Influence of Periodontal Disease Treatment on Serum Levels of Sirtuin 1 and Mannose-binding Lectin

Overview

The premise of the relationship between the atherosclerotic process of coronary artery disease and periodontal disease is the immunoinflammatory process, which causes a significant increase in serum concentration of mannose-binding lectin. This protein is part of the innate immunity and has the ability to bind to the mannose residues common to various pathogens. Animal studies also showed that increased serum concentration of sirtuin-1 was associated with reduced inflammation. Evidence indicates that sirtuin-1 plays an important role in vascular protection and is associated with aging. OBJECTIVES: This study examined the influence of non-surgical treatment of periodontal disease on the serum concentration of mannose-binding lectin and sirtuin-1 in patients with periodontal disease and coronary artery disease. METHODS: Seventy-eight patients, 38 women and 40 men, mean age 58 ± 8 years old, were divided into 4 groups: 20 healthy subjects (group 1), 18 patients with coronary artery disease and without periodontal disease (group 2), 20 patients with periodontal disease and without coronary artery disease (group 3) and 20 patients with coronary artery disease and periodontal disease (group 4). Peripheral blood samples were collected at the beginning and at the end of the treatment of periodontal disease.

Inclusion criteria for PD were: presence of at least 15 teeth and clinical diagnosis of PD. Excluding third molars. This diagnosis was confirmed by the presence of at least 6 teeth with at least one noncontiguous interproximal site with Probing Pocket Depth (PPD) and Clinical Attachment Loss (CAL) ≥ 5 mm, as well as 30% of Sites with PPD and CAL ≥ 4mm and bleeding on Probing (BOP). Periodontal disease currently classified as Stage III Degree B. Periodontal healthy was defined as individuals who presented a periodontium without loss of insertion, with PPD ≤3 mm, BOP in less than 10% of the sites and without radiographic bone loss. Non-surgical periodontal treatment was performed, including oral hygiene education, scaling, smoothing and coronal-radicular polishing (RAR). Six sites were evaluated in each tooth (mesiobuccal, buccal, distobuccal, distolingual/palatal, lingual/palatal and mesiolingual/palatal surfaces). Scaling and root planing were performed using mechanical devices - ultrasound and manual instruments. The treatment was with local anesthesia, 3% lidocaine with vasoconstrictor, for PPD ≥ 5 mm. The objective of each session was to achieve a smooth surface, devoid of biofilm and calculus. The following parameters are evaluated during clinical examination: Probing Pocket Depth (PPD), distance of the enamel-cementum line at the gingival margin, clinical Attachment Loss (CAL), plaque index (IP) and bleeding on probing (BOP), PPD and CAL measurements are rounded to the nearest millimeter using a North Carolina periodontal probe (Chicago, USA).