Exenatide and Sitagliptin Decrease Interleukin 1β, Matrix Metalloproteinase 9, and Nitric Oxide Synthase 2 Gene Expression But Does Not Reduce Alveolar Bone Loss in Rats With Periodontitis

Moraes, Renata Mendonça; Lima, Gabriela Moreira; Oliveira, Felipe Eduardo de; Brito, Ana Carolina V.; Pereira, Rodrigo Dantas; Oliveira, Luciane Dias de; Barros, Patrícia Pimentel de; Franco, Gilson César Nobre; Anbinder, Ana Lia

doi:10.1902/jop.2015.150278

Cited by 17 publications

(14 citation statements)

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“…Recent study showed that inhibition of CD 26 signaling inhibited human osteoclast development and humanized anti-CD26 monoclonal antibody may have therapeutic potential for the treatment of osteolytic lesions [33]. Recently some studies reported that DPP4i had anti-inflammatory effects and it also becomes the another possibility [34,35]. And increased levels of GIP might be able to affect the result though we did not measure [25,26].…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Vildagliptin against Pioglitazone-Induced Bone Loss in Type 2 Diabetic Rats

et al. 2016

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Long-term use of thiazolidinediones (TZDs) is associated with bone loss and an increased risk of fracture in patients with type 2 diabetes (T2DM). Incretin-based drugs (glucagon-like peptide-1 (GLP-1) agonists and dipeptidylpeptidase-4 (DPP-4) inhibitors) have several benefits in many systems in addition to glycemic control. In a previous study, we reported that exendin-4 might increase bone mineral density (BMD) by decreasing the expression of SOST/sclerostin in osteocytes in a T2DM animal model. In this study, we investigated the effects of a DPP-4 inhibitor on TZD-induced bone loss in a T2DM animal model. We randomly divided 12-week-old male Zucker Diabetic Fatty (ZDF) rats into four groups; control, vildagliptin, pioglitazone, and vildagliptin and pioglitazone combination. Animals in each group received the respective treatments for 5 weeks. We performed an intraperitoneal glucose tolerance test (IPGTT) before and after treatment. BMD and the trabecular micro-architecture were measured by DEXA and micro CT, respectively, at the end of the treatment. The circulating levels of active GLP-1, bone turnover markers, and sclerostin were assayed. Vildagliptin treatment significantly increased BMD and trabecular bone volume. The combination therapy restored BMD, trabecular bone volume, and trabecular bone thickness that were decreased by pioglitazone. The levels of the bone formation marker, osteocalcin, decreased and that of the bone resorption marker, tartrate-resistant acid phosphatase (TRAP) 5b increased in the pioglitazone group. These biomarkers were ameliorated and the pioglitazone-induced increase in sclerostin level was lowered to control values by the addition of vildagliptin. In conclusion, our results indicate that orally administered vildagliptin demonstrated a protective effect on pioglitazone-induced bone loss in a type 2 diabetic rat model.

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Section: Discussionmentioning

confidence: 99%

Protective Effects of Vildagliptin against Pioglitazone-Induced Bone Loss in Type 2 Diabetic Rats

et al. 2016

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“…It is reported that severe periodontitis has been associated with a robust increase in plasma TG (Maekawa et al 2011 ; D’Aiuto et al 2006 ), which is agreed by the present study. NSPT improved plasma lipid, which might be another mechanism by which NSPT decreased inflammatory response in the arterial wall (Moraes et al 2015 ; Cho 2002 ; Lemaitre et al 2009 ).…”

Section: Discussionmentioning

confidence: 99%

Nonsurgical periodontal treatment reduced aortic inflammation in ApoE−/− mice with periodontitis

