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Levels of Serum Interleukin (IL)‐6 and Gingival Crevicular Fluid of IL‐1β and Prostaglandin E2 Among Non‐Smoking Subjects With Gingivitis and Type 2 Diabetes
Background: The goal of this study was to assess whether non‐smoking patients with type 2 diabetes present with increased levels of local and systemic proinflammatory mediators and, if so, whether such an increase is associated with enhanced clinical gingival inflammation compared to non‐smoking pat...
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| Published in: | Journal of periodontology (1970) 2009-02, Vol.80 (2), p.307-316 |
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| container_end_page | 316 |
| container_issue | 2 |
| container_start_page | 307 |
| container_title | Journal of periodontology (1970) |
| container_volume | 80 |
| creator | Andriankaja, O.M. Barros, S.P. Moss, K. Panagakos, F.S. DeVizio, W. Beck, J. Offenbacher, S. |
| description | Background: The goal of this study was to assess whether non‐smoking patients with type 2 diabetes present with increased levels of local and systemic proinflammatory mediators and, if so, whether such an increase is associated with enhanced clinical gingival inflammation compared to non‐smoking patients without diabetes.
Methods: We used a cross‐sectional database consisting of 725 self‐reported lifelong non‐smokers aged 53 to 74 years. Gingival crevicular fluid (GCF) levels of interleukin (IL)‐1β and prostaglandin E2 (PGE2) and serum levels of IL‐6 were measured using enzyme‐linked immunosorbent assay. No participant had probing depth >3 mm. Participants with bleeding on probing (BOP) in |
| doi_str_mv | 10.1902/jop.2009.080385 |
| format | article |
| fullrecord | <record><control><sourceid>wiley_pasca</sourceid><recordid>TN_cdi_pascalfrancis_primary_21242633</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>JPER0307</sourcerecordid><originalsourceid>FETCH-LOGICAL-p1467-d43b86c1c47b61d72e1076b31a7bccadb8adeb90d735b2720c0557ae4749420b3</originalsourceid><addsrcrecordid>eNo9kUtOwzAQQC0EEuWzZusNEixSxp_EzRKVFooiqGgRy8h23OLiJlGcFHXHETgEJ-AgHIKTkFLEymPNm7d5CJ0Q6JIY6MWiKLsUIO5CD1gv3EEdEnMWsEjALuoAUBowHtN9dOD9ov0SzqCDPhKzMs7jYoYnpmqWeJTXpnKmebE5Phsl599v7xGWeYavbT63K-lwvzIrqxsnKzx0jc02t6Ok5cjX5y85rgpfy7lr51YyoPhyWeRzfFfkLTRZFq16jieNWhhde_xk6-c_ua2t_zVM16XBFF9ZqUxt_BHam0nnzfHfe4geh4Np_yZI7q9H_cskKAmPRJBxpnqRJpoLFZFMUENARIoRKZTWMlM9mRkVQyZYqKigoCEMhTRc8JhTUOwQnW69pfRaulklc219WlZ2Kat1SgnlNGKs5cIt92qdWf_vCaSbEmlbIt2USLcl0tvx4AEYCPYDQk-CBg</addsrcrecordid><sourcetype>Index Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Levels of Serum Interleukin (IL)‐6 and Gingival Crevicular Fluid of IL‐1β and Prostaglandin E2 Among Non‐Smoking Subjects With Gingivitis and Type 2 Diabetes</title><source>Wiley-Blackwell Read & Publish Collection</source><creator>Andriankaja, O.M. ; Barros, S.P. ; Moss, K. ; Panagakos, F.S. ; DeVizio, W. ; Beck, J. ; Offenbacher, S.</creator><creatorcontrib>Andriankaja, O.M. ; Barros, S.P. ; Moss, K. ; Panagakos, F.S. ; DeVizio, W. ; Beck, J. ; Offenbacher, S.</creatorcontrib><description>Background: The goal of this study was to assess whether non‐smoking patients with type 2 diabetes present with increased levels of local and systemic proinflammatory mediators and, if so, whether such an increase is associated with enhanced clinical gingival inflammation compared to non‐smoking patients without diabetes.
Methods: We used a cross‐sectional database consisting of 725 self‐reported lifelong non‐smokers aged 53 to 74 years. Gingival crevicular fluid (GCF) levels of interleukin (IL)‐1β and prostaglandin E2 (PGE2) and serum levels of IL‐6 were measured using enzyme‐linked immunosorbent assay. No participant had probing depth >3 mm. Participants with bleeding on probing (BOP) in <10% of sites were classified as healthy, whereas those with BOP in ≥10% of sites were defined as having biofilm–gingival interface (BGI) gingivitis.
