Salivary interleukin-17 and tumor necrosis factor-α in relation to periodontitis and glycemic status in type 2 diabetes mellitus
Background Poorly‐controlled glycemic status in type 2 diabetes mellitus (T2DM) is suggested to play a role in the periodontal inflammatory process by aggregating the local cytokine response. Our objectives were to profile salivary interleukin (IL)‐17 and tumor necrosis factor (TNF)‐α levels in subj...
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Published in | Journal of diabetes Vol. 7; no. 5; pp. 681 - 688 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Australia
Blackwell Publishing Ltd
01.09.2015
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Subjects | |
Online Access | Get full text |
ISSN | 1753-0393 1753-0407 1753-0407 |
DOI | 10.1111/1753-0407.12228 |
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Abstract | Background
Poorly‐controlled glycemic status in type 2 diabetes mellitus (T2DM) is suggested to play a role in the periodontal inflammatory process by aggregating the local cytokine response. Our objectives were to profile salivary interleukin (IL)‐17 and tumor necrosis factor (TNF)‐α levels in subjects with T2DM and to examine their relevance for the periodontal health status and glycemic control levels.
Methods
Unstimulated whole saliva samples, together with full‐mouth periodontal recordings (plaque index [PI], bleeding on probing [BOP %], gingival index [GI], probing pocket depth [PPD], and clinical attachment level [CAL]), were collected from 123 subjects with T2DM. Additionally, demographic and general health parameters, including fasting blood glucose, glycated hemoglobin (HbA1c), were collected. Salivary IL‐17 and TNF‐α concentrations were analyzed using the Luminex®‐xMAP™ technique.
Results
Subjects with poorly‐controlled T2DM (HbA1c ≥ 7) had elevated serum triglyceride (P < 0.001) concentration as well as elevated scores of BOP % (P = 0.014), PI (P = 0.048), GI (P = 0.033), and CAL (P = 0.003) in comparison to those of well‐controlled T2DM (HbA1c < 7). When the subjects with detectable salivary IL‐17 were categorized in tertiles, the scores of PPD and BOP%, and salivary TNF‐α concentrations were significantly elevated in the highest (P = 0.007, P = 0.002 and P < 0.001, respectively) and middle (P = 0.052, P = 0.022, and P = 0.003, respectively) tertiles compared to subjects with non‐detectable salivary IL‐17. The adjusted association between PPD measurements and salivary IL‐17 concentrations was significant (P = 0.008).
Conclusions
Poorly‐controlled glycemic status relates to the severity of periodontal disease in T2DM. The association between PPD and IL‐17 in saliva, however, is independent from the effect of glycemic status.
摘要
背景:
目前认为血糖水平控制不佳在2型糖尿病(T2DM)患者牙周炎症发生过程中对聚集局部细胞因子反应有影响。我们的目的是描述T2DM受试者唾液中的白细胞介素(IL)‐17以及肿瘤坏死因子(TNF)‐α的水平,调查它们与牙周健康状态以及血糖控制水平之间的相关性。
方法:
从123名T2DM受试者中收集非刺激性的全唾液样本以及全口腔牙周记录(菌斑指数[plaque index,PI],探查时出血[bleeding on probing,BOP %],牙龈指数[gingival index,GI],探测袋深度[probing pocket depth,PPD]以及临床附着水平[clinical attachment level,CAL])。另外,还收集了人口统计学以及一般的健康指标,包括空腹血糖与糖化血红蛋白(HbA1c)。使用Luminex®‐xMAP™技术来分析唾液中的IL‐17与TNF‐α浓度。
结果:
与血糖控制良好的T2DM受试者(HbA1c < 7)相比,血糖控制不佳的T2DM受试者(HbA1c ≥ 7)血清中的甘油三酯浓度升高(P < 0.001),除此之外BOP %(P = 0.014)、PI(P = 0.048)、GI(P = 0.033)以及CAL(P = 0.003)的评分也更高。与唾液中检测不到IL‐17的受试者相比较,唾液中可检测到IL‐17的受试者按照IL‐17浓度三等分为3组,发现PPD与BOP %评分以及唾液中的TNF‐α浓度在浓度最高组(分别P = 0.007,P = 0.002与P < 0.001)与中间组(分别P = 0.052,P = 0.022与P = 0.003)都显著升高。经过校正之后发现PPD测量结果与唾液中的TNF‐α浓度具有显著相关性(P = 0.008)。
结论:
T2DM患者血糖水平控制不佳与牙周病的严重程度相关。PPD与唾液中的IL‐17相关,然而,这种相关性独立于血糖状态的影响。 |
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AbstractList | Poorly-controlled glycemic status in type 2 diabetes mellitus (T2DM) is suggested to play a role in the periodontal inflammatory process by aggregating the local cytokine response. Our objectives were to profile salivary interleukin (IL)-17 and tumor necrosis factor (TNF)-α levels in subjects with T2DM and to examine their relevance for the periodontal health status and glycemic control levels.
