Periodontitis is a chronic inflammatory disease caused by dysregulated microbial-host interactions, with Porphyromonas gingivalis (P. gingivalis) playing a pivotal role. This bacterium expresses a variety of virulence factors that disrupt both innate and adaptive immunity, allowing it to survive and proliferate in the host, leading to the destruction of periodontal tissues and its association with systemic diseases. P. gingivalis can breach the gingival epithelial barrier, internalize into epithelial cells, enhance autophagy, invade host tissues, and survive. Moreover, the bacterium can promote its evasion through the dysregulation of the complement system, degradation of antimicrobial peptides, and impairment of phagocytic cell functions. Investigating the immune evasion mechanisms of P. gingivalis is of significant importance for developing new therapeutic strategies against periodontitis.