Pyrroloquinoline quinone inhibits ligature-induced alveolar bone loss through regulation of redox balance and cell senescence.

It has been demonstrated that oxidative stress is related to periodontitis, and that pyrroloquinoline quinine (PQQ) acts as a powerful antioxidant. This study aimed to explore the effect of PQQ on ligature-induced alveolar bone loss in experimental periodontitis (EP) mice with/without PQQ in the diet. EP mice received a diet supplemented with PQQ for 2 weeks and were compared with sham (control) mice as well as untreated EP mice. Additionally, human periodontal ligament cells (hPDLCs) were treated with PQQ in the presence or absence of lipopolysaccharide (LPS). We found that the bone volume fraction, alkaline phosphatase activity, and the number of antioxidant cells were significantly decreased in EP mice compared with the sham mice, whereas PQQ administration rescued the above effects. In contrast, alveolar bone loss, osteoclast number, cell senescence-associated cells, and cytokines' expression were significantly increased in EP mice compared with the sham mice but were significantly decreased with PQQ supplementation in periodontal tissues. Furthermore, we found that antioxidant enzymes and Bmi-1 protein expression levels were downregulated, whereas the protein expression levels of cell senescence-related proteins including γ-H2AX, IL-6, IL-1β, p16, and p21 were significantly up-regulated in LPS-induced hPDLCs compared with the control cells. However, PQQ administration partially prevented these changes. These findings suggest that PQQ may alleviate periodontal damage through regulation of the redox balance and cell senescence. AJTR