Unstimulated whole saliva samples, together with full-mouth periodontal recordings (plaque index [PI], bleeding on probing [BOP %], gingival index [GI], probing pocket depth [PPD], and clinical attachment level [CAL]), were collected from 123 subjects with T2DM. Additionally, demographic and general health parameters, including fasting blood glucose, glycated hemoglobin (HbA1c), were collected. Salivary IL-17 and TNF-α concentrations were analyzed using the Luminex®-xMAP™ technique.
Subjects with poorly-controlled T2DM (HbA1c ≥ 7) had elevated serum triglyceride (P < 0.001) concentration as well as elevated scores of BOP % (P = 0.014), PI (P = 0.048), GI (P = 0.033), and CAL (P = 0.003) in comparison to those of well-controlled T2DM (HbA1c < 7). When the subjects with detectable salivary IL-17 were categorized in tertiles, the scores of PPD and BOP%, and salivary TNF-α concentrations were significantly elevated in the highest (P = 0.007, P = 0.002 and P < 0.001, respectively) and middle (P = 0.052, P = 0.022, and P = 0.003, respectively) tertiles compared to subjects with non-detectable salivary IL-17. The adjusted association between PPD measurements and salivary IL-17 concentrations was significant (P = 0.008).
Poorly-controlled glycemic status relates to the severity of periodontal disease in T2DM. The association between PPD and IL-17 in saliva, however, is independent from the effect of glycemic status. Background Poorly‐controlled glycemic status in type 2 diabetes mellitus (T2DM) is suggested to play a role in the periodontal inflammatory process by aggregating the local cytokine response. Our objectives were to profile salivary interleukin (IL)‐17 and tumor necrosis factor (TNF)‐α levels in subjects with T2DM and to examine their relevance for the periodontal health status and glycemic control levels. Methods Unstimulated whole saliva samples, together with full‐mouth periodontal recordings (plaque index [PI], bleeding on probing [BOP %], gingival index [GI], probing pocket depth [PPD], and clinical attachment level [CAL]), were collected from 123 subjects with T2DM. Additionally, demographic and general health parameters, including fasting blood glucose, glycated hemoglobin (HbA1c), were collected. Salivary IL‐17 and TNF‐α concentrations were analyzed using the Luminex®‐xMAP™ technique. Results Subjects with poorly‐controlled T2DM (HbA1c ≥ 7) had elevated serum triglyceride (P < 0.001) concentration as well as elevated scores of BOP % (P = 0.014), PI (P = 0.048), GI (P = 0.033), and CAL (P = 0.003) in comparison to those of well‐controlled T2DM (HbA1c < 7). When the subjects with detectable salivary IL‐17 were categorized in tertiles, the scores of PPD and BOP%, and salivary TNF‐α concentrations were significantly elevated in the highest (P = 0.007, P = 0.002 and P < 0.001, respectively) and middle (P = 0.052, P = 0.022, and P = 0.003, respectively) tertiles compared to subjects with non‐detectable salivary IL‐17. The adjusted association between PPD measurements and salivary IL‐17 concentrations was significant (P = 0.008). Conclusions Poorly‐controlled glycemic status relates to the severity of periodontal disease in T2DM. The association between PPD and IL‐17 in saliva, however, is independent from the effect of glycemic status. 摘要 背景: 目前认为血糖水平控制不佳在2型糖尿病(T2DM)患者牙周炎症发生过程中对聚集局部细胞因子反应有影响。我们的目的是描述T2DM受试者唾液中的白细胞介素(IL)‐17以及肿瘤坏死因子(TNF)‐α的水平,调查它们与牙周健康状态以及血糖控制水平之间的相关性。 方法: 从123名T2DM受试者中收集非刺激性的全唾液样本以及全口腔牙周记录(菌斑指数[plaque index,PI],探查时出血[bleeding on probing,BOP %],牙龈指数[gingival index,GI],探测袋深度[probing pocket depth,PPD]以及临床附着水平[clinical attachment level,CAL])。另外,还收集了人口统计学以及一般的健康指标,包括空腹血糖与糖化血红蛋白(HbA1c)。使用Luminex®‐xMAP™技术来分析唾液中的IL‐17与TNF‐α浓度。 结果: 与血糖控制良好的T2DM受试者(HbA1c < 7)相比,血糖控制不佳的T2DM受试者(HbA1c ≥ 7)血清中的甘油三酯浓度升高(P < 0.001),除此之外BOP %(P = 0.014)、PI(P = 0.048)、GI(P = 0.033)以及CAL(P = 0.003)的评分也更高。与唾液中检测不到IL‐17的受试者相比较,唾液中可检测到IL‐17的受试者按照IL‐17浓度三等分为3组,发现PPD与BOP %评分以及唾液中的TNF‐α浓度在浓度最高组(分别P = 0.007,P = 0.002与P < 0.001)与中间组(分别P = 0.052,P = 0.022与P = 0.003)都显著升高。经过校正之后发现PPD测量结果与唾液中的TNF‐α浓度具有显著相关性(P = 0.008)。 结论: T2DM患者血糖水平控制不佳与牙周病的严重程度相关。