NLRC4 and Hyperglycemia: In 2021, a study [90] found that hyperglycemia induces macrophage scorch death and leads to impaired cell function and gingival destruction may be involved in the pathogenesis of diabetic periodontal disease, and that GSDMD activation and pyroptosis in the hyperglycemic state is mediated by NLRC4 inflammatory vesicles, then NLRC4 phosphorylation may be a potential therapeutic target to inhibit this process; a contemporaneous study [91] demonstrated that metformin also delayed the damage to periodontal tissue from hyperglycemia-induced macrophage scorching inflammatory response.