BACKGROUND Periodontal ligament stem cells (PDLSCs) possess characteristics of multi-potential differentiation and immuno-modulation, and PDLSCs-mediated periodontal tissue regeneration is regarded as a hopeful method for periodontitis treatment. Recent studies demonstrated that RIP3 and caspase8 regulate bacteria-induced innate immune response and programmed necrosis, which is also called necroptosis. This study aimed to determine the role of the RIP3/Caspase8 signal pathway on necroptosis of PDLSCs under the inflammatory microenvironment, both [i]in vitro[/i] and [i]in vivo[/i]. MATERIAL AND METHODS PDLSCs were cultured, and transmission electron microscopy and flow cytometry were used to detect necroptosis. PCR, ALP, and Alizarin Red S staining were used to assess the effect of necroptosis on osteogenesis differentiation of PDLSCs [i]in vitro[/i], while HE and Masson staining were taken after the nude mouse subcutaneous transplant experiment. RESULTS Our research indicates that RIP3/caspase8 can regulate the immune response of PDLSCs, and blockade of RIP3/caspase8 can protect the biological characteristics of the PDLSCs, effectively promoting periodontal tissue regeneration in the inflammatory microenvironment. CONCLUSIONS Inhibiting RIP3/caspase8 can effectively promote periodontal tissue regeneration in the inflammatory microenvironment.
Keywords: Necrosis; Periodontal Ligament; Receptor-Interacting Protein Serine-Threonine Kinases; periodontitis.