PPD与唾液中的IL‐17相关,然而,这种相关性独立于血糖状态的影响。 Poorly-controlled glycemic status in type 2 diabetes mellitus (T2DM) is suggested to play a role in the periodontal inflammatory process by aggregating the local cytokine response. Our objectives were to profile salivary interleukin (IL)-17 and tumor necrosis factor (TNF)-α levels in subjects with T2DM and to examine their relevance for the periodontal health status and glycemic control levels.BACKGROUNDPoorly-controlled glycemic status in type 2 diabetes mellitus (T2DM) is suggested to play a role in the periodontal inflammatory process by aggregating the local cytokine response. Our objectives were to profile salivary interleukin (IL)-17 and tumor necrosis factor (TNF)-α levels in subjects with T2DM and to examine their relevance for the periodontal health status and glycemic control levels.Unstimulated whole saliva samples, together with full-mouth periodontal recordings (plaque index [PI], bleeding on probing [BOP %], gingival index [GI], probing pocket depth [PPD], and clinical attachment level [CAL]), were collected from 123 subjects with T2DM. Additionally, demographic and general health parameters, including fasting blood glucose, glycated hemoglobin (HbA1c), were collected. Salivary IL-17 and TNF-α concentrations were analyzed using the Luminex®-xMAP™ technique.METHODSUnstimulated whole saliva samples, together with full-mouth periodontal recordings (plaque index [PI], bleeding on probing [BOP %], gingival index [GI], probing pocket depth [PPD], and clinical attachment level [CAL]), were collected from 123 subjects with T2DM. Additionally, demographic and general health parameters, including fasting blood glucose, glycated hemoglobin (HbA1c), were collected. Salivary IL-17 and TNF-α concentrations were analyzed using the Luminex®-xMAP™ technique.Subjects with poorly-controlled T2DM (HbA1c ≥ 7) had elevated serum triglyceride (P < 0.001) concentration as well as elevated scores of BOP % (P = 0.014), PI (P = 0.048), GI (P = 0.033), and CAL (P = 0.003) in comparison to those of well-controlled T2DM (HbA1c < 7). When the subjects with detectable salivary IL-17 were categorized in tertiles, the scores of PPD and BOP%, and salivary TNF-α concentrations were significantly elevated in the highest (P = 0.007, P = 0.002 and P < 0.001, respectively) and middle (P = 0.052, P = 0.022, and P = 0.003, respectively) tertiles compared to subjects with non-detectable salivary IL-17. The adjusted association between PPD measurements and salivary IL-17 concentrations was significant (P = 0.008).RESULTSSubjects with poorly-controlled T2DM (HbA1c ≥ 7) had elevated serum triglyceride (P < 0.001) concentration as well as elevated scores of BOP % (P = 0.014), PI (P = 0.048), GI (P = 0.033), and CAL (P = 0.003) in comparison to those of well-controlled T2DM (HbA1c < 7). When the subjects with detectable salivary IL-17 were categorized in tertiles, the scores of PPD and BOP%, and salivary TNF-α concentrations were significantly elevated in the highest (P = 0.007, P = 0.002 and P < 0.001, respectively) and middle (P = 0.052, P = 0.022, and P = 0.003, respectively) tertiles compared to subjects with non-detectable salivary IL-17. The adjusted association between PPD measurements and salivary IL-17 concentrations was significant (P = 0.008).Poorly-controlled glycemic status relates to the severity of periodontal disease in T2DM. The association between PPD and IL-17 in saliva, however, is independent from the effect of glycemic status.CONCLUSIONSPoorly-controlled glycemic status relates to the severity of periodontal disease in T2DM. The association between PPD and IL-17 in saliva, however, is independent from the effect of glycemic status. |
Author | Doğan, Başak Gürsoy, Ulvi Kahraman Yildiz Çiftlikli, Sinem Gürsoy, Mervi Könönen, Eija |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25327309$$D View this record in MEDLINE/PubMed |
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Keywords | saliva type 2 diabetes mellitus interleukin-17 tumor necrosis factor-α 关键词:白细胞介素-17,牙周病,唾液,肿瘤坏死因子-α,2型糖尿病 periodontal disease |
