A Study Into Systemic and Oral Levels of Proinflammatory Biomarkers Associated With Endpoints After Active Non-Surgical Periodontal Therapy.

aimTo analyse whether some selected inflammatory biomarkers collected from venous blood and gingival crevicular fluid (GCF) were associated with the outcome of non-surgical periodontal therapy. MATERIALS AND

methodsTwo-hundred and nine patients affected by periodontitis were enrolled in the study, who had undergone steps I and II therapy as well as a non-surgical re-instrumentation (NSRI) of periodontal pockets after 6 months. Serum (SE), plasma (PL) and GCF samples were quantitatively analysed for the following inflammatory biomarkers: active matrix metalloproteinase-8 (aMMP-8), prostaglandin E2 (PGE2) and surfactant protein D (SP-D). Therapy outcomes were evaluated using a 'treat-to-target' endpoint (T2T) at the patient level, defined as ≤ 4 sites with pocket depth ≥ 5 mm.

resultsPatients presented with 23 ± 6 teeth (mean ± SD) at baseline. After steps I and II therapy, 41.6% of the patients reached T2T and after NSRI 47.4%. Univariate analysis identified a potential association between high levels of PL-SP-D and more favourable treatment outcomes. Multivariate binary logistic regression adjusted for sex, mean baseline probing depth, diabetes and current smoking status confirmed an independent relationship between baseline PL-SP-D and the T2T after steps I and II therapy (aOR 0.432, p = 0.011), implying that a higher level PL-SP-D at baseline is associated with a > 50% reduced risk of failing T2T. However, no such association was found for PL-SP-D and NSRI.

conclusionHigher baseline PL-SP-D levels might be associated with more favourable treatment outcomes after steps I and II therapy. This may be due to its role in the regulation of neutrophil function. However, further investigation is required to confirm this hypothesis. If proven, PL-SP-D could play a role as a biomarker for identifying individuals who respond differentially to primary therapy.