Under inflammatory conditions, HIF‐1α is rapidly upregulated, driving glycolytic flux and shifting macrophage polarization toward the pro‐inflammatory M1 phenotype.[28] Additional analysis of macrophage polarization markers demonstrated that pro‐inflammatory genes associated with the M1 phenotype, such as HIF‐1α, NOD‐like receptor thermal protein domain‐associated protein 3 (NLRP3), and IL‐1β, were significantly elevated in periodontitis‐associated macrophages (Figure S1a—c, Supporting Information). Here, IL1B is linked to periodontitis.