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References | Miossec P, Kolls JK. Targeting IL-17 and TH17 cells in chronic inflammation. Nat Rev Drug Discov. 2012; 11: 763-776. Eke PI, Page RC, Wei L, Thornton-Evans G, Genco RJ. Update of the case definitions for population-based surveillance of periodontitis. J Periodontol. 2012; 83: 1449-1454. Wilensky A, Segev H, Mizraji G et al. Dendritic cells and their role in periodontal disease. Oral Dis. 2014; 20: 119-126. Javed F, Al-Askar M, Al-Hezaimi K. Cytokine profile in the gingival crevicular fluid of periodontitis patients with and without type 2 diabetes: A literature review. J Periodontol. 2012; 83: 156-161. Gursoy UK, Marakoglu I, Oztop AY. Relationship between neutrophil functions and severity of periodontitis in obese and/or type 2 diabetic chronic periodontitis patients. Quintessence Int. 2008; 39: 485-489. Turner-Brannen E, Choi KY, Arsenault R, El-Gabalawy H, Napper S, Mookherjee N. Inflammatory cytokines IL-32 and IL-17 have common signaling intermediates despite differential dependence on TNF-receptor 1. J Immunol. 2011; 186: 7127-7135. Serrano C, Perez C, Rodriguez M. Periodontal conditions in a group of Colombian type 2 diabetic patients with different degrees of metabolic control. Acta Odontol Latinoam. 2012; 25: 132-139. Gürsoy UK, Könönen E, Uitto VJ et al. Salivary interleukin-1beta concentration and the presence of multiple pathogens in periodontitis. J Clin Periodontol. 2009; 36: 922-927. Ji L, Hu D, Pan C et al. Primacy of the 3B approach to control risk factors for cardiovascular disease in type 2 diabetes patients. Am J Med. 2013; 126: 925 e11-92522. Preshaw PM, Alba AL, Herrera D et al. Periodontitis and diabetes: A two-way relationship. Diabetologia. 2012; 55: 21-31. Miller CS, Foley JD, Bailey AL et al. Current developments in salivary diagnostics. Biomark Med. 2010; 4: 171-189. Silva JA, Ferrucci DL, Peroni LA et al. Sequential IL-23 and IL-17 and increased Mmp8 and Mmp14 expression characterize the progression of an experimental model of periodontal disease in type 1 diabetes. J Cell Physiol. 2012; 227: 2441-2450. Cheng WC, Hughes FJ, Taams LS. The presence, function and regulation of IL-17 and Th17 cells in periodontitis. J Clin Periodontol. 2014; Epub ahead of print; 41: 541-549. Taylor JJ, Preshaw PM, Lalla E. A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes. J Clin Periodontol. 2013; 40 (Suppl. 14): S113-134. Mealey BL, Ocampo GL. Diabetes mellitus and periodontal disease. Periodontol 2000. 2007; 44: 127-153. Hotamisligil GS, Shargill NS, Spiegelman BM. Adipose expression of tumor necrosis factor-alpha: Direct role in obesity-linked insulin resistance. Science. 1993; 259: 87-91. Santos VR, Ribeiro FV, Lima JA, Napimoga MH, Bastos MF, Duarte PM. Cytokine levels in sites of chronic periodontitis of poorly controlled and well-controlled type 2 diabetic subjects. J Clin Periodontol. 2010; 37: 1049-1058. Song X, Qian Y. IL-17 family cytokines mediated signaling in the pathogenesis of inflammatory diseases. Cell Signal. 2013; 25: 2335-2347. Katagiri S, Nitta H, Nagasawa T et al. Effect of glycemic control on periodontitis in type 2 diabetic patients with periodontal disease. J Diabetes Investig. 2013; 4: 320-325. Koenders MI, Marijnissen RJ, Devesa I et al. Tumor necrosis factor-interleukin-17 interplay induces S100A8, interleukin-1beta, and matrix metalloproteinases, and drives irreversible cartilage destruction in murine arthritis: Rationale for combination treatment during arthritis. Arthritis Rheum. 2011; 63: 2329-2339. Gürsoy UK, Könönen E, Huumonen S et al. Salivary type I collagen degradation end-products and related matrix metalloproteinases in periodontitis. J Clin Periodontol. 2013; 40: 18-25. Hajishengallis G. Immunomicrobial pathogenesis of periodontitis: Keystones, pathobionts, and host response. Trends Immunol. 2014; 35: 3-11. Lalla E, Lamster IB, Feit M et al. Blockade of RAGE suppresses periodontitis-associated bone loss in diabetic mice. J Clin Invest. 