ArticleClinical oral investigations2025
Estimation of salivary protectin D1 in periodontitis patients with metabolic syndrome following non-surgical periodontal therapy.
Article in Clinical oral investigations, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectivesThis 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
methodsForty 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.
resultDemographic 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.
conclusionPeriodontitis 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.
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