Salivary inflammatory markers and microbiome in normoglycemic lean and obese children compared to obese children with type 2 diabetes
There is emerging evidence linking diabetes with periodontal disease. Diabetes is a well-recognized risk factor for periodontal disease. Conversely, pro-inflammatory molecules released by periodontally-diseased tissues may enter the circulation to induce insulin resistance. While this association ha...
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Abstract | There is emerging evidence linking diabetes with periodontal disease. Diabetes is a well-recognized risk factor for periodontal disease. Conversely, pro-inflammatory molecules released by periodontally-diseased tissues may enter the circulation to induce insulin resistance. While this association has been demonstrated in adults, there is little information regarding periodontal status in obese children with and without type 2 diabetes (T2D). We hypothesized that children with T2D have higher rates of gingivitis, elevated salivary inflammatory markers, and an altered salivary microbiome compared to children without T2D.
Three pediatric cohorts ages 10-19 years were studied: lean (normal weight-C), obese (Ob), and obese with T2D (T2D). Each subject completed an oral health survey, received a clinical oral examination, and provided unstimulated saliva for measurement of inflammatory markers and microbiome analysis.
The diabetes group was less likely to have had a dental visit within the last six months. Body mass index (BMI) Z-scores and waist circumference/height ratios were similar between Ob and T2D cohorts. The number of carious lesions and fillings were similar for all three groups. The gingival index was greater in the T2D group compared to the Ob and C groups. Although salivary microbial diversity was minimal between groups, a few differences in bacterial genus composition were noted.
Obese children with T2D show a trend toward poorer oral health compared to normal weight and obese children without T2D. This study characterizes the salivary microbiome of children with and without obesity and T2D. This study supports a modest link between T2D and periodontal inflammation in the pediatric population. |
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AbstractList | BACKGROUND:There is emerging evidence linking diabetes with periodontal disease. Diabetes is a well-recognized risk factor for periodontal disease. Conversely, pro-inflammatory molecules released by periodontally-diseased tissues may enter the circulation to induce insulin resistance. While this association has been demonstrated in adults, there is little information regarding periodontal status in obese children with and without type 2 diabetes (T2D). We hypothesized that children with T2D have higher rates of gingivitis, elevated salivary inflammatory markers, and an altered salivary microbiome compared to children without T2D. METHODS:Three pediatric cohorts ages 10-19 years were studied: lean (normal weight-C), obese (Ob), and obese with T2D (T2D). Each subject completed an oral health survey, received a clinical oral examination, and provided unstimulated saliva for measurement of inflammatory markers and microbiome analysis. RESULTS:The diabetes group was less likely to have had a dental visit within the last six months. Body mass index (BMI) Z-scores and waist circumference/height ratios were similar between Ob and T2D cohorts. The number of carious lesions and fillings were similar for all three groups. The gingival index was greater in the T2D group compared to the Ob and C groups. Although salivary microbial diversity was minimal between groups, a few differences in bacterial genus composition were noted. CONCLUSIONS:Obese children with T2D show a trend toward poorer oral health compared to normal weight and obese children without T2D. This study characterizes the salivary microbiome of children with and without obesity and T2D. This study supports a modest link between T2D and periodontal inflammation in the pediatric population. There is emerging evidence linking diabetes with periodontal disease. Diabetes is a well-recognized risk factor for periodontal disease. Conversely, pro-inflammatory molecules released by periodontally-diseased tissues may enter the circulation to induce insulin resistance. While this association has been demonstrated in adults, there is little information regarding periodontal status in obese children with and without type 2 diabetes (T2D). We hypothesized that children with T2D have higher rates of gingivitis, elevated salivary inflammatory markers, and an altered salivary microbiome compared to children without T2D. Three pediatric cohorts ages 10-19 years were studied: lean (normal weight-C), obese (Ob), and obese with T2D (T2D). Each subject completed an oral health survey, received a clinical oral examination, and provided unstimulated saliva for measurement of inflammatory markers and microbiome analysis. The diabetes group was less likely to have had a dental visit within the last six months. Body mass index (BMI) Z-scores and waist circumference/height ratios were similar between Ob and T2D cohorts. The number of carious lesions and fillings were similar for all three groups. The gingival index was greater in the T2D group compared to the Ob and C groups. Although salivary microbial diversity was minimal between groups, a few differences in bacterial genus