Background Chronic inflammation is believed to be a major mechanism underlying the pathophysiology of type 2 diabetes. Periodontitis is a cause of systemic inflammation. We aimed to assess the effects of periodontal treatment on glycaemic control in people with type 2 diabetes. Methods In this 12 month, single-centre, parallel-group, investigator-masked, randomised trial, we recruited patients with type 2 diabetes, moderate-to-severe periodontitis, and at least 15 teeth from four local hospitals and 15 medical or dental practices in the UK. We randomly assigned patients (1:1) using a computer-generated table to receive intensive periodontal treatment (IPT; whole mouth subgingival scaling, surgical periodontal therapy [if the participants showed good oral hygiene practice; otherwise dental cleaning again], and supportive periodontal therapy every 3 months until completion of the study) or control periodontal treatment (CPT; supra-gingival scaling and polishing at the same timepoints as in the IPT group). Treatment allocation included a process of minimisation in terms of diabetes onset, smoking status, sex, and periodontitis severity. Allocation to treatment was concealed in an opaque envelope and revealed to the clinician on the day of first treatment. With the exception of dental staff who performed the treatment and clinical examinations, all study investigators were masked to group allocation. The primary outcome was between-group difference in HbA,, at 12 months in the intention-to-treat population. This study is registered with the ISRCTN registry, number ISRCTN83229304.

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Context Periodontitis confers an increased risk of developing type 2 diabetes and, in patients with obesity, it might interfere with the incretin axis. The effect of periodontal treatment on glucoregulatory hormones remains unknown. Objective To evaluate the effect of periodontal treatment on incretin axis in obese and lean non-diabetic individuals. Setting King's College Dental Hospital and Institute, London, UK. Participants and Methods The metabolic profile of obese and BMI-normal individuals affected by periodontitis was studied at baseline, 2 and 6 months after intensive periodontal treatment, by measuring plasma insulin, glucagon, GLP-1 and GIP and markers of systemic inflammation and oxidative stress. Main Outcome Measure(s) Circulating levels of incretins and inflammatory markers. Results At baseline, periodontal parameters were worse for obese than non-obese; this was accompanied by higher levels of circulating hs-CRP, insulin and GLP-1. The response to periodontal treatment was less favourable in the obese group, without significant variations of hs-CRP or malondialdehyde. Gluco-regulatory hormones changed differently after treatment: while insulin and glucagon did not vary at 2 and 6 months, GLP-1 and GIP significantly increased at 6 months in both groups. In particular, GLP-1 increased more rapidly in obese participants, while the increase of GIP followed similar trends across visits in both groups. Conclusions Nonsurgical treatment of periodontitis is associated with increased GLP-1 and GIP levels in non-obese and obese patients; changes in GLP-1 were more rapid in obese participants. This might have positive implications for the metabolic risk of these individuals.

Aim The study aim was to investigate the predictive role of obesity on clinical response following non‐surgical periodontal therapy in individuals with severe periodontitis. Methods A total of 57 BMI obese and 58 BMI normal non‐smoker adults with periodontitis (defined as probing pocket depths (PPD) of ≥5 mm and alveolar bone loss of >30% with >50% of the teeth affected) received non‐surgical periodontal therapy. Periodontal status was based upon PPD, clinical attachment level (CAL) and full‐mouth bleeding score (FMBS). Mean PPD, percentage sites PPD >4 mm, percentage sites PPD >5 mm and FMBS at 2 and 6 months were outcome variables. Propensity score analysis was used to assess the effect of obesity on outcome variables after adjusting for confounders. Results Statistically significant higher clinical measures (mean PPD, mean percentage of sites with PPD >4 mm, mean percentage of sites with PPD >5 mm and FMBS) were observed in the obese group than the normal group at baseline, 2 and 6 months after therapy (p < .01). At 2 and 6 months, obesity was associated with worse mean PPD (p < .05), percentage sites with PPD >4 mm (p < .05), percentage sites with PPD > 5mm (p < .05) and FMBS (p < .01), independent of age, gender, ethnicity or plaque levels. Conclusions Obesity compared to normal BMI status was an independent predictor of poorer response following non‐surgical periodontal therapy.