Abstract
Background. Periodontitis is an infectious and inflammatory disease of the supporting tissues of the tooth caused by specific microorganisms or a group of microorganisms and, if not treated, leads to progressive degradation of the supporting tissues and subsequent loss of the teeth affected. The aim of this study was to evaluate the effects of IL-36γ on periodontitis by enhancing the TLR4 and MAPK signaling pathways.
Methods. In this pilot study, 50 patients with generalized moderate-to-severe chronic periodontitis and 50 individuals with healthy periodontium, who were candidates for crown lengthening (CL), were selected based on inclusion criteria. The tissue samples were taken during pocket depth surgery (for the test group) and CL surgery (for the control group). The macrophage cells of the inflammatory tissues were extracted and stimulated by TLR4 proteins in a time-dependent manner; then IL-36γ levels in macrophages were investigated. Data were analyzed using descriptive statistics (means ± standard deviations and frequency percentages). Repeat measurement test was used to compare IL36γ expression in MAPK and TLR4 pathways at different time intervals. ANCOVA was used to compare IL36γ expression at different time intervals between the two pathways. Statistical analysis was performed using SPSS 17 at a significance level of P<0.05.
Results. The results of the current study showed a significant relation between TLR4 and IL-36γ (P<0.001); in tissues with generalized moderate-to-severe chronic periodontitis, there was a significant relation between the condition and IL-36γ (P<0.0001). This study also showed that TLR4 and MAPK levels increased in the presence of IL-36γ.
Conclusion. According to the present study, it was concluded that IL-36γ concentrations increased in periodontitis, which could trigger MAPK and TLR4 pathways.