2000; 105: 1117-1124. Lalla E, Papapanou PN. Diabetes mellitus and periodontitis: A tale of two common interrelated diseases. Nat Rev Endocrinol. 2011; 7: 738-748. Liu Y, Mei J, Gonzales L et al. IL-17A and TNF-alpha exert synergistic effects on expression of CXCL5 by alveolar type II cells in vivo and in vitro. J Immunol. 2011; 186: 3197-3205. Donath MY, Shoelson SE. Type 2 diabetes as an inflammatory disease. Nat Rev Immunol. 2011; 11: 98-107. Teles RP, Likhari V, Socransky SS, Haffajee AD. Salivary cytokine levels in subjects with chronic periodontitis and in periodontally healthy individuals: A cross-sectional study. J Periodontal Res. 2009; 44: 411-417. Darveau RP. Periodontitis: A polymicrobial disruption of host homeostasis. Nat Rev Microbiol. 2010; 8: 481-490. Pihlstrom BL, Michalowicz BS, Johnson NW. Periodontal diseases. Lancet. 2005; 366: 1809-1820. Ribeiro FV, de Mendonca AC, Santos VR, Bastos MF, Figueiredo LC, Duarte PM. Cytokines and bone-related factors in systemically healthy patients with chronic periodontitis and patients with type 2 diabetes and chronic periodontitis. J Periodontol. 2011; 82: 1187-1196. Gürsoy UK, Könönen E. Understanding the roles of gingival beta-defensins. J Oral Microbiol. 2012; 4: 15127. doi:10.3402/jom.v4i0.15127 Loe H, Silness J. Periodontal Disease in Pregnancy. I. Prevalence and Severity. Acta Odontol Scand. 1963; 21: 533-551. Preshaw PM, Bissett SM. Periodontitis: Oral complication of diabetes. Endocrinol Metab Clin North Am. 2013; 42: 849-867. Silness J, Loe H. Periodontal disease in pregnancy. Ii. Correlation between oral hygiene and periodontal condtion. Acta Odontol Scand. 1964; 22: 121-135. Gürsoy UK, Könönen E, Pradhan-Palikhe P et al. Salivary MMP-8, TIMP-1, and ICTP as markers of advanced periodontitis. J Clin Periodontol. 2010; 37: 487-493. 2012; 83 2009; 44 2010; 37 1963; 21 2013; 4 2013; 25 2013; 40 2011; 82 2013; 126 2013; 42 2008; 39 1964; 22 2011; 11 2014; 41 2012; 55 2012; 227 2012; 11 2011; 7 2014; 20 2009; 36 2005; 366 2000; 105 2011; 63 2014; 35 2012; 25 2007; 44 1993; 259 2012; 4 2010; 4 2010; 8 2011; 186 |
References_xml | – reference: Hajishengallis G. Immunomicrobial pathogenesis of periodontitis: Keystones, pathobionts, and host response. Trends Immunol. 2014; 35: 3-11. – reference: Mealey BL, Ocampo GL. Diabetes mellitus and periodontal disease. Periodontol 2000. 2007; 44: 127-153. – reference: Gürsoy UK, Könönen E, Pradhan-Palikhe P et al. Salivary MMP-8, TIMP-1, and ICTP as markers of advanced periodontitis. J Clin Periodontol. 2010; 37: 487-493. – reference: Preshaw PM, Alba AL, Herrera D et al. Periodontitis and diabetes: A two-way relationship. Diabetologia. 2012; 55: 21-31. – reference: Loe H, Silness J. Periodontal Disease in Pregnancy. I. Prevalence and Severity. Acta Odontol Scand. 1963; 21: 533-551. – reference: Lalla E, Papapanou PN. Diabetes mellitus and periodontitis: A tale of two common interrelated diseases. Nat Rev Endocrinol. 2011; 7: 738-748. – reference: Cheng WC, Hughes FJ, Taams LS. The presence, function and regulation of IL-17 and Th17 cells in periodontitis. J Clin Periodontol. 2014; Epub ahead of print; 41: 541-549. – reference: Serrano C, Perez C, Rodriguez M. Periodontal conditions in a group of Colombian type 2 diabetic patients with different degrees of metabolic control. Acta Odontol Latinoam. 2012; 25: 132-139. – reference: Turner-Brannen E, Choi KY, Arsenault R, El-Gabalawy H, Napper S, Mookherjee N. Inflammatory cytokines IL-32 and IL-17 have common signaling intermediates despite differential dependence on TNF-receptor 1. J Immunol. 2011; 186: 7127-7135. – reference: Katagiri S, Nitta H, Nagasawa T et al. Effect of glycemic control on periodontitis in type 2 diabetic patients with periodontal disease. J Diabetes Investig. 2013; 4: 320-325. – reference: Miller CS, Foley JD, Bailey AL et al. Current developments in salivary diagnostics. Biomark Med. 2010; 4: 171-189. – reference: Koenders MI, Marijnissen RJ, Devesa I et al. Tumor necrosis factor-interleukin-17 interplay induces S100A8, interleukin-1beta, and matrix metalloproteinases, and drives irreversible cartilage destruction in murine arthritis: Rationale for combination treatment during arthritis. Arthritis Rheum. 