Results: Approximately 53% (n = 385) and 11% (n = 80) of the sample had BGI gingivitis and type 2 diabetes, respectively. The mean age‐adjusted level of GCF IL‐1β was significantly elevated in the diabetic group compared to the non‐diabetic group (P = 0.048), but serum IL‐6 (P = 0.14) and GCF PGE2 were not (P = 0.98). The mean GCF IL‐1β and PGE2 levels were significantly elevated in subjects with BGI gingivitis (136.2 ± 112.9 ng/ml and 277.2 ± 187.2 ng/ml, respectively) compared to subjects with gingival health (95.9 ± 82.9 ng/ml and 205.7 ± 149.6 ng/ml, respectively), regardless of diabetic status (P <0.001 for both). However, serum IL‐6 was elevated in subjects with BGI gingivitis compared to subjects with gingival health only among subjects with diabetes (2.9 ± 3.2 pg/ml versus 1.5 ± 1.4 pg/ml; P = 0.008). With the exception of serum IL‐6 in subjects without diabetes, an increase in the levels of proinflammatory mediators was associated with increased odds of having BGI gingivitis. The associations were stronger in the diabetic group.
Conclusions: Type 2 diabetes may increase the host inflammatory response to oral biofilm, which, in turn, may exacerbate preconditions associated with gingivitis in susceptible individuals. Furthermore, systemic inflammation, as demonstrated by the increased level of serum IL‐6, is associated with BGI gingivitis among non‐smoking patients with diabetes.</description><identifier>ISSN: 0022-3492</identifier><identifier>EISSN: 1943-3670</identifier><identifier>DOI: 10.1902/jop.2009.080385</identifier><language>eng</language><publisher>Chicago, IL: American Academy of Periodontology</publisher><subject>Biological and medical sciences ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Facial bones, jaws, teeth, parodontium: diseases, semeiology ; Gingivitis ; interleukin‐1 beta ; interleukin‐6 ; Medical sciences ; Non tumoral diseases ; Otorhinolaryngology. Stomatology ; prostaglandin E2 ; Tobacco, tobacco smoking ; Toxicology ; type 2 diabetes</subject><ispartof>Journal of periodontology (1970), 2009-02, Vol.80 (2), p.307-316</ispartof><rights>2009 American Academy of Periodontology</rights><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21242633$$DView record in Pascal Francis$$Hfree_for_read</backlink></links><search><creatorcontrib>Andriankaja, O.M.</creatorcontrib><creatorcontrib>Barros, S.P.</creatorcontrib><creatorcontrib>Moss, K.</creatorcontrib><creatorcontrib>Panagakos, F.S.</creatorcontrib><creatorcontrib>DeVizio, W.</creatorcontrib><creatorcontrib>Beck, J.</creatorcontrib><creatorcontrib>Offenbacher, S.</creatorcontrib><title>Levels of Serum Interleukin (IL)‐6 and Gingival Crevicular Fluid of IL‐1β and Prostaglandin E2 Among Non‐Smoking Subjects With Gingivitis and Type 2 Diabetes</title><title>Journal of periodontology (1970)</title><description>Background: The goal of this study was to assess whether non‐smoking patients with type 2 diabetes present with increased levels of local and systemic proinflammatory mediators and, if so, whether such an increase is associated with enhanced clinical gingival inflammation compared to non‐smoking patients without diabetes.
Methods: We used a cross‐sectional database consisting of 725 self‐reported lifelong non‐smokers aged 53 to 74 years. Gingival crevicular fluid (GCF) levels of interleukin (IL)‐1β and prostaglandin E2 (PGE2) and serum levels of IL‐6 were measured using enzyme‐linked immunosorbent assay. No participant had probing depth >3 mm. Participants with bleeding on probing (BOP) in <10% of sites were classified as healthy, whereas those with BOP in ≥10% of sites were defined as having biofilm–gingival interface (BGI) gingivitis.
