Overexpression of interleukin‐1β and interleukin‐6 may play an important role in periodontal breakdown in type 2 diabetic patients

Duarte, Poliana Mendes; Oliveira, Maria Cláudia G.; Tambeli, Cláudia Herrera; Parada, Carlos A.; Casati, Márcio Z.; Nociti, Francisco Humberto

doi:10.1111/j.1600-0765.2006.00961.x

Cited by 59 publications

(63 citation statements)

References 29 publications

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“…In a previous study, we have reported that expression of the angiogeneic factor VEGF in the periodontium is increased in rats with diabetes mellitus when compared to that in healthy rats 22) . Hyperglycemia-induced increases in levels of inflammatory cytokines, such as TNF- 10) , IL-1 11) and IL-6 11) , cause progression of periodontitis in diabetes mellitus. However, how VEGF, a cytokine expressed and present in the periodontium under hyperglycemic conditions, affects bone resorption caused by periodontitis is unknown.…”

Section: Discussionmentioning

confidence: 99%

“…Hyperglycemia causes formation and accumulation of irreversible advanced glycation end products (AGEs) in the body 31) and induces expression of their primary receptor RAGE 32) . Interactions between the AGEs and RAGE result in the dysfunction of immune cells 6,7) and functional alterations of various cells 8,9) , causing cytokine imbalance associated with inflammatory cytokine increases 10,11) . Furthermore, hyperglycemia shifts the balance of the RANKL/OPG interaction in the direction of tissue destruction through AGEs/RAGE interaction 33,34) .…”

Section: Discussionmentioning

confidence: 99%

“…Among them, the main mechanisms involve immune dysfunction 6,7 ) , cellular stress 8,9 ) , and cytokine imbalance 10,11) caused by hyperglycemia, which enhances tissue destruction of periodontitis and impairs tissue repair. The mechanism of exacerbation of alveolar bone resorption due to cytokine imbalance is initiated when hyperglycemia increases the level of inflammatory cytokines, such as TNF- 10) , IL-1 11) , and IL-6 11) . These cytokines affect the interaction between RANKL and OPG 12) , and as a result, osteoclast differentiation is promoted.…”

Section: Introductionmentioning

confidence: 99%

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VEGF Expression in Diabetic Rats Promotes Alveolar Bone Resorption by <i>Porphyromonas gingivalis</i> LPS

Tsumori

Kono

Shigematsu

et al. 2016

J. Hard Tissue Biology.

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Diabetes mellitus is an important risk factor for periodontitis. Although numerous complications are associated with the disease, all of these are attributed to vascular disorders and are closely related to the potent angiogeneic factor vascular endothelial growth factor (VEGF). However, it remains unknown how diabetes mellitus/hyperglycemia-associated VEGF expression affects alveolar bone resorption in the periodontium. The aim of this study was to determine the level of adverse effect on bone resorption of diabetes mellitus-associated VEGF. Therefore, we induced experimental periodontitis with injections of the endotoxin lipopolysaccharide (LPS) from Porphyromonas gingivalis in diabetic rats, measured the level of bone resorption, and observed VEGF expression and localization of osteoclasts in the periodontium. Eight-week-old male Goto-Kakizaki (GK) rats were in the experimental group, and male Wistar rats were in the control group. Experimental periodontitis was induced by injecting P. gingivalis LPS and inserting ligatures. All rats were euthanized and underwent micro X-ray computed tomography (CT) to acquire bone resorption image, in which the distance between the cement-enamel junction and the alveolar bone crest was measured to determine the amount of bone resorption. Samples were prepared and underwent immunohistochemical staining with an anti-VEGF monoclonal antibody and tartrate-resistant acid phosphatase (TRAP) staining. The amount of bone resorption measured by micro X-ray CT images was significantly greater in the experimental group than in the control group. Immunohistochemical staining showed that VEGF expression levels on the alveolar bone surface and around microvessels in the gingival connective tissue were higher in the experimental group than in the control group. On the alveolar bone surface, localization of TRAP-positive cells and bone resorption lacunae from the same sites were observed in both groups. These results suggest that VEGF expression in the periodontium caused by hyperglycemia in rats with diabetes mellitus affects P. gingivalis LPS-induced alveolar bone resorption.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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VEGF Expression in Diabetic Rats Promotes Alveolar Bone Resorption by <i>Porphyromonas gingivalis</i> LPS

Tsumori

Kono

Shigematsu

et al. 2016

J. Hard Tissue Biology.

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“…Duarte et al 25 found higher levels of IL-6 in diabetic patients with chronic periodontitis and suggested that a high level of IL-6 may contribute to periodontal destruction in diabetic patients, which may be relevant for the modulation of periodontal disease in these patients.…”

Section: Group S (N =mentioning

confidence: 99%

Glycemic control and the production of cytokines in diabetic patients with chronic periodontal disease

Franco

Moraes

Duarte

et al. 2017

RGO, Rev. Gaúch. Odontol.

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ObjectiveTo evaluate the association of glycemic control and cytokine production in type 2 diabetic subjects with chronic periodontitis Methods Gingival biopsies were performed in 40 patients, divided into four groups: systemically healthy subjects without periodontal disease (S); systemically healthy patients with chronic periodontitis (P); patients with well-controlled type 2 diabetes mellitus (DM) with chronic periodontitis (C); poorly controlled type 2 diabetes mellitus with chronic periodontitis (D). The production of interleukin (IL) -4, -6, -10, -17 and interferon (IFN) -γ was quantified by ELISA. Results The production of IL-4, IL-10, IL-17 and INF-γ was higher on group D when compared to other groups (p <0.05), which in turn were similar (p ≥0.05). In addition, there was no difference in the production of IL-6 in any of the evaluated groups (p≥0.05). ConclusionWere observed significantly elevated levels of pro-inflammatory and anti-inflammatory cytokines in patients with poorly controlled type 2 diabetes and chronic periodontitis, demonstrating that glycemic control may be associated to the immune inflammatory response of sites with chronic periodontitis.

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“…Compared to infected normoglycaemic control T2DM rats have a 2 to 4-fold rise in osteoclasts induced by periodontal infection [39]. Correspondingly, human subjects with T2DM and periodontitis have significantly increased levels of TNF-α, IL-1β and IL-6 connected with delayed inflammation and increased lipid peroxidation and dyslipidaemia [38, 40,41]. Increased RANKL/OPG ratios and TNF-α levels that contribute to greater bone resorption are observed in diabetes.…”

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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Overexpression of interleukin‐1β and interleukin‐6 may play an important role in periodontal breakdown in type 2 diabetic patients

Cited by 59 publications

References 29 publications

VEGF Expression in Diabetic Rats Promotes Alveolar Bone Resorption by <i>Porphyromonas gingivalis</i> LPS

VEGF Expression in Diabetic Rats Promotes Alveolar Bone Resorption by <i>Porphyromonas gingivalis</i> LPS

Glycemic control and the production of cytokines in diabetic patients with chronic periodontal disease

Bone Restoration in Diabetic Osteolysis and Therapeutic Targets

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