Cui

Lei

et al. 2016

SpringerPlus

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BackgroundAlthough the correlation between periodontal infection and atherosclerotic lesions has been well recognized, whether and how the nonsurgical periodontal treatment (NSPT) can improve the vascular inflammation has not been investigated clearly.MethodsThirty-two apolipoprotein E−/− (apoE−/−) mice were randomly divided into four groups: (1) Con group: no treatment, blank control group; (2) Lig group: ligature-induced-periodontitis group; (3) Lig-N group: ligatures were removed on the 7th day; (4) Lig-SRP group: ligatures were removed on the 7th day, and scaling and root planing (SRP) were performed on the 9th day. All the animals were euthanized on the 30th day. Alveolar bone loss (ABL) was assessed under microcomputed tomography. Systemic inflammatory status and lipid contents in the plasma were detected. Expression of several surrogate markers for vascular inflammation was evaluated by immunohistology and quantitative real time PCR.ResultsNSPT reduced ABL, improved lipid profile, and inhibited systemic inflammation with reduced plasma interleukin-6 (IL-6) level in apoE−/− mice; in addition, reduced inflammation in arterial wall was observed in NSPT treated mice, showing less vascular cell adhesion molecule-1 expression and less macrophage adhesion; furthermore, NSPT improved elastic fiber fragmentation disorder in the aortic wall, thus preserved elasticity of aortic artery.ConclusionLigature-induced periodontitis can lead to inflammatory response in the vascular wall and NSPT has beneficial effect on the early stage of atherosclerosis process in the articular wall by reducing systemic inflammation and improving lipid profile.

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“…without effect on alveolar bone loss in periodontally affected rats 114. Intensified metabolic treatment with glycated hemoglobin reduction resulted in an improved inflammation state, characterized by decreased levels of C-reactive protein 115.…”

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confidence: 96%

Periodontal complications of hyperglycemia/diabetes mellitus: Epidemiologic complexity and clinical challenge

Kocher

König

Borgnakke

et al. 2018

Periodontology 2000

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170

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This report provides a comprehensive overview of the adverse effects of hyperglycemia on the periodontium. It combines data from literature reviews of original data from two large, population-based epidemiologic studies with comprehensive periodontal health assessment. Emphasis is placed on the exploration of hitherto sparsely reported effects of prediabetes and poorly controlled (uncontrolled) diabetes, in contrast to the umbrella term "diabetes." This stems from the realization that it is not simply having a diagnosis of diabetes that may adversely affect periodontal health. Rather, it is the level (severity) of hyperglycemia that is the determining factor, not the case definition of the diagnosis of diabetes or the type of diabetes in question. Importantly, based on existing evidence this paper also attempts to estimate the improvements in periodontal probing depth and clinical attachment level that can be expected upon successful nonsurgical periodontal treatment in people with chronic periodontitis, with and without diabetes, respectively. This exploration includes the implentation of new systematic reviews and meta-analyses that allow comparison of such intervention outcomes between hyperglycemic and normoglycemic subjects. Based on both existing literature and original analyses of population-based studies, we try to answer questions such as: Is there a glycated hemoglobin concentration threshold for periodontitis risk? Does short-term periodontal probing depth reduction and clinical attachment level gain after scaling and root planing depend on glycemic control in type 2 diabetes? Are short-term scaling and root planing outcomes in people with hyperglycemia/diabetes inferior to those in people without diabetes? Do periodontitis patients with diabetes benefit more from the use of adjuvant antibiotics with nonsurgical periodontal treatment than people without diabetes? Does hyperglycemia lead to greater tooth loss in patients in long-term post-periodontal treatment maintenance programs? Throughout this review, we compare our new findings with previous data and report whether the results of these new analyses corroborate, or are in discord with, similar scientific reports in the literature. We also explore the potential role of dental health-care professionals in helping patients control the risk factors that are identical for periodontitis and diabetes. Finally, we suggest various topics that still need exploration in future research.

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Exenatide and Sitagliptin Decrease Interleukin 1β, Matrix Metalloproteinase 9, and Nitric Oxide Synthase 2 Gene Expression But Does Not Reduce Alveolar Bone Loss in Rats With Periodontitis

Abstract: Regardless of the reduction of the expression of Il1b, Nos2, and Mmp9, the drugs were not effective in the stabilization or reduction of alveolar bone loss and collagen degradation in rats.

Cited by 17 publications

References 44 publications

Protective Effects of Vildagliptin against Pioglitazone-Induced Bone Loss in Type 2 Diabetic Rats

Protective Effects of Vildagliptin against Pioglitazone-Induced Bone Loss in Type 2 Diabetic Rats

Nonsurgical periodontal treatment reduced aortic inflammation in ApoE−/− mice with periodontitis

Periodontal complications of hyperglycemia/diabetes mellitus: Epidemiologic complexity and clinical challenge

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