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There has been a systematic review of studies that used FEA in dental sciences, but no adequate risk of bias (RoB) analysis technique has been developed. Therefore, the development and validation process of RoB in studies using the finite element analysis in dentistry (ROBFEAD) tool is described. In the first phase of development, the scope of the tool and possible modifications were covered, and validation was done in the second phase. The developed tool comprised 6 domains and a total of 22 guiding questions in these domains. This article proposes the development and validation of ROBFEAD, a tool for measuring RoB in finite element research in dentistry. [ABSTRACT FROM AUTHOR]

Intracellular signaling complexes of the innate immune system orchestrate the development of inflammation. Porphyromonas gingivalis is a commensal bacterium that induces periodontal pyroptosis. The transcription factor Dec1 can regulate the expression of inflammatory molecules. In this study, we investigated whether a deficiency of Dec1 activates/represses Caspase-1 and/or Gasdermin-D in periodontal pyroptosis, resulting in the release of the proinflammatory mediator interleukin-1β. Dec1 expression in human periodontal ligament fibroblasts (HPDLFs) treated with P. gingivalis lipopolysaccharide (LPS) was assessed and pyroptosis activation was determined by microscopy, qRT-PCR and Western blot analysis. Moreover, a siRNA targeting Dec1 was introduced into HPDLFs to determine the function of Dec1 in periodontal pyroptosis and a Dec1-deficient experimental mouse model of periodontitis was used. Treatment of HPDLFs with P. gingivalis LPS-stimulated levels of cleaved-Caspase-1 and cleaved-GSDMD and increased levels of phosphorylated NF-κB and interleukin-1β. In contrast, Dec1 knockdown maintained cellular homeostasis with low levels of pyroptosis. Treatment with P. gingivalis alleviated periodontal pyroptosis in PDLFs of wild-type mice and a Dec1 deficiency subsequently repressed the inflammatory effect of P. gingivalis. These results reveal for the first time the novel function of Dec1 in periodontal pyroptosis, suggesting that Dec1 is a crucial target to prevent periodontal inflammation. [ABSTRACT FROM AUTHOR]