Abstract
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 nondiabetic individuals. Setting: King's College Dental Hospital and Institute, London, UK. Participants and Methods: The metabolic profile of obese and normal-body-mass-index individuals affected by periodontitis was studied at baseline, 2, and 6 months after intensive periodontal treatment, by measuring plasma insulin, glucagon, glucagon-like peptide-1(GLP-1), and glucose-dependent insulinotropic polypeptide (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 nonobese; this was accompanied by higher levels of circulating high-sensitivity C-reactive protein (hs-CRP), insulin, and GLP-1. The response to periodontal treatment was less favorable in the obese group, without significant variations of hs-CRP or malondialdehyde. Glucoregulatory 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 nonobese 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.
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Suvan, J., Masi, S., Harrington, Z., Santini, E., Raggi, F., D’Aiuto, F., & Solini, A. (2021). Effect of treatment of periodontitis on incretin axis in obese and nonobese individuals: A cohort study. Journal of Clinical Endocrinology and Metabolism, 106(1), E74–E82. https://doi.org/10.1210/clinem/dgaa757
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