TY - JOUR
T1 - Treatment of periodontitis reduces systemic inflammation in type 2 diabetes
AU - Preshaw, Philip M.
AU - Taylor, John J.
AU - Jaedicke, Katrin M.
AU - De Jager, Marko
AU - Bikker, Jan Willem
AU - Selten, Wieke
AU - Bissett, Susan M.
AU - Whall, Kerry M.
AU - van de Merwe, Rachel
AU - Areibi, Aisha
AU - Jitprasertwong, Paiboon
AU - Al-Shahwani, Rana
AU - Weaver, Jolanta
AU - Taylor, Roy
AU - Wassall, Rebecca R.
N1 - Funding Information:
The authors thank all of the patients who participated in this research. Funding for this study was received from the UK National Institute for Health Research (NIHR) via a Clinician Scientist Fellowship awarded to P.M. Preshaw (ref. DHCS/03/G121/46), and research grants from the Dunhill Medical Trust (ref. R63/1107) and a PhD studentship grant from Philips Research (ref. DRC‐0417). The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the UK Department of Health. The research was supported by the Newcastle Dental Clinical Research Facility, Newcastle University School of Dental Sciences, the Newcastle upon Tyne Hospitals NHS Foundation Trust and the Gateshead Health NHS Foundation Trust. The study sponsor was the Newcastle upon Tyne Hospitals NHS Foundation Trust. Philips Research provided funding for the commercial statistical consultants (CQM, The Netherlands) to assist with the analysis of the data. P.M. Preshaw and J.J. Taylor have received research grants from Philips for the submitted work, and P.M. Preshaw has received research funding, honoraria and travel grants from Philips Research and from Colgate. M. De Jager is an employee of Philips Research.
Publisher Copyright:
© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
PY - 2020/5/28
Y1 - 2020/5/28
N2 - 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.
AB - 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.
KW - diabetes mellitus
KW - inflammation
KW - periodontitis
KW - type 2
UR - http://www.scopus.com/inward/record.url?scp=85084472705&partnerID=8YFLogxK
U2 - 10.1111/jcpe.13274
DO - 10.1111/jcpe.13274
M3 - Article
C2 - 32106333
AN - SCOPUS:85084472705
SN - 0303-6979
VL - 47
SP - 737
EP - 746
JO - Journal of Clinical Periodontology
JF - Journal of Clinical Periodontology
IS - 6
ER -