2011; 63: 2329-2339. – reference: Hotamisligil GS, Shargill NS, Spiegelman BM. Adipose expression of tumor necrosis factor-alpha: Direct role in obesity-linked insulin resistance. Science. 1993; 259: 87-91. – reference: Santos VR, Ribeiro FV, Lima JA, Napimoga MH, Bastos MF, Duarte PM. Cytokine levels in sites of chronic periodontitis of poorly controlled and well-controlled type 2 diabetic subjects. J Clin Periodontol. 2010; 37: 1049-1058. – reference: Darveau RP. Periodontitis: A polymicrobial disruption of host homeostasis. Nat Rev Microbiol. 2010; 8: 481-490. – reference: Ribeiro FV, de Mendonca AC, Santos VR, Bastos MF, Figueiredo LC, Duarte PM. Cytokines and bone-related factors in systemically healthy patients with chronic periodontitis and patients with type 2 diabetes and chronic periodontitis. J Periodontol. 2011; 82: 1187-1196. – reference: Silness J, Loe H. Periodontal disease in pregnancy. Ii. Correlation between oral hygiene and periodontal condtion. Acta Odontol Scand. 1964; 22: 121-135. – reference: Eke PI, Page RC, Wei L, Thornton-Evans G, Genco RJ. Update of the case definitions for population-based surveillance of periodontitis. J Periodontol. 2012; 83: 1449-1454. – reference: Miossec P, Kolls JK. Targeting IL-17 and TH17 cells in chronic inflammation. Nat Rev Drug Discov. 2012; 11: 763-776. – reference: Gürsoy UK, Könönen E, Huumonen S et al. Salivary type I collagen degradation end-products and related matrix metalloproteinases in periodontitis. J Clin Periodontol. 2013; 40: 18-25. – reference: Javed F, Al-Askar M, Al-Hezaimi K. Cytokine profile in the gingival crevicular fluid of periodontitis patients with and without type 2 diabetes: A literature review. J Periodontol. 2012; 83: 156-161. – reference: Wilensky A, Segev H, Mizraji G et al. Dendritic cells and their role in periodontal disease. Oral Dis. 2014; 20: 119-126. – reference: Gursoy UK, Marakoglu I, Oztop AY. Relationship between neutrophil functions and severity of periodontitis in obese and/or type 2 diabetic chronic periodontitis patients. Quintessence Int. 2008; 39: 485-489. – reference: Preshaw PM, Bissett SM. Periodontitis: Oral complication of diabetes. Endocrinol Metab Clin North Am. 2013; 42: 849-867. – reference: Pihlstrom BL, Michalowicz BS, Johnson NW. Periodontal diseases. Lancet. 2005; 366: 1809-1820. – reference: Lalla E, Lamster IB, Feit M et al. Blockade of RAGE suppresses periodontitis-associated bone loss in diabetic mice. J Clin Invest. 2000; 105: 1117-1124. – reference: Silva JA, Ferrucci DL, Peroni LA et al. Sequential IL-23 and IL-17 and increased Mmp8 and Mmp14 expression characterize the progression of an experimental model of periodontal disease in type 1 diabetes. J Cell Physiol. 2012; 227: 2441-2450. – reference: Gürsoy UK, Könönen E, Uitto VJ et al. Salivary interleukin-1beta concentration and the presence of multiple pathogens in periodontitis. J Clin Periodontol. 2009; 36: 922-927. – reference: Taylor JJ, Preshaw PM, Lalla E. A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes. J Clin Periodontol. 2013; 40 (Suppl. 14): S113-134. – reference: Ji L, Hu D, Pan C et al. Primacy of the 3B approach to control risk factors for cardiovascular disease in type 2 diabetes patients. Am J Med. 2013; 126: 925 e11-92522. – reference: Song X, Qian Y. IL-17 family cytokines mediated signaling in the pathogenesis of inflammatory diseases. Cell Signal. 2013; 25: 2335-2347. – reference: Teles RP, Likhari V, Socransky SS, Haffajee AD. Salivary cytokine levels in subjects with chronic periodontitis and in periodontally healthy individuals: A cross-sectional study. J Periodontal Res. 2009; 44: 411-417. – reference: Liu Y, Mei J, Gonzales L et al. IL-17A and TNF-alpha exert synergistic effects on expression of CXCL5 by alveolar type II cells in vivo and in vitro. J Immunol. 2011; 186: 3197-3205. – reference: Donath MY, Shoelson SE. Type 2 diabetes as an inflammatory disease. Nat Rev Immunol. 