Diabetes Enhances Periodontal Bone Loss through Enhanced Resorption and Diminished Bone Formation

Liu, Rongkun; Bal, Harbinder S.; Desta, Tesfahun; Krothapalli, Nanarao; Alyassi, Monaf; Luan, Qingxian; Graves, Dana T.

doi:10.1177/154405910608500606

Cited by 238 publications

(269 citation statements)

References 32 publications

(35 reference statements)

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“…The levels of serum insulin and inflammatory cell infiltration in Zucker fatty rats were significantly higher than those of lean rats (data not shown), which were similar to other studies. 39,40 We have already reported that periodontitis induces the initial stage of atherosclerosis in normal rats. 19 Therefore, we focused on the combined effects of periodontitis and obesity on aorta in this study.…”

Section: Discussionmentioning

confidence: 99%

Effects of periodontitis on aortic insulin resistance in an obese rat model

Ekuni

Tomofuji

Irie

et al. 2010

Laboratory Investigation

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The combination of obesity and its associated risk factors, such as insulin resistance and inflammation, results in the development of atherosclerosis. However, the effects of periodontitis on atherosclerosis in an obese body remain unclear. The aim of the study was to investigate the effects of ligature-induced periodontitis in Zucker fatty rats on initiation of atherosclerosis by evaluating aortic insulin resistance. Zucker fatty rats (n ¼ 24) were divided into two groups. In the periodontitis group, periodontitis was ligature-induced for 4 weeks, whereas the control group was left unligated. After the 4-week experimental period, descending aorta was used for measuring the levels of lipid deposits, immunohistochemical analysis, and evaluation of gene expression. Levels of serum C-reactive protein (CRP), tumor necrosis factora (TNF-a), and insulin were also measured. Rats in the periodontitis group had significantly enhanced lipid deposits in the aorta, but not in the control group. Expression of suppressor of cytokine signaling 3, vascular cell adhesion molecule 1, reactive oxygen species, nitrotyrosine, and endothelin-1 in the periodontitis group was more intense than that in the control group. Significantly decreased levels of phosphatidylinositol 3-kinase (Pi3k) catalytic b-polypeptide (Pi3kcb), Pi3kp85, and insulin receptor substrate 1 and 2 were observed in the periodontitis group. Levels of serum CRP and TNF-a were significantly increased in the periodontitis group. Under insulin-stimulated conditions, aorta in the periodontitis group altered the Akt phosphorylation. Periodontitis in obesity induced the initial stage of atherosclerosis and disturbed aortic insulin signaling.

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Section: Discussionmentioning

confidence: 99%

Effects of periodontitis on aortic insulin resistance in an obese rat model

Ekuni

Tomofuji

Irie

et al. 2010

Laboratory Investigation

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“…Also, hyperglycemia can increase the inflammatory response and the osteoclastic activity, which can compromise the bone neoformation during bone repair 4,5 .…”

Section: Introductionmentioning

confidence: 99%

Aqueous-ozone irrigation of bone monocortical wounds in hyperglycemic rats

Frascino

Mantesso²,

Corrêa³

et al. 2013

Acta Cir. Bras.

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PURPOSE:To analyze the effects of aqueous ozone irrigation over bone healing in hyperglycemia-induced rats. METHODS:Forty-eight male Wistar rats were allocated into Group H (hyperglycemic) or Group N (control). Monocortical bone wound were performed on femurs' anterolateral face. Wounds were treated with a trans-operatory single irrigation of 100ml of aqueous ozone [0.004mg/ml] whereas control groups received 100ml of pure water (Milli-Q ® ). Histomorphological and histomorphometrical analyses were accomplished after seven, 14 and 21 days. Kruskal-Wallis and Mann-Whitney statistical tests were applied for bone neoformation quantification and assessment. RESULTS:Aqueous ozone wounds irrigated revealed diffuse hemorrhage and increased neoformed of blood vessels number. There was no statistical significant difference in bone trabeculae neoformation. After seven and 14 days, the number of osteoclasts was higher in aqueous ozone groups than in those treated with pure water. CONCLUSION:Independently of blood glucose levels, aqueous ozone allowed an increase in blood vessels neoformation and osteoclast migration, without affect bone trabeculae neoformation.

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“…One of the mechanisms through which diabetes affects osteoblasts is elevated apoptosis. For example, AGEs induce osteoblast apoptosis through the MAP kinase pathway (Liu et al, 2006). Diabetes also increases the loss of periodontal ligament (PDL) cells that is induced by periodontal infection by accelerating apoptosis (Isaka et al, 2001).…”

Section: Bone Loss Is One Of the Complications In Diabetesmentioning

confidence: 99%

Effects on Alveolar Bone of Diabetes Mellitus Induced by Streptozotocin in Rats. Histopathologic and Immunohistochemical Study

Yilmaz¹,

Uysal²,

Eratilla³

et al. 2018

Int. J. Morphol.

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SUMMARY:The purpose of this study was to investigate effects of diabetes mellitus (DM) on the alveolar bone with histopathological and immunohistochemical methods. Wistar rats were divided into two groups, control and diabetes group. Control group was fed standard rat chow and drinking water for 8 weeks. Single dose (Streptozotocin) STZ (55 mg/kg), was dissolved in sodium citrate buffer and introduced intraperitoneal injection. Diabetes group and control group were compared in terms of glucose values. The blood glucose concentration in diabetic rats was significantly high (p <0.05). In diabetes group; periodontal membrane and the dilation of blood vessels, hemorrhage has also been a significant increase in inflammatory cells. In the diabetes group, osteonectin showed positive expression in periodontal membrane and showed negative expression in osteocytes of alveolar bone. Osteopontin expression in fibroblast cells and periodontal membrane collagen fibrils was positive, alveolar cells, osteocytes and bone matrix bone was found positive. Diabetes results showed that there formed periodontitis; due to the increase in inflammation inhibiting bone formation delaying the development of early bone cells.

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Diabetes Enhances Periodontal Bone Loss through Enhanced Resorption and Diminished Bone Formation

Cited by 238 publications

References 32 publications

Effects of periodontitis on aortic insulin resistance in an obese rat model

Effects of periodontitis on aortic insulin resistance in an obese rat model

Aqueous-ozone irrigation of bone monocortical wounds in hyperglycemic rats

Effects on Alveolar Bone of Diabetes Mellitus Induced by Streptozotocin in Rats. Histopathologic and Immunohistochemical Study

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