Presentations

1678-7757-jaos-22-02-0103

Categories
Published
of 6
All materials on our website are shared by users. If you have any questions about copyright issues, please report us to resolve them. We are always happy to assist you.
Related Documents
Share
Description
jurnalll
Transcript
  J Appl Oral Sci.   ABSTRACT www.scielo.br/jaos         diabetes patients with chronic periodontitis    1      2      2    1     2     2           1 1- Department of Microbiology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil.2- Division of Periodontics, Department of Stomatology, School of Dentistry, University of São Paulo, São Paulo, SP, Brazil.3- Department of Endocrinology, School of Medicine, Federal University of São Paulo, São Paulo, SP, Brazil.    Priscila Larcher Longo - Departamento de Microbiologia, Instituto de Ciências Biomédicas - Universidade de São Paulo - Av. Lineu Prestes, 1374 - São Paulo - SP - 05508-900 - Brazil - Phone: 55-11-3091-7348 - e-mail: pllongo@usp.br                D iabetes has been associated with periodontitis, but the mechanisms through which periodontal diseases affect the metabolic control remain unclear. Objective: This              chemoattractant protein 1 (MCP-1), in type 2 diabetic patients in the presence of chronic periodontitis. Material and Methods: Forty two individuals were enrolled in this study                                              Periodontal clinical examination included visible plaque index (PL), gingival bleeding index (GB), probing depth (PD), attachment level (AL) and bleeding on probing (BP). Glycemic control was evaluated by serum concentration of glycated hemoglobin (HbA1c).                                       IL-6, IL-8 and MCP-1 serum levels. Conclusions: Although periodontitis was more severe              differ among the groups. Keywords:       INTRODUCTION Type 2 diabetes mellitus (T2DM) is the most common endocrine disorder and its incidence is increasing worldwide. This condition is a serious public health concern due to the need for lifelong care, premature death and the fact that it remains incurable 22 . It is characterized by a progressive        resistance, whereby target tissues do not respond to this hormone, is a characteristic of the disease’s         hyperinsulinemia 1 . This resistance comes together       of diabetes chronic complications 32 . Among these complications, periodontal diseases (PD) are very common and immune modulating factors are necessary for pathogen clearance, but also contribute to host tissues damage, as those seen in PD.       diabetes date back to more than a century ago. Proinflammatory molecules as tumor necroses       monocyte chemoattractant protein-1 (MCP-1) and visfatin, among others, are expressed at high levels in activated macrophages and/or other              classical receptor-mediated mechanisms which are also activated by pattern recognition receptors, bound to substances as lipopolissacharide (LPS) from gram negative bacteria. These include the Toll Like Receptors (TLRs) and the receptor for advanced glycation end products (RAGE). Prolonged   J Appl Oral Sci.  104 hyperglycemia and the accompanying production of excess amounts of advanced glycation end products        resistance through the phosphorylation of serine residues in insulin receptor signaling (IRS)-1 that negatively regulates normal signaling through the       resistance by promoting the expression of numerous target genes as those for TNF- α , IL-6, IL-8, MCP-1,      29 .                 is exacerbated in patients with T2DM where TLR-4          induce responses by oral epithelial cells 2 .The local production of cytokines in response to periodontal bacteria and their products results in      biomarkers 13 and a poor glycemic control in T2DM patients is associated with a loss of mucosal barrier integrity and accumulation of innate immune receptor ligands resulting in an exacerbation of   2 .Thus, the adverse effect of periodontitis in T2DM may be explained by an increase in       resistance 19 .The interrelation between more severe PD and DM is established 8,32 and there are evidences on the importance of cytokine analysis in T2DM evolution 29  and therapy blockade 21 .      