Treatment of periodontitis reduces systemic inflammation in type 2 diabetes

Aims To assess the impact of periodontal treatment on systemic inflammation in type 2 diabetes. Materials and Methods Adults with type 2 diabetes (n = 83) and without diabetes (controls, n = 75) were recruited, and participants with periodontitis received periodontal treatment and 12 months’ follow‐...

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Veröffentlicht in:Journal of clinical periodontology 2020-06, Vol.47 (6), p.737-746
Hauptverfasser: Preshaw, Philip M., Taylor, John J., Jaedicke, Katrin M., De Jager, Marko, Bikker, Jan Willem, Selten, Wieke, Bissett, Susan M., Whall, Kerry M., Merwe, Rachel, Areibi, Aisha, Jitprasertwong, Paiboon, Al‐Shahwani, Rana, Weaver, Jolanta, Taylor, Roy, Wassall, Rebecca R.
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container_end_page 746
container_issue 6
container_start_page 737
container_title Journal of clinical periodontology
container_volume 47
creator Preshaw, Philip M.
Taylor, John J.
Jaedicke, Katrin M.
De Jager, Marko
Bikker, Jan Willem
Selten, Wieke
Bissett, Susan M.
Whall, Kerry M.
Merwe, Rachel
Areibi, Aisha
Jitprasertwong, Paiboon
Al‐Shahwani, Rana
Weaver, Jolanta
Taylor, Roy
Wassall, Rebecca R.
description Aims To assess the impact of periodontal treatment on systemic inflammation in type 2 diabetes. Materials and Methods Adults with type 2 diabetes (n = 83) and without diabetes (controls, n = 75) were recruited, and participants with periodontitis received periodontal treatment and 12 months’ follow‐up. Biomarkers for periodontal inflammation (gingival crevicular fluid interleukin‐6, tumour necrosis factor‐α, interleukin‐1β, interferon‐γ, matrix metalloproteinase‐8, matrix metalloproteinase‐9, adiponectin) and serum markers of inflammation and diabetes control (glycated haemoglobin, high sensitivity C‐reactive protein, interleukin‐6, tumour necrosis factor‐α, interleukin‐1β, interferon‐γ, leptin, adiponectin) were measured. Structural equation modelling was used to evaluate periodontal treatment effects on oral and systemic inflammation. Results Periodontal treatment resulted in significant improvements in clinical status and reductions in gingival crevicular fluid biomarkers from baseline to month 12. Structural equation modelling identified that, at baseline, individuals with diabetes and periodontitis had significantly higher systemic inflammation than non‐diabetic controls with periodontitis (Δ = 0.20, p = .002), with no significant differences between groups for oral inflammation. There was a greater reduction in systemic inflammation following periodontal treatment in individuals with diabetes and periodontitis compared to those with periodontitis but not diabetes (Δ = −0.25, p = .01). Conclusions Diabetes and periodontitis together appear to increase systemic inflammation, with evidence of reductions following periodontal treatment.
doi_str_mv 10.1111/jcpe.13274
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Materials and Methods Adults with type 2 diabetes (n = 83) and without diabetes (controls, n = 75) were recruited, and participants with periodontitis received periodontal treatment and 12 months’ follow‐up. Biomarkers for periodontal inflammation (gingival crevicular fluid interleukin‐6, tumour necrosis factor‐α, interleukin‐1β, interferon‐γ, matrix metalloproteinase‐8, matrix metalloproteinase‐9, adiponectin) and serum markers of inflammation and diabetes control (glycated haemoglobin, high sensitivity C‐reactive protein, interleukin‐6, tumour necrosis factor‐α, interleukin‐1β, interferon‐γ, leptin, adiponectin) were measured. Structural equation modelling was used to evaluate periodontal treatment effects on oral and systemic inflammation. Results Periodontal treatment resulted in significant improvements in clinical status and reductions in gingival crevicular fluid biomarkers from baseline to month 12. Structural equation modelling identified that, at baseline, individuals with diabetes and periodontitis had significantly higher systemic inflammation than non‐diabetic controls with periodontitis (Δ = 0.20, p = .002), with no significant differences between groups for oral inflammation. There was a greater reduction in systemic inflammation following periodontal treatment in individuals with diabetes and periodontitis compared to those with periodontitis but not diabetes (Δ = −0.25, p = .01). Conclusions Diabetes and periodontitis together appear to increase systemic inflammation, with evidence of reductions following periodontal treatment.