Elucidating the molecular healing of intrabony defects following non‐surgical periodontal therapy: A pilot study

Objective To elucidate the molecular healing of intrabony defects following non‐surgical periodontal therapy (NSPT) using gingival crevicular fluid (GCF). Background Data Currently limited information is available regarding the GCF of intrabony defects and the change in biomarker levels in the GCF a...

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Veröffentlicht in:Journal of periodontal research 2024-02, Vol.59 (1), p.53-62
Hauptverfasser: Koidou, Vasiliki P., Hagi‐Pavli, Eleni, Nibali, Luigi, Donos, Nikolaos
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Sprache:eng
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Zusammenfassung:Objective To elucidate the molecular healing of intrabony defects following non‐surgical periodontal therapy (NSPT) using gingival crevicular fluid (GCF). Background Data Currently limited information is available regarding the GCF of intrabony defects and the change in biomarker levels in the GCF at early time points following treatment interventions. Methods Twenty‐one patients (Periodontitis Stage III or IV) who have received NSPT, contributing one intrabony defect and one healthy site were included in this study. GCF sampling was performed at baseline, 1 day, 5 days and 3 months after NSPT. Multiplex bead immunoassays allowed the profiling of GCF for 27 markers, associated with inflammation and repair/regeneration. A mixed effects model with Bonferroni correction for multiple comparisons was employed to compare the changes in the levels of GCF markers over time. Results Following NSPT, changes were observed for several GCF markers, marked by significant increases 1 day post‐intervention, before returning to baseline levels by 3 months. Specifically, GCF concentrations of IL‐2, IL‐4, IL‐6, IL‐8, MMP‐1, MMP‐3, TIMP‐1 and FGFb significantly increased 1 day after NSPT. Signs of activation of cellular senescence were observed 1 day following treatment of intrabony defects, rapidly regressing by 5 days. Conclusion Significant molecular changes are observed as early as 1 day following NSPT in intrabony defects, along with activation of cellular senescence.
ISSN:0022-3484
1600-0765
DOI:10.1111/jre.13207