to an aberrant continuation of acute phase response and may also lead to further diabetes complications, such as micro and macroangiopathy and impaired healing 14,28 , it is suggested that periodontal disease        systemic levels 30  may collaborate to insulin resistance       evidence on the effects of chronic periodontitis on diabetes mellitus remains inadequate and inconclusive 9 . Furthermore, whether periodontal therapy may help to control serum levels of      5 . While some studies showed an effective improvement      markers and glycemic control after periodontal treatment in patients with T2DM 9,17,32 , others have shown that these responses were inconsistent across individuals and not sustainable over time 3,5,19 .      mediators, such as IL-6, in obesity or metabolic syndrome enhance the host response to periodontal pathogens, hence increasing the chance of periodontal destruction. IL-6 is a multifunctional cytokine produced by a variety of cells including macrophages, neutrophils, and endothelial cells. The double edge        molecule entail complexity in investigating its role and, until now, no evidence from animal or human studies supports the hypothetical model in which metabolic syndrome-induced IL-6 increases the risk of destructive periodontal disease 18 .Interleukin 8 (IL-8) is a chemokine important for recruiting neutrophils during healing and its levels were shown to be tightly linked to increased susceptibility to periodontitis 12 .Monocyte chemoattractant protein 1 (MCP-1) is also thought to play an important role in       as a key factor in recruitment and activation of peripheral blood leukocytes in atherosclerotic lesions and adipose tissue. Elevated levels of circulating MCP-1 have been found in patients with T2DM, and experimental data have shown that this protein      insulin resistance in transgenic mice 26 .Some studies 3,6,9,17,24  have evaluated markers        (TNF-        related them to insulin resistance 24  and glycemic control 3       Based on the evidences that IL-6, IL-8 and MCP-1 are important key markers of immune response, which have been considered as critical mediators of initiation, progression and/or suppression of chronic periodontitis, and that no previous study had analyzed this combination of mediators in groups with and without diabetes and periodontal disease, this study aimed to evaluate serum levels         type 2 diabetic patients in the presence of chronic periodontitis. PATIENTS AND METHODS This study was conducted between January 2012 and March 2013 in full accordance with the Helsinki Declaration of 1975, as revised in 2000. The study protocol and the informed consent form were reviewed and approved by the Biomedical Sciences Institute Ethics Committee (#011/CEP) from the University of São Paulo (São Paulo, Brazil). T2DM individuals were recruited from the Diabetes Center at the Federal University of São Paulo. Non-diabetic patients were recruited from the School of Dentistry, University of São Paulo. Detailed medical and dental history was obtained from all patients. All volunteers received full mouth periodontal clinical examination performed at six sites  per   tooth (excluding third molars) from a calibrated examiner (HPCA). Intraexaminer reliability for detecting PDs within 1 mm was >90%. The presence of supragingival         gingival bleeding was recorded as gingival bleeding                J Appl Oral Sci.  105 (GB); bleeding on probing (BP), probing depth (PD) and attachment level (AL) were also evaluated. The probe used was North Caroline (UNC-15, Hu-Friedy ® , Chicago, IL, USA). PL, GB and BP were recorded as absent (0) or present (1). Inclusion criteria were: age         over 3 years (for individuals with T2DM), generalized moderate to severe chronic periodontitis (American Academy of Periodontology, 1998)      with PD >4 mm and bleeding on probing) and       patients with Body Mass Index (BMI) >40 kg/m 2  or who received periodontal therapy, antibiotic or antiseptic therapy 6 months prior to the study were excluded. Blood samples were obtained and glycated hemoglobin (HbA1c) levels were determined for all individuals at the clinical laboratory of the University of São Paulo Hospital. Approximately 5 ml of blood were collected by venipuncture in untreated