Serum IL-17, IL-34, and CXCL12 in Plaque-Induced Gingivitis: An Exploratory Case-Control Study

Abstract

Background: Plaque-induced gingivitis is a common inflammatory periodontal condition in which alterations in inflammatory and immune mediators such as IL-17, IL-34, and CXCL12 may reflect the host response to dental plaque.

Objective: This study assessed whether plaque-induced gingivitis was accompanied by altered serum concentrations of three types of interleukin IL-17, IL-34, and CXCL12 and, in a small ancillary subset, whether these markers varied with the dominant cultured isolate.

Methodology: This exploratory case-control study enrolled 30 adults: 15 with plaque-induced gingivitis and 15 periodontally healthy controls. Serum IL-17, IL-34, and CXCL12 were measured by enzyme-linked immunosorbent assay. Between-group comparisons were based on two-sided Mann-Whitney U tests with Holm adjustment for the three prespecified biomarkers, and Welch unequal-variance t tests were used as sensitivity analyses. In eight gingivitis cases, dominant aerobic isolates were recovered by culture and the corresponding cytokine distributions were summarized descriptively.

Results: Compared with controls, gingivitis cases showed higher serum IL-17 (median 83.62 vs 65.07 pg/mL; Holm-adjusted p = 0.0084) and a markedly higher serum IL-34 concentration (766.17 vs 64.98 pg/mL; Holm-adjusted p = 1.02 × 10^-5). Serum CXCL12 remained similar in the two groups (p = 0.8682). Within the ancillary bacterial subset, cytokine values differed numerically across isolates, but the subgroup sizes were too small to support organism-level inference.

Conclusion: In this exploratory cohort, plaque-induced gingivitis was accompanied by higher circulating IL-17 and, more strikingly, IL-34. Among the three analytes, IL-34 yielded the clearest separation between groups and deserves validation in larger serum-based studies of early gingival inflammation. The ancillary bacterial findings were descriptive and should not be read as evidence for isolate-specific effects.

Bangladesh Journal of Infectious Diseases, June 2026;13(1):300-307