ArticleFrontiers in cellular and infection microbiology2026
Non-surgical periodontal therapy and systemic inflammatory biomarkers in patients with periodontitis and carotid plaque burden: a pilot study.
Article in Frontiers in cellular and infection microbiology, 2026. 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
Introduction: Systemic inflammation is a key contributor to the pathophysiology of carotid plaque burden (CpB). Increasing evidence supports a link between periodontitis and systemic conditions, including endothelial dysfunction, and CpB. This study aimed to explore inflammatory mediators involved in cardiovascular disease that may represent shared mechanistic pathways between periodontitis and carotid plaque burden, and to determine whether non-surgical periodontal therapy modulates systemic inflammatory activity. Methods: A pilot study was conducted on subjects presenting with both periodontitis and CpB. Of 87 initially screened participants, 10 met the inclusion criteria and completed the study. Periodontal parameters-probing pocket depth (PPD), clinical attachment loss (CAL), and bleeding on probing (BOP)-were recorded. Systemic inflammatory biomarkers, including matrix metalloproteinase-8 (MMP-8), myeloperoxidase (MPO), lipoprotein-associated phospholipase A2 (Lp-PLA2), and soluble CD40 ligand (sCD40L), were analyzed. Results: Participants demonstrated severe periodontal disease, with mean PPD of 5.5 mm (maximum 8 mm), mean CAL of 6.46 mm (maximum 12 mm), and BOP of 67%. Periodontal therapy was associated with significant reductions for MMP-8 (25.64 ± 20.31 vs. 10.60 ± 3.41ng/mL post-treatment; p = 0.010) and Lp-PLA2 (p = 0.0195). MPO and sCD40L showed decreasing trends that did not reach statistical significance (p = 0.097 and p = 0.156, respectively). Correlation analyses demonstrated limited associations between baseline biomarker levels and periodontal clinical parameters, except for an inverse correlation between sCD40L and probing pocket depth (ρ = -0.77, p = 0.015). Conclusion: Inflammatory biomarkers may represent important mechanistic links between periodontitis and imaging-confirmed carotid atherosclerotic plaques. Within the limitations of this pilot study, non-surgical periodontal therapy was associated with reductions in selected systemic inflammatory biomarkers, supporting the feasibility of investigating the periodontitis-carotid plaque axis in larger translational cohorts. Larger studies are needed to validate these findings.
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