Periodontitis is a chronic inflammatory disease characterized by dysbiotic biofilms and a dysregulated host immune response that drives progressive destruction of periodontal supporting tissues. Conventional mechanical and antimicrobial therapies primarily target bacterial burden but often fail to achieve long-term disease control due to persistent host-mediated inflammation. Increasing evidence highlights the complement system, particularly complement component C3, as a central regulator of periodontal inflammation and bone loss. Dysregulated C3 activation amplifies inflammatory signaling through generation of C3a and C5a, promotes osteoclastogenesis, and sustains tissue destruction via crosstalk with Toll-like receptors. C3-targeted therapies, especially peptide-based inhibitors such as compstatin analogs and AMY-101, have demonstrated significant anti-inflammatory and bone-protective effects in experimental models and early-phase clinical trials. These agents offer a novel host-modulatory approach that suppresses pathogenic inflammation while preserving essential immune functions. This review summarizes the role of C3 in periodontal pathogenesis, evaluates current evidence on C3 inhibition, and discusses future perspectives for precision-based periodontal and peri-implant therapy.