抄録
Dysregulation of growth and inflammatory mediators might contribute to defective tissue homeostasis and healing, as commonly observed in sedentary lifestyles and in conditions such as diabetes mellitus and periodontitis. Periodontitis is an inflammatory disease characterized by extensive bone resorption. Sodium fluoride (NaF) causes proliferation and differentiation, and modulates the activity of growth factors. In this study, we investigated the effects of NaF on insulin-like growth factor (IGF) 1 and 2 in Goto-Kakizaki (GK) rats, a spontaneous model of type 2 diabetes induced by Porphyromonas gingivalis, an important colonizer of the oral cavity that has been implicated in periodontitis. NaF strongly inhibited the P. gingivalis-induced alveolar bone loss. That effect was accompanied by decreased levels of TNF-α, IL-1β, and RM4, which were up-regulated in P. gingivalis-induced diabetes model. Consistent with the anti-inflammatory effect, NaF inhibited osteoclast markers, the receptor activator of nuclear factor kappa B ligand (RANKL) and Cathepsin K protein expression. IGF-1, -2 was strongly expressed by periodontal ligament, fibroblasts, particularly those in areas close to cementum and bone surfaces in NaF-treated groups. In the periodontal ligament, strong staining was noted in the fiber bundles inserting into alveolar bone and cementum. Our findings suggest the mechanism of IGF signaling by which NaF alters periodontal tissue repair in type 2 diabetes.
