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Gingival tissue human beta-defensin levels in relation to infection and inflammation.

Authors
  • Özdemir, Meltem1, 2
  • Caglayan, Feriha2
  • Bikker, Floris J3
  • Pussinen, Pirkko4
  • Könönen, Eija1, 5
  • Yamalik, Nermin2
  • Gürsoy, Mervi1
  • Fteita, Dareen1
  • Nazmi, Kamran3
  • Güncü, Güliz N2
  • Pietiäinen, Milla4
  • Tolvanen, Mimmi1
  • Gürsoy, Ulvi Kahraman1
  • 1 Department of Periodontology, Institute of Dentistry, University of Turku, Turku, Finland. , (Finland)
  • 2 Department of Periodontology, Faculty of Dentistry, Hacettepe University, Ankara, Turkey. , (Turkey)
  • 3 Department of Oral Biochemistry, Academic Centre for Dentistry Amsterdam, Free University and University of Amsterdam, Amsterdam, The Netherlands. , (Netherlands)
  • 4 Department of Oral and Maxillofacial Diseases, University of Helsinki, Helsinki, Finland. , (Finland)
  • 5 Oral Health Care, Welfare Division, City of Turku, Turku, Finland. , (Finland)
Type
Published Article
Journal
Journal Of Clinical Periodontology
Publisher
Wiley (Blackwell Publishing)
Publication Date
Dec 03, 2019
Identifiers
DOI: 10.1111/jcpe.13227
PMID: 31799742
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

To profile gingival tissue levels of human beta-defensin (hBD)-2 and hBD-3 in relation to gingival inflammation, Th17-related cytokine concentrations, Porphyromonas gingivalis counts, and gingipain and total protease activities. Gingival tissue and subgingival plaque samples were collected from 21 periodontitis patients including 48 periodontal pocket sites with marginal, mild, or moderate to severe inflammation. hBD levels were determined by immunodetection, P. gingivalis counts with real-time polymerase chain reaction, protease activities with fluorogenic substrates, and cytokine concentrations with Luminex technique. Data were statistically analysed using Kruskal-Wallis and Mann-Whitney U tests and Spearman correlation coefficients. Subgingival plaque counts of P. gingivalis (p = .001) and gingipain activity (p < .001), as well as interleukin (IL)-1β (p = .012), IL-10 (p = .024), IL-17A (p = .002), IL-17F (p = .006), and IL-23 (p = .036) concentrations were elevated in severely inflamed sites, whereas no change was observed in hBD-2 and hBD-3 levels. Negative correlations were found between protease activity and hBD-2 (p = .033) and hBD-3(p = .003) levels. Shift in gingival inflammation from marginal to mild stage is related to elevations in subgingival plaque P. gingivalis counts and gingipain activity, but not to tissue hBD levels. Negative correlations between hBDs and total protease activity suggest the degradation of these antimicrobial peptides in progressed inflammation. © 2019 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

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