期刊
JOURNAL OF CLINICAL PERIODONTOLOGY
卷 47, 期 3, 页码 309-318出版社
WILEY
DOI: 10.1111/jcpe.13227
关键词
antimicrobial peptides; gingipain; hBD-2; hBD-3; inflammatory cytokines; periodontitis; Porphyromonas gingivalis
资金
- Turku University Foundation
- Suomen Hammaslaakariseura Apollonia
- Paulo foundation, Finland
- Hacettepe University Scientific Research Projects Coordination Units
- Scientific and Research Council of Turkey (TUBITAK) [BIDEB-1059B141700759]
- Sigrid Juselius foundation, Finland
- Finnish Dental Society Apollonia [12194]
- Hacettepe University
- University of Turku
Aim 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. Materials and Methods 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. Results Subgingival plaque counts of P. gingivalis (p = .001) and gingipain activity (p < .001), as well as interleukin (IL)-1 beta (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. Conclusions 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.
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