Periodontitis is a chronic inflammatory disease characterized by progressive destruction of periodontal supporting tissues and alveolar bone loss. Emerging evidence suggests that ferroptosis contributes to oxidative imbalance and periodontal tissue damage, however, the role of SC6 in regulating ferroptosis during periodontal inflammation remainsunclear. This study investigated the protective effects of SC6 against inflammation, ferroptosis, and osteogenic impairment in vitro. Human periodontal ligament cells (HPDLCs) were stimulated with Porphyromonas gingivalis lipopolysaccharide (Pg-LPS) to establish an inflammatory microenvironment and subsequently treated with SC6. SC6 significantly attenuated Pg-LPS–induced inflammatory responses, reduced lipid peroxidation and intracellular iron accumulation, and restored the expression of ferroptosis-suppressive markers. Moreover, SC6 alleviated Pg-LPS–induced osteogenic dysfunction, as evidenced by increased expression of osteogenic markers and enhanced mineralization capacity. Mechanistically, SC6 suppressed Bach1 expression and promoted HO-1 activation. Bach1 silencing partially diminished the ferroptosis-suppressive effects of SC6, indicating that its protective effects are mediated through the Bach1/HO-1 signaling pathway. Collectively, these findings suggest that SC6 mitigates periodontal cellular injury by regulating ferroptosis via the Bach1/HO-1 pathway.