The aim of this study was to evaluate the anti-inflammatory activities of the main constituents and epoxides derived from the essential oils (EOs) obtained from Tagetes lucida, Cymbopogon citratus, Lippia alba and Eucalyptus citriodora. The main constituents were isolated and then epoxidized with dimethyldioxirane (DMDO) in an acetone solution. The anti-inflammatory effects were studied in vitro on murine macrophages stimulated with bacterial lipopolysaccharide. All tested samples inhibited both nitric oxide (NO) and prostaglandin E2 (PGE2) production, but the EO from T. lucida and carvone exhibited the highest inhibitory effects. Most of the studied samples altered the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). The studied epoxides inhibited both NO and PGE2 production, but at the RNA level, they primarily inhibited COX-2. These results show, for the first time, the anti-inflammatory effects of epoxides generated from the main components of EOs from Colombian plants.
Apical periodontitis (AP) is a chronic immunoinflammatory disease influenced by complex interactions between microbial factors and host immune response. Although genetic susceptibility has been implicated in AP, evidence is limited, particularly in admixed populations. This exploratory study aimed to assess whether functional polymorphisms in MMP1 (rs1799750), IL10 (rs1800872), and IL17A (rs7747909) are associated with susceptibility to radiographically defined AP in a Colombian population. A case–control design was employed, including individuals with radiographic evidence of AP and controls without periapical lesions. Genotyping was performed using TaqMan® assay. The association between single-nucleotide polymorphisms and AP was evaluated using a dominant inheritance model. Effect sizes were estimated as odds ratios (ORs) with 95% confidence intervals (CIs), and p-values were adjusted using the Benjamini–Hochberg false discovery rate (FDR) procedure. The MMP1 rs1799750 polymorphism was associated with increased susceptibility to AP (OR = 3.47, 95% CI = 1.40–8.58; FDR = 0.013). Similarly, the IL10 rs1800872 variant was significantly associated with AP risk (OR = 3.00, 95% CI = 1.52–5.91; FDR = 0.007). The strongest association was observed for IL17A rs7747909 (OR = 8.95, 95% CI = 3.61–22.15; FDR < 0.001). This exploratory candidate-gene study provides preliminary evidence suggesting that genetic variations in MMP1, IL10, and IL17A may contribute to susceptibility to AP in the Colombian population. Given the exploratory design, modest sample size, and absence of ancestry adjustment or functional validation, these findings should be interpreted cautiously and confirmed in larger ancestry-informed cohorts integrating host genetic and microbial data.