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Increased levels of interleukin‐32 isoforms alpha, beta, gamma, and delta in the gingival crevicular fluid and plasma of the patients with periodontitis
Author(s) -
Öngöz Dede Figen,
Gökmenoğlu Ceren,
Deveci Emre Taha,
Çelen Selman,
Avci Bahattin,
Kara Cankat,
Çanakçi Varol
Publication year - 2021
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/jre.12796
Subject(s) - periodontitis , medicine , gastroenterology , interleukin , chronic periodontitis , alpha (finance) , interleukin 1β , gene isoform , beta (programming language) , dentistry , cytokine , chemistry , surgery , construct validity , computer science , patient satisfaction , programming language , biochemistry , gene
Background and Objective Interleukin (IL)‐32, which has been recently reported to be associated with periodontitis, has been suggested to have pleiotropic effect due to its 9 different isoforms. The aim of this study was to investigate the levels of IL‐32α, IL‐32β, IL‐32γ, IL‐32δ isoforms in gingival crevicular fluid (GCF) and plasma before and after non‐surgical periodontal treatment in patients with periodontitis (P). Materials and Methods Twenty‐seven P and 27 periodontally healthy controls (C) were recruited in this study. Non‐surgical periodontal treatment was performed to periodontitis patients. GCF and plasma sampling and clinical periodontal parameters were evaluated before and 1 month after treatment. Enzyme‐linked immunosorbent assay was used to analyze the levels of IL‐32α, IL‐32β, IL‐32γ, IL‐32δ isoforms in GCF and plasma samples. Results The levels of IL‐32α, IL‐32β, IL‐32γ, and IL‐32δ in plasma and GCF were significantly higher in patients with periodontitis than healthy controls ( P < .001). In P group, plasma and GCF IL‐32α, IL‐32β, IL‐32γ, and IL‐32δ levels after non‐surgical periodontal treatment were lower when compared to baseline ( P < .001). Moreover, there was a positive correlation between GCF and plasma IL‐32α, IL‐32β, IL‐32γ, and IL‐32δ levels in all groups at baseline and after treatment ( P < .05). Conclusion The study supported that there was a relationship between elevated levels of IL‐32 isoforms and periodontitis. Also, our novel findings suggest that the pro‐inflammatory role of IL‐32 in the periodontitis may be originated from IL‐32α, IL‐32β, IL‐32γ, and IL‐32δ isoforms.