Diabetes modulates gene expression in the gingival tissues of patients with chronic periodontitis

Duarte, Poliana Mendes; Neto, José Brandão; Casati, Márcio Z.; Sallum, Enílson Antônio; Nociti, Francisco Humberto

doi:10.1111/j.1601-0825.2006.01348.x

Cited by 51 publications

(62 citation statements)

References 25 publications

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“…The high levels of glucose in diabetic animals result in greater destruction of periodontal tissues [Graves et al, 2007]. Together with the findings of Duarte et al [2007] and Taka yanagi [2010], our results suggest that the exacerbated inflammation that occurs in DM1 rats might be associated with advanced glycation end products and other mechanisms of bone resorption in addition to RANKL/OPG regulation.…”

Section: Discussionsupporting

confidence: 67%

“…This seems to be particularly true given the fact that the bone-lining cells (osteoblasts), which are important players of the RANKL signaling pathway, undergo apoptosis immediately after PD induction [Liu et al, 2006;Graves et al, 2007]. In addition, Duarte et al [2007] demonstrated that the Th1 response-associated cytokine IL-6 induces osteoclast formation in vitro through a RANKLindependent mechanism. Similarly, Takayanagi [2010] reported that TNF-␣ plus TGF-␤ induces osteoclastogenesis using a not-yet characterized intracellular signaling system distinct from the RANKL pathway.…”

Section: Discussionmentioning

confidence: 99%

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Periodontal Disease-Associated Compensatory Expression of Osteoprotegerin Is Lost in Type 1 Diabetes Mellitus and Correlates with Alveolar Bone Destruction by Regulating Osteoclastogenesis

Silva

Ferrucci

Peroni

et al. 2012

Cells Tissues Organs

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Alveolar bone resorption results from the inflammatory response to periodontal pathogens. Systemic diseases that affect the host response, such as type 1 diabetes mellitus (DM1), can potentiate the severity of periodontal disease (PD) and accelerate bone resorption. However, the biological mechanisms by which DM1 modulates PD are not fully understood. The aim of this study was to determine the influence of DM1 on alveolar bone resorption and to evaluate the role of receptor activator of nuclear factor-kappaB ligand (RANKL)/osteoprotegerin (OPG) in osteoclastogenesis in rats. PD was induced by means of ligature in nondiabetic and in streptozotocyn-induced DM1 rats. Morphological and morphometric analyses, stereology and osteoclast counting were performed. RANKL and OPG mRNA levels, protein content, and location were determined. PD caused alveolar bone resorption, increased the number of osteoclasts in the alveolar bone crest and also promoted changes in RANKL/OPG mRNA expression. DM1 alone showed alveolar bone destruction and an increased number of osteoclasts at the periapical and furcal regions. DM1 exacerbated these characteristics, with a greater impact on bone structure, resulting in a low OPG content and a higher RANKL/OPG ratio, which correlated with prominent osteoclastogenesis. This work demonstrates that the effects of PD and DM1 enhance bone destruction, confirms the importance of the RANKL signaling pathway in bone destruction in DM1 in animal models and suggests the existence of alternative mechanisms potentiating bone degradation in PD.

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Section: Discussionsupporting

confidence: 67%

Section: Discussionmentioning

confidence: 99%

Periodontal Disease-Associated Compensatory Expression of Osteoprotegerin Is Lost in Type 1 Diabetes Mellitus and Correlates with Alveolar Bone Destruction by Regulating Osteoclastogenesis

Silva

Ferrucci

Peroni

et al. 2012

Cells Tissues Organs

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“…The role of TNF-a (and IL-6) in the enhanced immune responses to periodontal bacteria in diabetic mouse models has also been highlighted (Graves et al 2005, Nishihara et al 2009, Takano et al 2010). However, evidence for any association between levels of TNF-a in oral fluids or gingival tissues and T2DM in chronic periodontitis is inconsistent (Duarte et al 2007b, Navarro-Sanchez et al 2007, Ross et al 2010, Santos et al 2010b. The majority of studies have focused on single or a limited number of mediators and most have investigated pro-inflammatory cytokines (Table 2).…”

Section: Cytokines and Adipokinesmentioning

confidence: 99%

“…A number of studies focusing on osteoclastogenesis-related factors have reported elevated levels of RANKL in diabetes-associated periodontal tissues (Mahamed et al 2005, Duarte et al 2007b, Lappin et al 2009). Studies in gingival crevicular fluid demonstrated that RANKL and the RANKL to OPG ratio are higher in poorly controlled diabetic patients with periodontitis compared to well-controlled or non-diabetic subjects with similar periodontal status (Santos et al 2010a, Vieira Ribeiro et al 2011.…”

Section: Hyperglycaemia and Alveolar Bone Homeostasismentioning

confidence: 99%

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

Taylor

Preshaw

Lalla

2013

Journal of Periodontology

218

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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“…Additionally, DM alters bacteria-host interactions by prolonging the inflammatory response and dysregulating cytokine production. 6,8 Although periodontal diseases are initiated by bacteria that colonize the tooth surface and gingival sulcus, the host response, which is primarily responsible for the destruction of connective tissue constituents and bone, has led to host-modulation therapies in the management of infectious diseases. 9,10 Host modulatory therapy (HMT) is a treatment concept that aims to decrease tissue destruction and stabilize or regenerate the periodontium by modifying or downregulating destructive aspects of the host response and upregulating protective or regenerative responses.…”

Section: öZmentioning

confidence: 99%

The Effect of Bisphosphonates and Low-Dose Doxcycline Therapy in Diabetics With Periodontitis: A Review

Doğan¹,

Dede²

2016

Atatürk Üniversitesi Diş Hekimliği Fakültesi Dergisi

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Diabetes modulates gene expression in the gingival tissues of patients with chronic periodontitis

Abstract: Taken together, these data suggest that decreased levels of IL-10 and OPG may play an important role in the periodontal breakdown in diabetic patients.

Cited by 51 publications

References 25 publications

Periodontal Disease-Associated Compensatory Expression of Osteoprotegerin Is Lost in Type 1 Diabetes Mellitus and Correlates with Alveolar Bone Destruction by Regulating Osteoclastogenesis

Periodontal Disease-Associated Compensatory Expression of Osteoprotegerin Is Lost in Type 1 Diabetes Mellitus and Correlates with Alveolar Bone Destruction by Regulating Osteoclastogenesis

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

The Effect of Bisphosphonates and Low-Dose Doxcycline Therapy in Diabetics With Periodontitis: A Review

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