King's College London

Research portal

Molecular profiling of intrabony defects' gingival crevicular fluid

Research output: Contribution to journalArticlepeer-review

Vasiliki P. Koidou, Eleni Hagi-Pavli, Samantha Cross, Luigi Nibali, Nikolaos Donos

Original languageEnglish
Number of pages10
JournalJournal of Periodontal Research
Issue number1
Early online date17 Nov 2021
Accepted/In press2021
E-pub ahead of print17 Nov 2021

Bibliographical note

Funding Information: This study was supported by Barts Charity Grant MGU0389, UK. Publisher Copyright: © 2021 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd

King's Authors


Aim: To profile, for the first time, the gingival crevicular fluid (GCF) of intrabony defects against a wide array of inflammatory and regenerative markers. Materials and methods: Twenty-one patients contributed one intrabony defect and one periodontally healthy site. Clinical and radiographic measures were obtained. GCF samples were analyzed with multiplex bead immunoassays over 27 markers previously identified by our group. Comparisons were performed using Wilcoxon matched-pairs signed-ranks tests, using a Bonferroni corrected α = 0.05/27 = 0.0019. Results: Intrabony defect sites presented significantly increased GCF volume and disease-associated clinical and radiographic characteristics (p <.05). Intrabony defect sites presented significantly increased IL-1α, IL-1β, IL-6, IFN-γ, and MMP-8 levels compared with periodontally healthy sites (p <.0019). For regeneration markers, significantly higher FGF basic and VEGF levels were observed (p <.0019). Notably, traits of cell senescence were identified for the first time in the GCF. Conclusions: The differentiation of intrabony defects from periodontally healthy control sites can be based on clinical and radiographic measures and on a differentiated GCF profile that is site-specific. Alongside catabolic processes, through significant up-regulation of inflammation and connective tissue remodeling, unique molecular characteristics of intrabony defects may render them a microenvironment amenable to regeneration. Traits of the senescence-associated secretory phenotype may suggest the existence of senescent cells during periodontal inflammation in intrabony defects.

View graph of relations

© 2020 King's College London | Strand | London WC2R 2LS | England | United Kingdom | Tel +44 (0)20 7836 5454