</description><identifier>ISSN: 0303-6979</identifier><identifier>EISSN: 1600-051X</identifier><identifier>DOI: 10.1111/jcpe.13274</identifier><identifier>PMID: 32106333</identifier><language>eng</language><publisher>United States: Blackwell Publishing Ltd</publisher><subject>Adiponectin ; Adult ; Biomarkers ; Chronic Periodontitis ; Cytokines ; Dentistry ; Diabetes ; diabetes mellitus ; Diabetes mellitus (non-insulin dependent) ; Diabetes Mellitus, Type 2 - complications ; Diabetes Mellitus, Type 2 - therapy ; Gingival Crevicular Fluid - chemistry ; Glycated Hemoglobin A - analysis ; Gum disease ; Hemoglobin ; Humans ; Inflammation ; Interferon ; Leptin ; Matrix metalloproteinase ; Metalloproteinase ; Periodontitis ; Periodontitis - complications ; Periodontitis - therapy ; Tumor necrosis factor ; Tumor necrosis factor-TNF ; Tumors ; type 2</subject><ispartof>Journal of clinical periodontology, 2020-06, Vol.47 (6), p.737-746</ispartof><rights>2020 John Wiley &amp; Sons A/S. Published by John Wiley &amp; Sons Ltd</rights><rights>2020 John Wiley &amp; Sons A/S. Published by John Wiley &amp; Sons Ltd.</rights><rights>Copyright © 2020 John Wiley &amp; Sons A/S. 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Materials and Methods Adults with type 2 diabetes (n = 83) and without diabetes (controls, n = 75) were recruited, and participants with periodontitis received periodontal treatment and 12 months’ follow‐up. Biomarkers for periodontal inflammation (gingival crevicular fluid interleukin‐6, tumour necrosis factor‐α, interleukin‐1β, interferon‐γ, matrix metalloproteinase‐8, matrix metalloproteinase‐9, adiponectin) and serum markers of inflammation and diabetes control (glycated haemoglobin, high sensitivity C‐reactive protein, interleukin‐6, tumour necrosis factor‐α, interleukin‐1β, interferon‐γ, leptin, adiponectin) were measured. Structural equation modelling was used to evaluate periodontal treatment effects on oral and systemic inflammation. Results Periodontal treatment resulted in significant improvements in clinical status and reductions in gingival crevicular fluid biomarkers from baseline to month 12. Structural equation modelling identified that, at baseline, individuals with diabetes and periodontitis had significantly higher systemic inflammation than non‐diabetic controls with periodontitis (Δ = 0.20, p = .002), with no significant differences between groups for oral inflammation. There was a greater reduction in systemic inflammation following periodontal treatment in individuals with diabetes and periodontitis compared to those with periodontitis but not diabetes (Δ = −0.25, p = .01). 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Materials and Methods Adults with type 2 diabetes (n = 83) and without diabetes (controls, n = 75) were recruited, and participants with periodontitis received periodontal treatment and 12 months’ follow‐up. Biomarkers for periodontal inflammation (gingival crevicular fluid interleukin‐6, tumour necrosis factor‐α, interleukin‐1β, interferon‐γ, matrix metalloproteinase‐8, matrix metalloproteinase‐9, adiponectin) and serum markers of inflammation and diabetes control (glycated haemoglobin, high sensitivity C‐reactive protein, interleukin‐6, tumour necrosis factor‐α, interleukin‐1β, interferon‐γ, leptin, adiponectin) were measured. Structural equation modelling was used to evaluate periodontal treatment effects on oral and systemic inflammation. Results Periodontal treatment resulted in significant improvements in clinical status and reductions in gingival crevicular fluid biomarkers from baseline to month 12. Structural equation modelling identified that, at baseline, individuals with diabetes and periodontitis had significantly higher systemic inflammation than non‐diabetic controls with periodontitis (Δ = 0.20, p = .002), with no significant differences between groups for oral inflammation. There was a greater reduction in systemic inflammation following periodontal treatment in individuals with diabetes and periodontitis compared to those with periodontitis but not diabetes (Δ = −0.25, p = .01). Conclusions Diabetes and periodontitis together appear to increase systemic inflammation, with evidence of reductions following periodontal treatment.</abstract><cop>United States</cop><pub>Blackwell Publishing Ltd</pub><pmid>32106333</pmid><doi>10.1111/jcpe.13274</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-7153-4865</orcidid><orcidid>https://orcid.org/0000-0002-2767-5361</orcidid><oa>free_for_read</oa></addata></record>
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source Wiley-Blackwell Journals; MEDLINE
subjects Adiponectin
Adult
Biomarkers
Chronic Periodontitis
Cytokines
Dentistry
Diabetes
diabetes mellitus
Diabetes mellitus (non-insulin dependent)
Diabetes Mellitus, Type 2 - complications
Diabetes Mellitus, Type 2 - therapy
Gingival Crevicular Fluid - chemistry
Glycated Hemoglobin A - analysis
Gum disease
Hemoglobin
Humans
Inflammation
Interferon
Leptin
Matrix metalloproteinase
Metalloproteinase
Periodontitis
Periodontitis - complications
Periodontitis - therapy
Tumor necrosis factor
Tumor necrosis factor-TNF
Tumors
type 2
title Treatment of periodontitis reduces systemic inflammation in type 2 diabetes
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