Effect of Periodontal Treatment on Salivary and Serum SIRT-1, MMP-9 and T-SOD Levels

Periodontitis is a dysbiotic chronic inflammatory disease that compromises the integrity of the tooth-supporting tissues. When periodontitis occurs, reactive oxygen species, which are overproduced mostly by hyperactive neutrophils, can not be balanced by the antioxidant defense system and cause tissue damage. Cytoprotective enzymes such as superoxide dismutase (SOD), catalase (Cat) and the regulatory pathways that influence them, play a critical role in the scavenging and detoxification of ROS. Sirtuin-1 (SIRT-1) is a nicotinamide adenine dinucleotide (NAD)dependent histone deacetylase. SIRT1 is known to deacetylate FOXO3a, which induces antioxidant responses via modulation in SOD2 and CAT. Moreover, SIRT1 overexpression downregulates the pro-inflammatory cytokines such as interleukin (IL)-1α, IL-6, IL-8 and tumor necrosis factor-α (TNF-α) synthesis which are associated with the onset and progression of the periodontal disease. MMP-9 is a host-derived proteolytic enzyme that leads to periodontal tissue breakdown and is activated by oxidative stress.

This study aims to examine the effect of non-surgical periodontal treatment (NSPT) on saliva and serum SIRT-1, SOD and MMP-9. It is the first controlled clinical study investigating the effect of NSPT on salivary SIRT-1 levels in different periodontitis groups. The sample size was calculated based on a previous study investigating the level of salivary MMP-9 and the power of the test was 95%, alfa value: 0.05. The estimated sample size was 10 individuals for each group. Therefore, a total of 49 systemically healthy patients; 17 periodontally healthy, 16 P-III-B, 16 P-III-C were included in this study. Periodontal examination was performed, and full medical and dental histories were collected by a single examiner at baseline and 3 months after NSPT. The whole mouth clinical periodontal examination included measurement of probing depth (PPD), clinical attachment level (CAL), presence of bleeding on probing (BOP), gingival index (GI), and plaque index (PI) at 6 sites per tooth, except the third molars. The presence and type of the alveolar bone loss were assessed on the digital panoramic radiograph in each participant, which was supplemented with periapical radiographs if necessary. Periodontal status of each patient was evaluated by a single calibrated periodontists with a manual probe. The diagnosis of periodontitis or periodontal health was determined according to the 2017 World Workshop on Classification of Periodontal and Peri-Implant Diseases and Conditions. Periodontally healthy individuals (n=17) in the control group had no sites with PD >3 mm and CAL >2 mm and also no radiographic evidence of alveolar bone loss. BOP was <10%.

The periodontitis stage III patients had a minimum of three teeth apart from the first molars and incisors showing CAL ≥5 mm and PD ≥6 mm and showed no>4 teeth loss because of periodontitis. Radiographic bone loss extending from coronal to middle third or beyond. Radiographic bone loss was determined from the tooth showing the most severe bone loss as a percentage of root length. If the values of bone loss %/age were between 0.25 and 1.0, the patients were assigned to grade B (n=16). If higher than 1.0, the patients were assigned to grade C (n=16).

Treatment

Patients in the periodontitis groups underwent quadrant-wise supra and subgingival mechanical scaling and root planing using ultrasonic scalers and manual instruments, after administration of local anesthesia. No periodontal intervention was carried out in the periodontally healthy controls.