Immunological pathways triggered by Porphyromonas gingivalis in periodontitis: New insights into molecular mechanisms

Periodontitis (PD) is one of the most common chronic inflammatory diseases worldwide. One of the keystone causative agents of PD is considered an anaerobic, Gram-negative, opportunistic oral bacterium - Porphyromonas gingivalis, which has evolved sophisticated mechanisms to evade host immune responses, thus contributing to persistent inflammation and periodontal tissue destruction. As reported in the literature, P. gingivalis interacts with various host receptors and manipulates key immunological signaling pathways, including Toll-like receptor (TLR) signaling, the complement system, and PI3K-AKT signaling. By disrupting these pathways, it subverts host defense mechanisms, promotes dysbiosis, and exacerbates PD progression. Furthermore, emerging evidence suggests, that P. gingivalis infections may have systemic implications, linking PD to conditions, such as, neurodegenerative disorders, rheumatoid arthritis, and cardiovascular diseases. We discussed in this review the molecular mechanisms by which P. gingivalis manipulates key signaling pathways of inflammation and provided a comprehensive review of the intricate molecular interactions between P. gingivalis and host immune responses, emphasizing the ability of this oral pathogen to alter fundamental signaling cascades. Continued exploration of the molecular interplay between this pathogen and the host immune system will not only enhance our knowledge of PD but may also have broader implications for understanding pathogenetic events of associated systemic inflammatory conditions.