2011; 11: 98-107. – reference: Gürsoy UK, Könönen E. Understanding the roles of gingival beta-defensins. J Oral Microbiol. 2012; 4: 15127. doi:10.3402/jom.v4i0.15127 – volume: 126 start-page: 925 e11 year: 2013 end-page: 92522 article-title: Primacy of the 3B approach to control risk factors for cardiovascular disease in type 2 diabetes patients publication-title: Am J Med – volume: 186 start-page: 7127 year: 2011 end-page: 7135 article-title: Inflammatory cytokines IL‐32 and IL‐17 have common signaling intermediates despite differential dependence on TNF‐receptor 1 publication-title: J Immunol – volume: 44 start-page: 127 year: 2007 end-page: 153 article-title: Diabetes mellitus and periodontal disease publication-title: Periodontol 2000 – volume: 4 start-page: 171 year: 2010 end-page: 189 article-title: Current developments in salivary diagnostics publication-title: Biomark Med – volume: 40 start-page: S113 issue: Suppl. 14 year: 2013 end-page: 134 article-title: A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes publication-title: J Clin Periodontol – volume: 44 start-page: 411 year: 2009 end-page: 417 article-title: Salivary cytokine levels in subjects with chronic periodontitis and in periodontally healthy individuals: A cross‐sectional study publication-title: J Periodontal Res – volume: 227 start-page: 2441 year: 2012 end-page: 2450 article-title: Sequential IL‐23 and IL‐17 and increased Mmp8 and Mmp14 expression characterize the progression of an experimental model of periodontal disease in type 1 diabetes publication-title: J Cell Physiol – volume: 40 start-page: 18 year: 2013 end-page: 25 article-title: Salivary type I collagen degradation end‐products and related matrix metalloproteinases in periodontitis publication-title: J Clin Periodontol – volume: 7 start-page: 738 year: 2011 end-page: 748 article-title: Diabetes mellitus and periodontitis: A tale of two common interrelated diseases publication-title: Nat Rev Endocrinol – volume: 42 start-page: 849 year: 2013 end-page: 867 article-title: Periodontitis: Oral complication of diabetes publication-title: Endocrinol Metab Clin North Am – volume: 82 start-page: 1187 year: 2011 end-page: 1196 article-title: Cytokines and bone‐related factors in systemically healthy patients with chronic periodontitis and patients with type 2 diabetes and chronic periodontitis publication-title: J Periodontol – volume: 22 start-page: 121 year: 1964 end-page: 135 article-title: Periodontal disease in pregnancy. Ii. Correlation between oral hygiene and periodontal condtion publication-title: Acta Odontol Scand – volume: 83 start-page: 156 year: 2012 end-page: 161 article-title: Cytokine profile in the gingival crevicular fluid of periodontitis patients with and without type 2 diabetes: A literature review publication-title: J Periodontol – volume: 25 start-page: 2335 year: 2013 end-page: 2347 article-title: IL‐17 family cytokines mediated signaling in the pathogenesis of inflammatory diseases publication-title: Cell Signal – volume: 20 start-page: 119 year: 2014 end-page: 126 article-title: Dendritic cells and their role in periodontal disease publication-title: Oral Dis – volume: 41 start-page: 541 year: 2014 end-page: 549 article-title: The presence, function and regulation of IL‐17 and Th17 cells in periodontitis publication-title: J Clin Periodontol – volume: 25 start-page: 132 year: 2012 end-page: 139 article-title: Periodontal conditions in a group of Colombian type 2 diabetic patients with different degrees of metabolic control publication-title: Acta Odontol Latinoam – volume: 36 start-page: 922 year: 2009 end-page: 927 article-title: Salivary interleukin‐1beta concentration and the presence of multiple pathogens in periodontitis publication-title: J Clin Periodontol – volume: 366 start-page: 1809 year: 2005 end-page: 1820 article-title: Periodontal diseases publication-title: Lancet – volume: 186 start-page: 3197 year: 2011 end-page: 3205 article-title: IL‐17A and TNF‐alpha exert synergistic effects on expression of CXCL5 by alveolar