Influence of the treatment of periodontal disease in serum concentration of sirtuin 1 and mannose-binding lectin.

Influence of the treatment of periodontal disease in serum concentration of sirtuin 1 and mannose-binding lectin.

Caribé, Pérola Michelle Vasconcelos;Villar, Cristina Cunha;Romito, Giuseppe Alexandre;Pacanaro, Ana Paula;Strunz, Célia Maria Cassaro;Takada, Júlio Yoshio;Cesar, Luiz Antônio Machado;Mansur, Antonio de Padua;
journal of periodontology 2019
345
carib2019influencejournal

Abstract

Increased levels of periodontal pathogens disrupt the homeostasis between the host and its microbiota and increase susceptibility to periodontal diseases. Periodontitis increases the serum concentration of mannose binding lectin (MBL), which exacerbates local inflammatory processes. In animal studies, sirtuin-1 (SIRT1) was associated with protection against inflammation. This study analyzed the influence of nonsurgical periodontal treatment on serum levels of MBL and SIRT1.Forty patients with periodontitis and 38 periodontally healthy individuals (aged 45-79 years) were included. Periodontitis patients received scaling and root planing using machine driven and hand instruments. Clinical parameters, inflammatory biomarkers, MBL and SIRT1 levels were measured at baseline and at post-treatment.For all patients, an inverse correlation was observed between serum concentrations of MBL and SIRT1 (r = -0.30; p = 0.006). Periodontal treatment reduced serum concentrations of MBL (1099.35 ± 916.59 to 861.42 ± 724.82 ng/mL; p <0.001) and C-reactive protein (CRP) (6.05 ± 8.99 to 2.49 ± 2.89 mg/L; p = 0.009). By contrast, SIRT1 serum levels increased (1.06 ± 1.03 to 1.66 ± 1.64 ng/mL; p<0.001) following periodontal treatment.Periodontal treatment was associated with decreased serum concentrations of MBL and CRP and increased serum levels of SIRT1. Prospective studies are needed to assess the impact of these biomarkers on pathophysiology of periodontitis. This article is protected by copyright. All rights reserved.

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70464
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10.1002/JPER.19-0236
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