Effect of Treatment of Periodontitis on Incretin Axis in Obese and Nonobese Individuals: A Cohort Study

• Published in: The journal of clinical endocrinology and metabolism Vol. 106; no. 1; pp. e74 - e82
• Main Authors: Suvan, Jeanie, Masi, Stefano, Harrington, Zoe, Santini, Eleonora, Raggi, Francesco, D'Aiuto, Francesco, Solini, Anna
• Format: Journal Article
• Language: English
• Published: United States Oxford University Press 01.01.2021
• Subjects: Analysis; C-reactive protein; Care and treatment; Development and progression; Dextrose; Diabetes mellitus (non-insulin dependent); Diabetes therapy; GIP protein; Glucagon; Glucagon-like peptide 1; Glucose; Gum disease; Inflammation; Insulin; Metabolism; Obesity; Oxidative stress; Patients; Periodontitis; Type 2 diabetes; incretin axis; obesity; periodontitis
• ISSN: 0021-972X; 1945-7197
• DOI: 10.1210/clinem/dgaa757

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. To evaluate the effect of periodontal treatment on incretin axis in obese and lean nondiabetic individuals. King's College Dental Hospital and Institute, London, UK. 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. Circulating levels of incretins and inflammatory markers. 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. 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.