Phloridzin Mitigates Aging-Associated Periodontitis by Restraining Inflammatory Cell Death

Aging is increasingly recognized as an important modifier of periodontitis progression. However, the direct impact of aging-related cellular processes on periodontal tissue degeneration remains insufficiently understood. This study aimed to investigate the protective effects of phloridzin on aging-associated experimental periodontitis and to elucidate its potential role in modulating aging-related alveolar bone loss.

HPDLCs were exposed to H₂O₂ to induce oxidative stress-induced premature senescence, after which the effects of phloridzin on cellular senescence, inflammatory responses, and osteogenic differentiation capacity were evaluated. In addition, an aging-associated experimental periodontitis model was established in Wistar rats through D-galactose administration combined with ligature placement. Phloridzin was concurrently administered, and alveolar bone loss, periodontal tissue morphology, and systemic aging-and inflammation-related markers were analyzed to assess the in vivo effects of phloridzin.

Phloridzin attenuated oxidative stress-induced senescence-associated changes, suppressed aging-associated inflammatory responses in HPDLCs, and preserved osteogenic differentiation capacity. In vivo, phloridzin administration significantly reduced alveolar bone loss and alleviated periodontal tissue damage in the aging-associated experimental periodontitis model. The protective effects observed in both cellular and animal models suggest that regulation of excessive inflammatory responses during aging is important for maintaining periodontal tissue integrity.

These findings indicate that phloridzin alleviates aging-associated alveolar bone loss by modulating aging-related inflammatory processes. Collectively, the results suggest that phloridzin may contribute to the improvement of periodontal tissue function under aging-related conditions.