Results: Approximately 53% (n = 385) and 11% (n = 80) of the sample had BGI gingivitis and type 2 diabetes, respectively. The mean age‐adjusted level of GCF IL‐1β was significantly elevated in the diabetic group compared to the non‐diabetic group (P = 0.048), but serum IL‐6 (P = 0.14) and GCF PGE2 were not (P = 0.98). The mean GCF IL‐1β and PGE2 levels were significantly elevated in subjects with BGI gingivitis (136.2 ± 112.9 ng/ml and 277.2 ± 187.2 ng/ml, respectively) compared to subjects with gingival health (95.9 ± 82.9 ng/ml and 205.7 ± 149.6 ng/ml, respectively), regardless of diabetic status (P <0.001 for both). However, serum IL‐6 was elevated in subjects with BGI gingivitis compared to subjects with gingival health only among subjects with diabetes (2.9 ± 3.2 pg/ml versus 1.5 ± 1.4 pg/ml; P = 0.008). With the exception of serum IL‐6 in subjects without diabetes, an increase in the levels of proinflammatory mediators was associated with increased odds of having BGI gingivitis. The associations were stronger in the diabetic group.
Conclusions: Type 2 diabetes may increase the host inflammatory response to oral biofilm, which, in turn, may exacerbate preconditions associated with gingivitis in susceptible individuals. Furthermore, systemic inflammation, as demonstrated by the increased level of serum IL‐6, is associated with BGI gingivitis among non‐smoking patients with diabetes.</description><subject>Biological and medical sciences</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Facial bones, jaws, teeth, parodontium: diseases, semeiology</subject><subject>Gingivitis</subject><subject>interleukin‐1 beta</subject><subject>interleukin‐6</subject><subject>Medical sciences</subject><subject>Non tumoral diseases</subject><subject>Otorhinolaryngology. Stomatology</subject><subject>prostaglandin E2</subject><subject>Tobacco, tobacco smoking</subject><subject>Toxicology</subject><subject>type 2 diabetes</subject><issn>0022-3492</issn><issn>1943-3670</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><recordid>eNo9kUtOwzAQQC0EEuWzZusNEixSxp_EzRKVFooiqGgRy8h23OLiJlGcFHXHETgEJ-AgHIKTkFLEymPNm7d5CJ0Q6JIY6MWiKLsUIO5CD1gv3EEdEnMWsEjALuoAUBowHtN9dOD9ov0SzqCDPhKzMs7jYoYnpmqWeJTXpnKmebE5Phsl599v7xGWeYavbT63K-lwvzIrqxsnKzx0jc02t6Ok5cjX5y85rgpfy7lr51YyoPhyWeRzfFfkLTRZFq16jieNWhhde_xk6-c_ua2t_zVM16XBFF9ZqUxt_BHam0nnzfHfe4geh4Np_yZI7q9H_cskKAmPRJBxpnqRJpoLFZFMUENARIoRKZTWMlM9mRkVQyZYqKigoCEMhTRc8JhTUOwQnW69pfRaulklc219WlZ2Kat1SgnlNGKs5cIt92qdWf_vCaSbEmlbIt2USLcl0tvx4AEYCPYDQk-CBg</recordid><startdate>200902</startdate><enddate>200902</enddate><creator>Andriankaja, O.M.</creator><creator>Barros, S.P.</creator><creator>Moss, K.</creator><creator>Panagakos, F.S.</creator><creator>DeVizio, W.</creator><creator>Beck, J.</creator><creator>Offenbacher, S.</creator><general>American Academy of Periodontology</general><scope>IQODW</scope></search><sort><creationdate>200902</creationdate><title>Levels of Serum Interleukin (IL)‐6 and Gingival Crevicular Fluid of IL‐1β and Prostaglandin E2 Among Non‐Smoking Subjects With Gingivitis and Type 2 Diabetes</title><author>Andriankaja, O.M. ; Barros, S.P. ; Moss, K. ; Panagakos, F.S. ; DeVizio, W. ; Beck, J. ; Offenbacher, S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p1467-d43b86c1c47b61d72e1076b31a7bccadb8adeb90d735b2720c0557ae4749420b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Biological and medical sciences</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Facial bones, jaws, teeth, parodontium: diseases, semeiology</topic><topic>Gingivitis</topic><topic>interleukin‐1 beta</topic><topic>interleukin‐6</topic><topic>Medical sciences</topic><topic>Non tumoral diseases</topic><topic>Otorhinolaryngology. Stomatology</topic><topic>prostaglandin E2</topic><topic>Tobacco, tobacco smoking</topic><topic>Toxicology</topic><topic>type 2 diabetes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Andriankaja, O.M.</creatorcontrib><creatorcontrib>Barros, S.P.</creatorcontrib><creatorcontrib>Moss, K.</creatorcontrib><creatorcontrib>Panagakos, F.S.</creatorcontrib><creatorcontrib>DeVizio, W.