virulence strategies of porphyromonas gingivalis: mechanisms of immune evasion and disease induction

Porphyromonas gingivalis is recognized as a keystone pathogen in periodontitis and has been linked to multiple systemic pathologies, including cardiovascular disease, rheumatoid arthritis, and cancer. its capacity to evade host immune responses and modulate inflammation contributes to chronic infection and progressive tissue damage. this review examines the virulence factors of p. gingivalis, emphasizing mechanisms of immune evasion, macrophage polarization, disruption of microbial balance, and its role in systemic disease. a critical evaluation of recent studies highlights the molecular interactions between p. gingivalis and host immune cells. notable findings include inhibition of phagosome maturation, activation of inflammasomes, deregulation of the complement system, and impairment of lysosomal exocytosis. p. gingivalis penetrates the gingival epithelial barrier, enters host cells, and utilizes autophagy to support intracellular survival. it suppresses phagocytosis by cleaving cd14 and blocking phagosome–lysosome fusion through the c5ar1–tlr2 signaling pathway. furthermore, it drives macrophage polarization toward a pro-inflammatory m1 phenotype, sustaining chronic inflammation. beyond the oral cavity, p. gingivalis contributes to systemic disease by inducing foam cell formation in atherosclerosis, intensifying macrophage-driven inflammation in rheumatoid arthritis, and upregulating pd-l1 to suppress anti-tumor t-cell activity. understanding these immune evasion strategies is essential for developing targeted therapies for periodontitis and its systemic implications. future directions include the development of innovative antimicrobial agents, host-targeted therapies, and improved diagnostic platforms to combat p. gingivalis-related diseases.