composition were noted. Obese children with T2D show a trend toward poorer oral health compared to normal weight and obese children without T2D. This study characterizes the salivary microbiome of children with and without obesity and T2D. This study supports a modest link between T2D and periodontal inflammation in the pediatric population. There is emerging evidence linking diabetes with periodontal disease. Diabetes is a well-recognized risk factor for periodontal disease. Conversely, pro-inflammatory molecules released by periodontally-diseased tissues may enter the circulation to induce insulin resistance. While this association has been demonstrated in adults, there is little information regarding periodontal status in obese children with and without type 2 diabetes (T2D). We hypothesized that children with T2D have higher rates of gingivitis, elevated salivary inflammatory markers, and an altered salivary microbiome compared to children without T2D. Three pediatric cohorts ages 10-19 years were studied: lean (normal weight-C), obese (Ob), and obese with T2D (T2D). Each subject completed an oral health survey, received a clinical oral examination, and provided unstimulated saliva for measurement of inflammatory markers and microbiome analysis. The diabetes group was less likely to have had a dental visit within the last six months. Body mass index (BMI) Z-scores and waist circumference/height ratios were similar between Ob and T2D cohorts. The number of carious lesions and fillings were similar for all three groups. The gingival index was greater in the T2D group compared to the Ob and C groups. Although salivary microbial diversity was minimal between groups, a few differences in bacterial genus composition were noted. Obese children with T2D show a trend toward poorer oral health compared to normal weight and obese children without T2D. This study characterizes the salivary microbiome of children with and without obesity and T2D. This study supports a modest link between T2D and periodontal inflammation in the pediatric population. Background There is emerging evidence linking diabetes with periodontal disease. Diabetes is a well-recognized risk factor for periodontal disease. Conversely, pro-inflammatory molecules released by periodontally-diseased tissues may enter the circulation to induce insulin resistance. While this association has been demonstrated in adults, there is little information regarding periodontal status in obese children with and without type 2 diabetes (T2D). We hypothesized that children with T2D have higher rates of gingivitis, elevated salivary inflammatory markers, and an altered salivary microbiome compared to children without T2D. Methods Three pediatric cohorts ages 10–19 years were studied: lean (normal weight—C), obese (Ob), and obese with T2D (T2D). Each subject completed an oral health survey, received a clinical oral examination, and provided unstimulated saliva for measurement of inflammatory markers and microbiome analysis. Results The diabetes group was less likely to have had a dental visit within the last six months. Body mass index (BMI) Z-scores and waist circumference/height ratios were similar between Ob and T2D cohorts. The number of carious lesions and fillings were similar for all three groups. The gingival index was greater in the T2D group compared to the Ob and C groups. Although salivary microbial diversity was minimal between groups, a few differences in bacterial genus composition were noted. Conclusions Obese children with T2D show a trend toward poorer oral health compared to normal weight and obese children without T2D. This study characterizes the salivary microbiome of children with and without obesity and T2D. This study supports a modest link between T2D and periodontal inflammation in the pediatric population. |
Audience | Academic |
Author | Scannapieco, Frank A Miecznikowski, Jeffrey C Berman, Harvey A Tsompana, Maria Janem, Waleed F Sabharwal, Amarpeet Haase, Elaine M Mastrandrea, Lucy D |
AuthorAffiliation | Medical University of South Carolina, UNITED STATES 2 Department of Oral Biology, School of Dental Medicine, University at Buffalo, Buffalo, NY, United States of America 5 Department of Biostatistics, School of Public Health and Health Professions, University at Buffalo, Buffalo, NY, United States of America 1 Department of Pediatrics, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY, United States of America 4 Department of Pharmacology and Toxicology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY, United States of America 3 Department of Epidemiology and Environmental Health, School of Public Health and Health Professions, University at Buffalo, Buffalo, NY, United States of America |
AuthorAffiliation_xml | – name: 4 Department of Pharmacology and Toxicology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY, United States of America – name: 2 Department of Oral Biology, School of Dental Medicine, University at Buffalo, Buffalo, NY, United States of America – name: 3 Department of Epidemiology and Environmental Health, School of Public Health and Health Professions, University at Buffalo, Buffalo, NY, United States of America – name: 5 Department of Biostatistics, School of Public Health and Health Professions, University at Buffalo, Buffalo, NY, United States of America – name: 1 Department of Pediatrics, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY, United States of America – name: Medical University of South Carolina, UNITED STATES |