</creatorcontrib><creatorcontrib>Beck, J.</creatorcontrib><creatorcontrib>Offenbacher, S.</creatorcontrib><collection>Pascal-Francis</collection><jtitle>Journal of periodontology (1970)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Andriankaja, O.M.</au><au>Barros, S.P.</au><au>Moss, K.</au><au>Panagakos, F.S.</au><au>DeVizio, W.</au><au>Beck, J.</au><au>Offenbacher, S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Levels of Serum Interleukin (IL)‐6 and Gingival Crevicular Fluid of IL‐1β and Prostaglandin E2 Among Non‐Smoking Subjects With Gingivitis and Type 2 Diabetes</atitle><jtitle>Journal of periodontology (1970)</jtitle><date>2009-02</date><risdate>2009</risdate><volume>80</volume><issue>2</issue><spage>307</spage><epage>316</epage><pages>307-316</pages><issn>0022-3492</issn><eissn>1943-3670</eissn><abstract>Background: The goal of this study was to assess whether non‐smoking patients with type 2 diabetes present with increased levels of local and systemic proinflammatory mediators and, if so, whether such an increase is associated with enhanced clinical gingival inflammation compared to non‐smoking patients without diabetes.
Methods: We used a cross‐sectional database consisting of 725 self‐reported lifelong non‐smokers aged 53 to 74 years. Gingival crevicular fluid (GCF) levels of interleukin (IL)‐1β and prostaglandin E2 (PGE2) and serum levels of IL‐6 were measured using enzyme‐linked immunosorbent assay. No participant had probing depth >3 mm. Participants with bleeding on probing (BOP) in <10% of sites were classified as healthy, whereas those with BOP in ≥10% of sites were defined as having biofilm–gingival interface (BGI) gingivitis.
Results: Approximately 53% (n = 385) and 11% (n = 80) of the sample had BGI gingivitis and type 2 diabetes, respectively. The mean age‐adjusted level of GCF IL‐1β was significantly elevated in the diabetic group compared to the non‐diabetic group (P = 0.048), but serum IL‐6 (P = 0.14) and GCF PGE2 were not (P = 0.98). The mean GCF IL‐1β and PGE2 levels were significantly elevated in subjects with BGI gingivitis (136.2 ± 112.9 ng/ml and 277.2 ± 187.2 ng/ml, respectively) compared to subjects with gingival health (95.9 ± 82.9 ng/ml and 205.7 ± 149.6 ng/ml, respectively), regardless of diabetic status (P <0.001 for both). However, serum IL‐6 was elevated in subjects with BGI gingivitis compared to subjects with gingival health only among subjects with diabetes (2.9 ± 3.2 pg/ml versus 1.5 ± 1.4 pg/ml; P = 0.008). With the exception of serum IL‐6 in subjects without diabetes, an increase in the levels of proinflammatory mediators was associated with increased odds of having BGI gingivitis. The associations were stronger in the diabetic group.
Conclusions: Type 2 diabetes may increase the host inflammatory response to oral biofilm, which, in turn, may exacerbate preconditions associated with gingivitis in susceptible individuals. Furthermore, systemic inflammation, as demonstrated by the increased level of serum IL‐6, is associated with BGI gingivitis among non‐smoking patients with diabetes.</abstract><cop>Chicago, IL</cop><pub>American Academy of Periodontology</pub><doi>10.1902/jop.2009.080385</doi><tpages>10</tpages></addata></record> |
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| ispartof | Journal of periodontology (1970), 2009-02, Vol.80 (2), p.307-316 |
| issn | 0022-3492 1943-3670 |
| language | eng |
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| source | Wiley-Blackwell Read & Publish Collection |
| subjects | Biological and medical sciences Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Facial bones, jaws, teeth, parodontium: diseases, semeiology Gingivitis interleukin‐1 beta interleukin‐6 Medical sciences Non tumoral diseases Otorhinolaryngology. Stomatology prostaglandin E2 Tobacco, tobacco smoking Toxicology type 2 diabetes |
| title | Levels of Serum Interleukin (IL)‐6 and Gingival Crevicular Fluid of IL‐1β and Prostaglandin E2 Among Non‐Smoking Subjects With Gingivitis and Type 2 Diabetes |
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