

View full text Add to dashboard Cite

show abstract

“…Increased RANKL/OPG ratios and TNF-α levels that contribute to greater bone resorption are observed in diabetes. In human subjects, the ratio of RANKL/OPG and TNF-α levels are increased in inadequately controlled diabetics [42]. In diabetic's fatty acid levels may also add to augmented osteoclastogenesis.…”

Section: Impact Of Diabetes On Bone and Osteoclastsmentioning

confidence: 99%

Bone Restoration in Diabetic Osteolysis and Therapeutic Targets

Thenmozhi¹,

Nagalakshmi²,

Samuel³

et al. 2017

Diabetes Case Rep

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Bone, being a key structural support of the body, undergoes dynamic micro structural remodelling all over life to control automatic stress and calcium requirement. Neurovascular, visual, renal complications added with osteopenia and osteoporosis are main unbearable problems in diabetes mellitus (DM). It is clear that hyperglycaemia in diabetes mellitus leads to glucose toxicity which directly suppresses adipogenic delineation of the osteoblast precursors which depreciate bone feature and strength which augment propensity to fracture. A number of risk factors including oxidative stress, apoptosis and abnormal intracellularCa 2+ metabolism have been postulated to play a function in the inception and progress of osteoporosis within diabetes. This review determines to discuss the most recent findings of mechanisms concerned in the progression of osteoporosis in diabetes. We emphasize the role of signalling molecules in osteoclastogenesis as therapeutic targets in the prevention and treatment of diabetic osteolysis. Increasing validation during the last decade suggests that zinc as neutraceutical suppresses calcium/calcineurin pathway and many compounds are potent inhibitors of osteoclast synthesis by blocking RANKL pathway, an emerging concept that is gaining acceptance. The characteristic of impediment and management of DM-induced osteolysis should be an effective glycaemic control. Hence, we propose to accentuate that Zinc combined with suitable anti-diabetic drugs and inhibitors of osteoclastogenesis may represent a potential therapeutic target in Diabetes mellitus for the prevention, reduction of fracture risk and treatment of osteolysis by suppressing osteoclastogenesis via calcium, calcineurin and RANKL pathway.

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“…6 Furthermore, previous studies described how uncontrolled type 2 diabetes patients with chronic periodontitis expressed higher RANKL and osteoprotegerin (OPG) than both control group patients and healthy individuals. 7,8 The aim of this study was to determine the correlation between RANKL expression of osteoblast and the number of osteoclast in alveolar bone of diabetic models under different mechanical force applications. From the application of varying mechanical forces, the optimal force that can be applied during the orthodontic treatment of diabetics could be estimated.…”

Section: Introductionmentioning

confidence: 99%

The RANKL expression and osteoclast in alveolar bone of rat diabetic model at different mechanical force application

Hikmah¹,

Shita²,

Maulana³

2018

Dent. J.

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Background: Diabetes is a serious and important public health problem, especially in relation to dental treatment. Because of its complications in periodontal tissue, diabetes can be contraindicated in patients undergoing orthodontic treatment. The receptor activator of nuclear factor-κb ligand (RANKL) is an essential cytokine inducing osteoclastogenesis. Osteoblasts produce this cytokine which has been suggested to play an integral role in osteoclast activation during bone remodeling of orthodontic tooth movement. Purpose: The aim of this study was to determine the correlation between RANKL expression of osteoblast and the number of osteoclasts in the alveolar bone of diabetic rat models at different mechanical force application. Methods: This study used animal subjects, white rats (Rattus norvegicus) of the Wistar strain (n=24) divided into six groups. The mechanical force to which they were subjected ranged between 10, 20, and 30 gramforce (grf). The animal models with diabetes were injected with a stratified dose of Streptozotocin. An orthodontic appliance was inserted in both the maxillary incisors for seven days. The tissue was subjected to histological analysis of osteoclasts and immunohistochemistry analysis of RANKL expression on the pressure and tension side of the alveolar bone. Results:The results of this study showed that the increase in mechanical force produced a rise in RANKL expression and osteoclast number on the pressure and tension side of the alveolar bone of diabetic rat models. Conclusion: There was a correlation between the RANKL of osteoblast and osteoclast numbers in the alveolar bone of diabetic models with different mechanical force application.

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Receptor Activator of Nuclear Factor‐Kappa B Ligand/Osteoprotegerin Ratio in Sites of Chronic Periodontitis of Subjects With Poorly and Well‐Controlled Type 2 Diabetes

Abstract: RANKL/OPG ratios in untreated and treated periodontitis sites may be negatively influenced by poor glycemic control in subjects with type 2 diabetes.

Cited by 75 publications

References 46 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

Bone Restoration in Diabetic Osteolysis and Therapeutic Targets

The RANKL expression and osteoclast in alveolar bone of rat diabetic model at different mechanical force application

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