Periodontal homeostasis is maintained by the dynamic equilibrium between cell death， differentiation and proliferation of resident cells in the periodontal microenvironment. Loss of resident periodontal ligament fibroblasts (PDLFs) has been a major challenge in the periodontal treatment. This study aimed to investigate the exact role of necroptotic cell death in periodontal diseases. Elevated levels of receptor-interacting protein serine-threonine kinases -1 (RIPK1)， phosphorylated RIPK3， mixed lineage kinase domain-like protein (MLKL)， phosphorylated MLKL and FLIP were observed in gingival tissues collected from patients with untreated chronic periodontitis; whereas no difference in caspase 8 was observed between the periodontitis and healthy control group. In contrast to the high incidence of necroptotic cell death in monocytes during live P. gingivalis infection with a low multiplicity of infection (MOI)， necroptosis was only observed in PDLFs with a high MOI. Priming PDLFs with frozen thawed monocytes enhanced proinflammatory responses to P. gingivalis infection; moreover， frozen thawed monocytes stimulation triggered RIPK1， RIPK3 and MLKL-mediated-necroptotic cell death in PDLFs. These results indicated that RIPK3 and MLKL-mediated-necroptotic cell death participated in the pathogenesis of periodontitis， and DAMPs released from monocytes after P. gingivalis stimulation by necroptosis triggered not only inflammatory responses， but also necroptosis of PDLFs.