type II cells in vivo and in vitro publication-title: J Immunol – volume: 35 start-page: 3 year: 2014 end-page: 11 article-title: Immunomicrobial pathogenesis of periodontitis: Keystones, pathobionts, and host response publication-title: Trends Immunol – volume: 11 start-page: 98 year: 2011 end-page: 107 article-title: Type 2 diabetes as an inflammatory disease publication-title: Nat Rev Immunol – volume: 259 start-page: 87 year: 1993 end-page: 91 article-title: Adipose expression of tumor necrosis factor‐alpha: Direct role in obesity‐linked insulin resistance publication-title: Science – volume: 4 start-page: 320 year: 2013 end-page: 325 article-title: Effect of glycemic control on periodontitis in type 2 diabetic patients with periodontal disease publication-title: J Diabetes Investig – volume: 21 start-page: 533 year: 1963 end-page: 551 article-title: Periodontal Disease in Pregnancy. I. Prevalence and Severity publication-title: Acta Odontol Scand – volume: 105 start-page: 1117 year: 2000 end-page: 1124 article-title: Blockade of RAGE suppresses periodontitis‐associated bone loss in diabetic mice publication-title: J Clin Invest – volume: 4 start-page: 15127 year: 2012 article-title: Understanding the roles of gingival beta‐defensins publication-title: J Oral Microbiol – volume: 63 start-page: 2329 year: 2011 end-page: 2339 article-title: Tumor necrosis factor‐interleukin‐17 interplay induces S100A8, interleukin‐1beta, and matrix metalloproteinases, and drives irreversible cartilage destruction in murine arthritis: Rationale for combination treatment during arthritis publication-title: Arthritis Rheum – volume: 8 start-page: 481 year: 2010 end-page: 490 article-title: Periodontitis: A polymicrobial disruption of host homeostasis publication-title: Nat Rev Microbiol – volume: 55 start-page: 21 year: 2012 end-page: 31 article-title: Periodontitis and diabetes: A two‐way relationship publication-title: Diabetologia – volume: 11 start-page: 763 year: 2012 end-page: 776 article-title: Targeting IL‐17 and TH17 cells in chronic inflammation publication-title: Nat Rev Drug Discov – volume: 39 start-page: 485 year: 2008 end-page: 489 article-title: Relationship between neutrophil functions and severity of periodontitis in obese and/or type 2 diabetic chronic periodontitis patients publication-title: Quintessence Int – volume: 37 start-page: 487 year: 2010 end-page: 493 article-title: Salivary MMP‐8, TIMP‐1, and ICTP as markers of advanced periodontitis publication-title: J Clin Periodontol – volume: 37 start-page: 1049 year: 2010 end-page: 1058 article-title: Cytokine levels in sites of chronic periodontitis of poorly controlled and well‐controlled type 2 diabetic subjects publication-title: J Clin Periodontol – volume: 83 start-page: 1449 year: 2012 end-page: 1454 article-title: Update of the case definitions for population‐based surveillance of periodontitis publication-title: J Periodontol |
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Poorly‐controlled glycemic status in type 2 diabetes mellitus (T2DM) is suggested to play a role in the periodontal inflammatory process by... Poorly-controlled glycemic status in type 2 diabetes mellitus (T2DM) is suggested to play a role in the periodontal inflammatory process by aggregating the... |
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SubjectTerms | Adult Blood Glucose - metabolism Diabetes Mellitus, Type 2 - complications Diabetes Mellitus, Type 2 - drug therapy Diabetes Mellitus, Type 2 - metabolism Female Glycated Hemoglobin A - analysis Humans Hypoglycemic Agents - therapeutic use interleukin-17 Interleukin-17 - analysis Male Middle Aged periodontal disease Periodontitis - complications Periodontitis - metabolism saliva Saliva - chemistry Tumor Necrosis Factor-alpha - analysis tumor necrosis factor-α type 2 diabetes mellitus 关键词:白细胞介素-17,牙周病,唾液,肿瘤坏死因子-α,2型糖尿病 |
Title | Salivary interleukin-17 and tumor necrosis factor-α in relation to periodontitis and glycemic status in type 2 diabetes mellitus |
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