IADR Abstract Archives
Avenanthramide-C shows alleviate inflammation and alveolar bone loss in periodontitis.
Objectives: Periodontal disease is a chronic inflammatory disease that leads to the gradual destruction of the supporting structures of the teeth including gums, periodontal ligaments, and alveolar bone. Recently, interests in alleviating symptoms of PD using natural compounds is increasing. Avenanthramide-C (Avn-C) is a polyphenol found only in oats. To date, the effect of Avn-C on PD pathogenesis has not been confirmed. Therefore, this study aimed to verify the protective effects of Avn-C on periodontal inflammation and subsequent alveolar bone erosion in vitro and in vivo.
Methods: To elucidate the effect of Avn-C on periodontal inflammation, we treated human GF and periodontal ligament (PDL) cells with different doses of Avn-C and examined the expression levels of inflammatory factors under in vitro periodontal pathological conditions by qRT-PCR. The total protein expression and phosphorylation level of three MAP kinases, namely, the ERK, p38 MAPK, and JNK, were determined in IL-1β-treated human GF. To explore the role of Avn-C in PD in vivo, we administered Avn-C to the ligature-induced PD mouse model via intra-gingival injection. The alveolar bone loss was evaluated as the cementum-enamel junction (CEJ) to alveolar bone crest (ABC) distance measured via μ-CT or histological analysis.
Results: Upregulated expression of catabolic factors, such as MMP1, MMP3, IL-6, IL-8, and COX2 induced by LPS and proinflammatory cytokines, IL-1β, and TNF-α, was dramatically decreased by Avn-C treatment in human gingival fibroblasts and periodontal ligament cells. Moreover, alveolar bone erosion in the ligature-induced PD mouse model was ameliorated by intra-gingival injection of Avn-C. Molecular mechanism studies revealed that the inhibitory effects of Avn-C on the upregulation of catabolic factors were mediated via ERK kinase and NF-κB pathway that was activated by IL-1β or p38 MAPK and JNK signaling that was activated by TNF-α, respectively.
Conclusions: Based on this study, we recommend that Avn-C may be a new natural compound that can be applied to PD treatment.
Methods: To elucidate the effect of Avn-C on periodontal inflammation, we treated human GF and periodontal ligament (PDL) cells with different doses of Avn-C and examined the expression levels of inflammatory factors under in vitro periodontal pathological conditions by qRT-PCR. The total protein expression and phosphorylation level of three MAP kinases, namely, the ERK, p38 MAPK, and JNK, were determined in IL-1β-treated human GF. To explore the role of Avn-C in PD in vivo, we administered Avn-C to the ligature-induced PD mouse model via intra-gingival injection. The alveolar bone loss was evaluated as the cementum-enamel junction (CEJ) to alveolar bone crest (ABC) distance measured via μ-CT or histological analysis.
Results: Upregulated expression of catabolic factors, such as MMP1, MMP3, IL-6, IL-8, and COX2 induced by LPS and proinflammatory cytokines, IL-1β, and TNF-α, was dramatically decreased by Avn-C treatment in human gingival fibroblasts and periodontal ligament cells. Moreover, alveolar bone erosion in the ligature-induced PD mouse model was ameliorated by intra-gingival injection of Avn-C. Molecular mechanism studies revealed that the inhibitory effects of Avn-C on the upregulation of catabolic factors were mediated via ERK kinase and NF-κB pathway that was activated by IL-1β or p38 MAPK and JNK signaling that was activated by TNF-α, respectively.
Conclusions: Based on this study, we recommend that Avn-C may be a new natural compound that can be applied to PD treatment.