Author_xml | – sequence: 1 givenname: Waleed F surname: Janem fullname: Janem, Waleed F organization: Department of Pediatrics, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY, United States of America – sequence: 2 givenname: Frank A surname: Scannapieco fullname: Scannapieco, Frank A organization: Department of Oral Biology, School of Dental Medicine, University at Buffalo, Buffalo, NY, United States of America – sequence: 3 givenname: Amarpeet surname: Sabharwal fullname: Sabharwal, Amarpeet organization: Department of Oral Biology, School of Dental Medicine, University at Buffalo, Buffalo, NY, United States of America – sequence: 4 givenname: Maria surname: Tsompana fullname: Tsompana, Maria organization: Department of Epidemiology and Environmental Health, School of Public Health and Health Professions, University at Buffalo, Buffalo, NY, United States of America – sequence: 5 givenname: Harvey A surname: Berman fullname: Berman, Harvey A organization: Department of Pharmacology and Toxicology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY, United States of America – sequence: 6 givenname: Elaine M surname: Haase fullname: Haase, Elaine M organization: Department of Oral Biology, School of Dental Medicine, University at Buffalo, Buffalo, NY, United States of America – sequence: 7 givenname: Jeffrey C surname: Miecznikowski fullname: Miecznikowski, Jeffrey C organization: Department of Biostatistics, School of Public Health and Health Professions, University at Buffalo, Buffalo, NY, United States of America – sequence: 8 givenname: Lucy D surname: Mastrandrea fullname: Mastrandrea, Lucy D organization: Department of Pediatrics, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY, United States of America |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28253297$$D View this record in MEDLINE/PubMed |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Conceptualization: WFJ FAS HAB LDM.Data curation: WFJ FAS AS MT JCM LDM.Formal analysis: WFJ FAS AS MT JCM LDM.Funding acquisition: WFJ FAS LDM.Investigation: WFJ MT LDM.Methodology: WFJ FAS AS MT JCM LDM.Project administration: FAS LDM.Resources: WFJ AS MT JCM LDM.Software: AS JCM.Supervision: FAS HAB EMH LDM.Validation: AS MT JCM LDM.Visualization: WFJ AS JCM LDM.Writing – original draft: WFJ FAS AS HAB EMH JCM LDM.Writing – review & editing: WFJ FAS AS MT HAB EMH JCM LDM. Competing Interests: Dr. Scannapieco and Dr. Mastrandrea received funding to perform this research from Colgate Palmolive. Receipt of funding does not alter our adherence to PLOS ONE policies on sharing data and materials. These authors also contributed equally to this work |
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References | 28813516 - PLoS One. 2017 Aug 16;12 (8):e0183600 PJ McMurdie (ref36) 2013; 8 P Jorth (ref61) 2014; 5 VM Barnes (ref45) 2014; 9 MK Crocker (ref1) 2011; 58 H Loe (ref56) 1965 JL Riis (ref47) 2014; 56 Y Benjamini (ref38) 1995 M Khorsavi Samani (ref51) 2012; 61 CL Ogden (ref2) 2014; 311 SP Engebretson (ref14) 2013; 310 PS Kumar (ref59) 2003; 82 PW Wilson (ref5) 2005; 112 F Javed (ref22) 2013; 85 CS Miller (ref49) 2010; 4 T Chen (ref39) 2010; 2010 V Barnes (ref20) 2014; 18 GG Nascimento (ref41) 2015 S Singh (ref11) 2008; 28 S Lal (ref18) 2007; 29 R Franchini (ref34) 2011; 38 R Teles (ref55) 2013; 62 CS Miller (ref24) 2006; 137 R Spooner (ref60) 2016; 6 JE Stewart (ref12) 2001; 28 UK Gürsoy (ref21) 2015; 7 D Dabelea (ref3) 2014; 311 JV Califano (ref46) 2005; 27 AJ Yoon (ref23) 2012; 39 ref35 RJ Kuczmarski (ref25) 2002 ref31 ref30 ref33 B Chee (ref9) 2013; 11 GW Taylor (ref7) 2001; 6 M Tremblay (ref10) 2011; 77 SS Socransky (ref57) 1998; 25 RCV Casarin (ref65) 2013; 48 JM Goodson (ref54) 2014; 9 MD Robinson (ref37) 2010; 26 M Shojaee (ref50) 2013; 2 RP Darveau (ref15) 2010; 8 EK Kim (ref42) 2013; 13 SR Parwani (ref52) 2012; 10 On Section (ref43) 2014; 134 ET Knight (ref8) 2016; 71 PD Schloss (ref32) 2009; 75 TE Rams (ref26) 1993; 20 X Ge (ref62) 2013; 8 SS Chukkapalli (ref16) 2015; 10 D Giustarini (ref28) 2008; 440 BW Chaffee (ref6) 2010; 81 S Katagiri (ref13) 2012; 3 ref29 J Katz (ref19) 2011; 42 NM Sundar (ref53) 2013; 7 BJ Paster (ref58) 2001; 183 M Zhou (ref64) 2013; 8 K Rai (ref17) 2011; 36 RT Demmer (ref63) 2015; 94 I Ouellet-Morin (ref48) 2011; 25 E Edblad (ref44) 2001; 25 J Suvan (ref40) 2011; 12 ACR Tanner (ref66) 2011; 90 H Löe (ref27) 1967; 38 AD Liese (ref4) 2006; 118 |
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Snippet | There is emerging evidence linking diabetes with periodontal disease. Diabetes is a well-recognized risk factor for periodontal disease. Conversely,... Background There is emerging evidence linking diabetes with periodontal disease. Diabetes is a well-recognized risk factor for periodontal disease. Conversely,... BACKGROUND:There is emerging evidence linking diabetes with periodontal disease. Diabetes is a well-recognized risk factor for periodontal disease. Conversely,... Background There is emerging evidence linking diabetes with periodontal disease. Diabetes is a well-recognized risk factor for periodontal disease. Conversely,... |
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Title | Salivary inflammatory markers and microbiome in normoglycemic lean and obese children compared to obese children with type 2 diabetes |
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