tubes (BD Vacutainer Rapid Serum Tube, Becton Dickinson Co., São Paulo, SP, Brazil). Serum was obtained by centrifugation at 2,500 g  for 2 minutes, aliquoted and        measurement of IL-6, IL-8 and MCP-1 was assayed by enzyme-linked immunosorbent assay (Human Standard ELISA Development Kit, PeproTech Inc., Rocky Hill, CT, USA) and read out using a Micro Plate reader (Model 680, Bio-Rad Laboratories Inc., Hercules, CA, USA). Serum from each patient was tested in triplicate, and a calibration curve was added to each plate.Forty-two individuals were enrolled in this study. Patients with T2DM and periodontitis were divided in two groups, as adequate glycemic control when                                      Periodontal clinical data were analyzed using appropriate statistical software (SPSS version 17.0 for Windows, SPSS Inc., Chicago, IL, USA) considering the individual as a study unit. The Kolmogorov-Smirnov test was used to test the variables normality distribution. Data were analyzed by non-parametric statistical methods since data were not normally distributed. Comparisons between groups were determined using Kruskal-Wallis test and Tukey test. Tests were based on median values with variability measures (25% and 75% quartiles).       p<0.05. For GB, PL and BOP data, percentages of positive sites were obtained  per   patient and, thereafter, median values were calculated for the groups. For PD and AL, measured by millimeters,         thereafter, as a median value for the group.Data from ELISA were analyzed by Kruskal-Wallis and Dunn’s Multiple Comparison Test (Prism 5.0 Project, Graph Pad Software Inc., La Jolla, CA, USA). Values were obtained per patient and a median value was calculated for each group. RESULTS A total of 546 patients were assessed for         (Figure 1). Demographic and HbA1c data from each group are described in Table 1.Table 2 provides periodontal clinical parameters    Flow diagram of patients included in the study                   J Appl Oral Sci.  106 for each group with periodontitis: DMI+P, DMA+P        diabetic (DMI+P and DMA+P) and non-diabetic         indicating a more severe disease among the diabetic patients. The other clinical parameters did not differ significantly among groups. Intergroup clinical parameters comparison for DMI+P and DMA+P       There were no differences between groups              male  BMI  H (n=6)250.0±4.3826.19±3.615.18±0.60P (n=6)547.0±5.2526.18±3.285.43±0.54DM (n=10)657.2±8.8026.18±2.377.33±0.78DMA+P (n=10)660.6±10.6727.34±4.386.83±0.78DMI+P (n=10)452.7±5.5428.92±6.3610.86±2.21 Table 1-  Demographic characteristics and glycated level (mean±standard deviation) for participants in each groupDM=type 2 diabetes mellitus; P=Periodontitis; BMI=body mass index. Groups: H (DM-P-), P (DM-P+), DM (DM+P-), DMA+P (DM+with adequate glycemic control P+), DMI+P (DM+with inadequate glycemic control P+) Clinical    p (n=10) (n=10) (n=6) value GB (%)71.35 (55.40-94.02)59.02 (40.16-90.69)58.85 (40.22-72.22)0.34PL (%)90.83 (68.00-97.90)66.70 (52.52-97.00)66.88 (52.40-81.62)0.25BOP (%)77.56 (68.24-94.54)67.55 (40.52-93.68)58.80(43.87-65.82)0.88PD (mm)3.60 (3.17-4.10)3.40 (3.00-4.10)3.00 (2.87-3.22)0.04* AL (mm)4.45 (3.82-5.05)4.20 (3.70-4.90)3.4 (3.25-3.65)0.01* Table 2-  Medians and quartiles (25–75%) of clinical parameters for the DMA+P, DMI+P and P groups            α =5%). GB= gingival bleeding index; PL=visible plaque index; BOP=bleeding on probing; PD=probing depth; AL=attachment level    IL-6 (A), IL-8 (B) and MCP-1 (C) serum levels in patients without periodontitis and T2DM (H), patients with periodontitis and without T2DM (P), patients with T2DM and without periodontitis (DM), patients with T2DM with adequate glycemic control and periodontitis (DMA+P) and patients with T2DM with inadequate glycemic control and periodontitis (DMI+P). MCP-1=monocyte chemoattractant protein-1; IL-6=interleukin 6; IL-8=interleukin 8; T2DM=Type 2 diabetes mellitus.              
We Need Your Support
Thank you for visiting our website and your interest in our free products and services. We are nonprofit website to share and download documents. To the running of this website, we need your help to support us.

Thanks to everyone for your continued support.

No, Thanks