Abstract

Introduction: Periodontitis, a bacterial infection affecting periodontal tissues, results in the alveolar bone destruction. In particular, periodontitis is associated with Porphyromonas gingivalis (Pg)-induced inflammation and an increase of macrophages infiltrated into the gingiva. Sprouty (Spry) proteins function as negative regulators, which interfere with the activation of fibroblast growth factor (FGF) pathway by suppressing the mitogen-activated protein kinase (MAPK) signaling. We have previously showed that the suppression of Spry2 effectively induces the periodontal ligament migration along the root surface of the tooth and an increase of the alveolar bone, whereas impeding gingival epithelial down-growth toward bone defects.
Results: In the recent paper in our laboratory, we showed that Spry2 knockdown by Pg lipopolysaccharide (LPS) and interferon (IFN) γ stimulation converts macrophages from the M1 to M2 phenotype, and may effectively resolve inflammation by releasing anti-inflammatory cytokines in macrophages.
Conclusion: These studies show that the topical application of Spry2 inhibitors to bone loss may generate an appropriate environment for periodontal remodeling by inducing M2 macrophages, resolving inflammation in periodontitis, activating the periodontal ligament migration along the root surface of a tooth, promoting growth of the alveolar bone, and interfering with gingival epithelial down-growth toward bone defects. These findings thus provide a molecular basis for novel therapeutic targets in periodontal remodeling.