Background and ObjectivePeriodontitis is an inflammatory disease that destroys periodontal tissues. Interleukin‐20 (IL‐20), on the other hand, is known as a potent angiogenic, chemotactic, and pro‐inflammatory cytokine associated with various chronic inflammatory disorders. IL‐20 has a significant role in the regulation of osteoclastogenesis and osteoblastogenesis. This study aimed to evaluate the effect of IL‐20 on periodontal destruction.MethodsIn this study, a total of 60 participants were included, 30 of whom were systemically and periodontally healthy (control group), and 30 were systemically healthy but had periodontitis (periodontitis group). Gingival crevicular fluid (GCF) and serum samples were collected from the participants for biochemical analysis. Enzyme‐linked immunosorbent assay was used to determine the levels of IL‐20, tumor necrosis factor (TNF)‐α, IL1β/IL‐10, RANKL/osteoprotegerin (OPG), and matrix metalloproteinase‐8 (MMP8). For statistical analysis, the independent t‐test, Pearson correlation coefficients, and the Chi‐square test were used.ResultsGCF IL‐20, RANKL, RANKL/OPG, serum IL‐20, RANKL, RANKL/OPG, MMP‐8, TNF‐α, IL‐1B, and IL‐1β/IL‐10 values were found to be statistically significantly higher in the periodontitis group than in the control group. GCF OPG and serum IL‐10 values were found to be statistically significantly higher in the control group than in the periodontitis group. No statistically significant difference was observed between the groups in serum OPG values. A statistically significantly positive correlation was observed between serum IL‐20 value and serum RANKL, RANKL/OPG, MMP‐8, TNF‐α, IL‐1β values, and periodontal clinical parameters. The ROC curves showed: AUC = 0.788 for GCF IL‐20, and AUC = 1.000 for serum IL‐20.ConclusionAccording to the results of the study, IL‐20 was found to be associated with periodontitis. The role of IL‐20 in periodontal pathogenesis is related to osteoclastogenesis and collagen degradation. It is conceivable that IL‐20 may increase bone destruction by both affecting the RANKL/OPG ratio and proinflammatory cytokines.