Estimation of salivary protectin D1 in periodontitis patients with metabolic syndrome following non-surgical periodontal therapy.

Abstract

Objectives: This study aims to assess periodontal and biochemical parameters and evaluate the salivary Protectin D1 levels in periodontitis patients with and without metabolic syndrome after non-surgical periodontal therapy.

Materials and methods: Forty patients were categorized into two groups: 20 patients in Group P (systemically healthy patients with stage II/III grade B periodontitis) and 20 patients in Group P+MS (patients with stage II/III grade B periodontitis and metabolic syndrome). Parameters including age, gender, height, weight, body mass index, waist circumference, socio-economic status, oral hygiene index (OHI), modified gingival index (MGI), probing pocket depth, clinical attachment levels, fasting blood glucose, HDL-c, total triglycerides, and blood pressure were recorded. Saliva samples were collected before scaling and root planing (PMPR). Full-mouth subgingival instrumentation (SGI) was performed on day 10, followed by reassessment on day 30.

Result: Demographic and baseline periodontal parameters were significantly higher in the P+MS group compared to the P group (p < 0.001). Both groups showed significant improvement in periodontal parameters after PMPR and SGI by the 30th day (p < 0.01). Salivary Protectin D1 levels increased significantly in both groups after treatment (p < 0.01), although no significant difference was observed between the groups at baseline and the 30th day. Protectin D1 levels positively correlated with HDL-c, blood pressure, and MGI at baseline, and with OHI, MGI, PPD, and CAL on the 30th day, but showed no significant association with periodontal parameters.

Conclusion: Periodontitis patients with metabolic syndrome exhibited worse baseline periodontal and biochemical profiles than periodontitis-only patients. Non-surgical periodontal therapy significantly improved periodontal health in both groups, with a concurrent increase in salivary PD1 levels, though no intergroup difference in PD1 expression was observed. While PD1 correlated with HDL-c, blood pressure, and periodontal indices, it did not differentiate the therapeutic response between groups, suggesting PD1 may reflect general resolution of inflammation rather than MS-specific pathways. Further research is needed to elucidate the role of PD1 in periodontitis with comorbid metabolic syndrome.

Clinical relevance: Protectin D1 holds promise as a biomarker for the effective management of periodontitis and metabolic syndrome, potentially aiding in both diagnosis and treatment strategies.